Cardionerds: A Cardiology Podcast

As the burden of cardiovascular disease increases in the United States, the importance of enhanced screening tools, early risk prediction, and prevention strategies grows. Novel risk scoring methods, including polygenic risk scores (PRS), may help identify patients that benefit from early intervention and risk modification. In this episode, we discuss how a PRS is calculated, how to incorporate a PRS into clinical practice, and current barriers to the equitable implementation of risk scores. In terms of frontiers in clinical genetics we also discuss the burgeoning field of pharmacogenetics and how pharmacogenetics may be used to identify responders and non-responders to certain therapies. Join CardioNerds Dr. Jessie Holtzman (CardioNerds Academy Chief and Chief Resident and soon FIT at UCSF), Dr. Alaa Diab (CardioNerds Academy Fellow and Medicine Resident at GBMC), and student doctor Hirsh Elhence (CardioNerds Academy Intern and medical student at USC Keck School of Medicine) as they discuss frontiers in clinical genetics with Dr. Pradeep Natarajan (Director of Preventive Cardiology, Massachusetts General Hospital). Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. This episode was developed in collaboration with the American Society of Preventive Cardiology and is supported with unrestricted educational funds from Illumina, Inc. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. This CardioNerds Cardiovascular Genomics series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Pearls • Notes • References CardioNerds Cardiovascular Genomics PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls – Frontiers in Clinical Genetics in Cardiovascular Prevention For common diseases like coronary artery disease, rare mutations may confer a several-fold increased risk of disease – for instance, in familial hypercholesterolemia, a single rare mutation may confer as much as a three-fold increase in risk of coronary artery disease. However, for most common diseases, the overall cumulative impact of several common genetic variants may be greater than that of a monogenetic trait. Family history is a particularly coarse predictor of CV risk, highlighting the need for polygenic risk scores. In particular, younger patients with borderline cardiovascular risk may benefit from the use of a polygenic risk score in the determination of their overall cardiovascular risk profile. A polygenic risk score (PRS) is a weighted sum of several risk-conferring alleles. The weight assigned to an allele is determined by the strength of the association between the allele and CV disease, as determined by genome-wide association studies (GWAS). The data used for genome-wide associated studies in cardiovascular disease have historically included populations primarily of European ancestry. However, more data is being collected from diverse patient cohorts to increase the external validity and broader applicability of such studies. Pharmacogenetic polygenic risk scores may be used to predict drug efficacy and toxicity, as well as to identify biologically plausible drug targets for clinical trial design. Show notes – Frontiers in Clinical Genetics in Cardiovascular Prevention What is a polygenic risk score (PRS)? Monogenic conditions are those in which a variant in a single gene causes a pathological phenotype. For example, familial hypercholesterolemia is often the result of a mutated allele in the LDL receptor gene. In contrast, polygenic risk suggests that there are variants in multiple genes that all confer risk independently, each with a small individual effect size. By aggregating many variants, a risk score may be able to provide an estimate as to the degree of one’s risk of cardiovascular disease. By comparing the allele frequencies of genes between patients with and without cardiovascular disease, risk-conferring alleles may be identified. These studies are called genome-wide association studies (GWAS). From GWAS, PRS can then be calculated by aggregating several risk-conferring alleles. What is the clinical utility of PRS? Current uses of PRS Family history is a coarse predictor of CV disease. The addition of a PRS to a risk assessment may improve the clinician’s ability to risk stratify patients. Calculating PRS can help identify patients who need early intervention, even in the absence of traditional risk factors (such as hypercholesterolemia or diabetes mellitus). For example, imagine a patient in the top 20th percentile for polygenic risk with a relatively normal LDL. Despite the lack of hyperlipidemia, some evidence may sugg

In this episode, we discuss the utility of veno-arterial extra-corporeal membrane oxygenation (VA-ECMO) for the temporary management of biventricular failure and cardiogenic shock requiring full cardiopulmonary support. Here, we define the types of ECMO and describe the unique physiology of this mechanical circulatory support platform, as well as review the potential complications and management strategies. Most notably, we highlight indications for and contraindications to the use of VA-ECMO and review the importance of patient selection.  Lastly, we discuss de-escalation and de-cannulation strategies for patients on VA-ECMO as a bridge to recovery. Join Dr. Amit Goyal (CardioNerds Cofounder and FIT at Cleveland Clinic), Dr. Yoav Karpenshif (Series Co-chair and FIT at University of Pennsylvania), and Dr. Megan Burke (Episode FIT Lead and FIT at University of Pennsylvania) as they learn about how to care for some of our sickest patients from Dr. Ann Gage, interventional and critical care cardiologist at Centennial Heart. At the beginning of the episode, enjoy a message from the very first CardioNerds Scholar, Dr. Katie Vaughan (Chief Resident and soon Cardiology Fellow at BIDMC). Episode notes were developed by Dr. Megan Burke. Audio editing by CardioNerds Academy Intern, Hirsh Elhence. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – Biventricular Failure and the Use of VA-ECMO Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a form of temporary mechanical circulatory support that can do the work of both the heart and lungs. The ECMO circuit is a narcissist, i.e. cannulas are named in reference to the circuit and not the patient (“inflow” vs “outflow”). The decision to utilize ECMO should be made by a multidisciplinary shock team and patient selection is KEY! ECMO physiology rule #1: VA-ECMO increases LV afterload Patients on VA-ECMO should be monitored with a PA catheter and an arterial line in the right arm Show notes – Biventricular Failure and the Use of VA-ECMO Notes drafted by Dr. Megan Burke. 1. What is ECMO and what are the different types? Extracorporeal membrane oxygenation (ECMO) is a temporary form of mechanical life support that comes in two flavors: veno-arterial, or “VA” and veno-venous, or “VV.”  VV-ECMO supports extracorporeal gas exchange in the setting of acute respiratory failure VA-ECMO provides full circulatory support in addition to gas exchange, doing the work of both the heart and lungs.  2. What are the components and “anatomy” of the VA-ECMO circuit? The circuit is made up of the following major components: Venous (inflow) cannula Centrifugal Pump Oxygenator (also responsible for CO2 removal) Arterial (outflow) cannula The cannulas are named in reference to the ECMO circuit, not the patient. Dr. Gage suggests that we think of the ECMO circuit (and mechanical circulatory support in general) as narcissistic, i.e. flow is always in reference to the device. Gas exchange happens in the oxygenator. In the oxygenator blood flows through thin filaments that allow for diffusion of oxygen and carbon dioxide. Gas flows in the opposite direction of blood flow to maximize diffusion through the countercurrent effect. Oxygenation is determined by rate of blood flow through the oxygenator and FiO2 delivered. Carbon dioxide removal is determined by rate of countercurrent gas flow, referred to as the sweep speed. 3. What are the indications for VA-ECMO? VA-ECMO is utilized in the setting of severe refractory cardiogenic shock (in the setting of left, right, or biventricular failure) and cardiac arrest. It is a temporary mechanical circulatory support platform, and should be used as a bridge to recovery or a more durable therapy (i.e. durable mechanical support or transplant). Due to lack of randomized data, there are no consensus guidelines for the use of VA-ECMO, and the decision to implement it should be made as part of a multidisciplinary cardiogenic shock team. Common indications include cardiogenic shock, refractory ventricular arrhythmias, massive pulmonary embolism, cardiac arrest, and failure to wean from cardiopulmonary bypass during surgery. The absolute and relative contra-indications to ECMO vary by institution. Given the high mortality rates for patients on VA-ECMO (hospital mortality is approxi

The CardioNerds Cardiovascular Genomics Series continues! In this episode Dr. Dan Ambinder (CardioNerds Cofounder and Interventional Cardiologist), Dr. Anjali Wagle (FIT Ambassador at Johns Hopkins) and Dr. James Sampognaro (medicine resident at Johns Hopkins Osler Medicine Residency) learn from Dr. Allison Hays (Associate Professor of Medicine, Division of Cardiology, Johns Hopkins CMR researcher and Medical Director of Echocardiography) and Dr. Cindy James (Associate Professor of Medicine and certified genetic counselor at Johns Hopkins with research focusing on cardiovascular genetic counseling and arrhythmogenic cardiomyopathies). They discuss arrhythmogenic RV cardiomyopathy as the context to learn about genetic counseling and family screening.  Episode script and notes were developed by Dr. Anjali Wagle. Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah. This episode was developed in collaboration with the American Society of Preventive Cardiology and is supported with unrestricted educational funds from Illumina, Inc. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. This CardioNerds Cardiovascular Genomics series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs. Check out this REVIEW describing the “Multimodality Imaging in Arrhythmogenic Right Ventricular Cardiomyopathy” by Nitin Malik, Allison Hays, and colleagues.   For related episodes, please enjoy these case-based discussions:  Ep 56. Case Report: Arrhythmogenic Desmoplakin Cardiomyopathy – Northwestern University  Ep 74. Case Report: Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) – Summa Health  Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Pearls • Notes • References CardioNerds Cardiovascular Genomics PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes – Genetic Counseling & Family Screening in Arrhythmogenic Cardiomyopathies Notes (developed by Dr. Anjali Wagle)   What is the underlying pathophysiology of arrhythmogenic RV cardiomyopathy (ARVC)?  Fibrofatty replacement cardiac myocytes  Associated with genetically mediated disruption of desmosomal proteins   This leads to thinning and weakness of the heart that can lead to aneurysms and progressive dilatation and failure of the right ventricle (RV)  How is ARVC diagnosed?  2010 taskforce criteria (Marcus et al, 2010):    RV structural abnormalities including findings seen on echocardiogram, MRI, and RV angiography  Pathological criteria  Repolarization abnormalities   Depolarization/conduction abnormalities   Ventricular arrhythmias   Genetics and/or family history   How does ARVC present?   Young, healthy individual will have symptoms of arrhythmias (syncope, pre-syncope, SCD) or heart failure  Family screening   What are the inheritance and genetic factors of ARVC?  Autosomal dominant pattern  Low penetrance and variable expressivity   Half of patients who are index cases will be found to have a mutation in the desmosomal gene.   What are the most common mutations associated with ARVC?  Most commonly the genes involved are plakophilin-2 (PKP-2) and desmoplakin.   For PKP-2 the most common mutations are truncating mutations.   In patients who have inherited two truncating mutations, this will result in neonatal lethality.   Is there a difference in the genetic factors of left and right arrhythmogenic cardiomyopathy?   ACM is disproportionally a right dominated cardiomyopathy. Left dominated cardiomyopathy has a different genetic profile.   Pathogenic variants in desmoplakin disproportionally cause biventricular forms of ACM or left dominated forms.   What are the echocardiographic findings in ACM?  Wall thinning and aneurysmal dilation in the sub-tricuspid region, RV outflow tract, or base also known as the “triangle of dysplasia.”  Progression of disease tends to be from the base to the apex.  Why is cardiac MRI the preferred imaging modality in ACM?  Higher spatial resolution and improved visualization of the right ventricle  Can imaging help define prognosis in ACM?  Top two strongest measures of prognostic value in ACM are:  RV fractional change area < 33%  Tricuspid annular plane systolic exertion < 1.7cm   References – Genetic Counseling & Family Screening in Arrhythmogenic Cardiomyopathies Malik, N., Mukherjee, M., Wu, K. C., Zimmerman, S. L., Zhan, J., Calkins, H., James,

Congenital heart disease is the most common birth defect, affecting 1 in 100 babies. Amongst these ventricular septal defects are very common with the majority of patients living into adulthood. In this episode we will be reviewing key features of VSDs including embryologic origin, anatomy, physiology, hemodynamic consequences, clinical presentation and management of VSDs. Dr. Tommy Das (CardioNerds Academy Program Director and FIT at Cleveland Clinic), Dr. Agnes Koczo (CardioNerds ACHD Series Co-Chair and FIT at UPMC), and Dr. Anu Dodeja (Associate Director for ACHD at Connecticut Children’s) discuss VSDs with expert faculty Dr. Keri Shafer. Dr. Shafer is an adult congenital heart disease specialist at Boston Children’s Hospital, and an assistant professor of pediatrics within Harvard Medical School. She is a medical educator and was an invited speaker for the inaugural CardioNerds Sanjay V Desai Lecture, on the topic of growth mindset. Script and notes were developed by Dr. Anu Dodeja. Audio editing by CardioNerds Academy Intern, Shivani Reddy. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls – Ventricular Septal Defects Most common VSDs: Perimembranous VSD The shunt volume in a VSD is determined largely by the size of the defect and the pulmonary vascular resistance. VSDs cause left to right shunt. The long-term effects are left sided chamber dilation, as is the case with PDAs (post-tricuspid shunts) VSDs can be associated with acquired RVOTO, double chamber right ventricle, LVOTO/sub aortic membrane formation, and aortic regurgitation from aortic valve prolapse. Eisenmenger syndrome results from long-term left-to-right shunt, usually at higher shunt volumes. The resulting elevated pulmonary artery pressure is irreversible and leads to a reversal in the ventricular level shunt, desaturation, cyanosis, and secondary erythrocytosis. Endocarditis prophylaxis is not indicated for simple VSD. It is required for 6 months post VSD closure, in patients post VSD closure with a residual shunt and in Eisenmenger patients with R—>L shunt and cyanosis. Show notes – Ventricular Septal Defects Notes (developed by Dr. Anu Dodeja): What are types OF VSD? (Please note that there are several nomenclatures) Perimembranous VSD Most common type of VSD – 80% of VSDs Occurs in the membranous septum and can be associated with inlet or outlet extension Located near the tricuspid and aortic valves, often time can be closed off by tissue from the septal leaflet of the tricuspid valve and associated with abnormalities in the septal leaflet of the tricuspid valve secondary to damage from the left to right shunt Can be associated with acquired RVOTO, double chamber right ventricle, LVOTO/sub aortic membrane formation On TTE, the parasternal short axis view at the base demonstrates this type of VSD at the 10-12 o’clock position. Muscular VSD Second most common VSD – 15-20% of VSDs Completely surrounded by muscle, usually restrictive, can be multiple defects These usually close spontaneously by direct apposition of the muscular borders. Supracristal (also known as sub-arterial/sub-pulmonary/conal/juxta-arterial) Represent 5% of VSDs Located beneath the semilunar valves in the conal or outlet septum Do not usually close spontaneously May be associated with progressive aortic regurgitation due to prolapse of the right aortic cusp and aneurysm of the sinus of Valsalva. Aortic valve prolapse: Prolapsing of the right or non-coronary aortic valve cusp may initially reduce the degree of left-to-right shunt but results in development of aortic regurgitation Aortic valve prolapse usually involves the right coronary cusp and less frequently the non-coronary cusp  In its early stage: prolapse occurs only in the systolic phase because of the venturi effect resulting from the rapid shunt flow through the defect In later stages the

The field of Cardiovascular Genomics has advanced tremendously over the past two decades, having a significant clinical impact and changing the perception of the role and scope of genetic testing in several cardiovascular domains. To kickstart the Cardiovascular Genomics series, CardioNerds Dr. Sara Coles (FIT at Duke University), Dr. Colin Blumenthal (CardioNerds Academy faculty and FIT at UPenn), and Dr. Karla Asturias (CardioNerds Academy fellow and medicine resident at Pennsylvania Hospital) have a great discussion with Dr. James Daubert, a clinical electrophysiologist at Duke University, with a particular interest in inherited arrhythmia syndromes and sports cardiology. In this episode, we review basic concepts of cardiovascular genomics and genetics in electrophysiology while discussing when to (and when not to!) test our patients and their families and how to approach those results. Audio editing by CardioNerds academy intern, Pace Wetstein. This episode was developed in collaboration with the American Society of Preventive Cardiology and is supported with unrestricted educational funds from Illumina, Inc. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. This CardioNerds Cardiovascular Genomics series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Pearls • Notes • References CardioNerds Cardiovascular Genomics PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – Genetics in Electrophysiology The first step is identifying the right phenotype! Getting the right phenotype is crucial, as genetic testing done in a patient without a clear phenotype (or an incorrect one) would lead to significant anxiety, unnecessary tests and interventions, and potentially misleading and dangerous conclusions for patients and their families. Genetic testing typically should be reserved for patients with a confirmed or suspected diagnosis of an inherited disease or for individuals with a previously diagnosed pathogenic variant in a first-degree relative.1 Discuss with your patient! Genetic counseling is essential and recommended for all patients before and after genetic testing. It should include a thorough discussion of risks, benefits, and possible outcomes, including variants of uncertain significance.2 Cardiovascular genetics is a dynamic and rapidly evolving field. New information can cause a variant of uncertain significance to be reclassified as a pathogenic or likely pathogenic variant or to be downgraded to benign or likely benign as variant databases expand. Another possibility is that new research might identify novel genes for a particular disease, which could warrant retesting, particularly for phenotype-positive and genotype-negative patients.1 Brugada syndrome is an inherited arrhythmogenic disorder characterized by ST-segment elevation in the right precordial leads and malignant ventricular arrhythmias, with occasional conduction disease and atrial arrhythmias. It is diagnosed in patients with ST-segment elevation ≥ 2 mm in ≥ 1 lead among the right precordial leads, with a type I morphology (J-point elevation with slowly descending or concave ST segment elevation merging into a negative T wave), shown in the image below. This pattern can be observed spontaneously or after provocative drug testing (e.g., procainamide). Pathogenic genetic variants in SCN5A that result in loss of function of the cardiac sodium channel are identified in approximately 20% of cases.3,4 Image adapted from Batchvarov VN. The Brugada Syndrome – Diagnosis, Clinical Implications and Risk Stratification. Eur Cardiol Rev. 2014;9(2):82. doi:10.15420/ECR.2014.9.2.82 Measure the QT interval yourself! A correct determination of the QT interval is essential. Although automatic measurements are widely available, the interval can be underestimated or overestimated, particularly in atrial arrhythmias or complex T-wave morphologies. Determining the end of the T-wave can be challenging in this setting, and can be assessed through the tangent method, which determines the end of the T-wave by the intersection between the baseline (U-P segment) and the “tangent” drawn to the steepest last limb of the presumed T-wave.5,6 Image adapted from Postema PG, De Jong JSSG, Van der Bilt IAC, Wilde AAM. Accurate electrocardiographic assessment of the QT interval: teach the tangent. Hear Rhythm. 2008;5(7):1015-1018. doi:10.1016/J.HRTHM.2008.03.037 When encountering a patient with prolonged QT, it is essential to exclude secondary causes like QT-prolonging drugs and electrolyte imbalances. As the acute cause is removed and the acute illness resolves, “see what happens

CardioNerds Cofounder Dr. Amit Goyal is joined by Dr. Douglas Salguero (Internal medicine resident), Dr. Francisco Ujueta (Cardiology fellow), and Dr. Priscilla Wessly (Chief cardiology fellow) from the Columbia University Division of Cardiology at Mount Sinai Medical Center in Miami to discuss a rare case of isolated non-compaction cardiomyopathy. Expert commentary is provided by Dr. Christos Mihos (Director, Echocardiography Laboratory, Columbia University Division of Cardiology, Mount Sinai Medical Center). Audio editing by CardioNerds Academy Intern, Shivani Reddy.   Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media – Non-Compaction Cardiomyopathy Episode Schematics & Teaching The etiology has been a constant debate since 1980. It has been debated among researchers and clinicians whether LVNC is a physiologic or a pathologic manifestation. Waning et al., classified 327 unrelated patients into 3 categories: 1) genetic, 2) probably genetic, or 3) sporadic, identifying the most common mutations: MYH7, MYBPC3 and TTN in the genetic LVNC patients, which mostly encode for sarcomere, Z-disc and nuclear-envelope proteins. This supports the hypothesis that the inherited phenotype can arise from a gene mutation possibly during embryogenesis, disrupting the physiologic compaction of normally developing myocardium, which progresses from the base to the apex of the cardiac tissue. It is estimated that genetic LVNC accounts approximately 18-44% of cases, with autosomal dominant transmission being the most common form of inheritance. Physiologic remodeling with prominent trabeculations may be noted in athletes and pregnant women, in comparison to pathologic remodeling which may be encountered in patients with cardiomyopathy (e.g. pressure or volume load).  (1) There is no pathognomonic signs or symptoms in LVNC. LVNC patients may encounter various potential clinical characteristics. Presentations are myriad and include heart failure symptoms (HFrEF or HFpEF), ventricular tachycardia (VT/VF), atrial fibrillation, thromboembolism including cerebrovascular accident (CVA), and syncope. In a cohort of 95 probands with LVNC investigated in Europe, as many as 32.3% had an ICD/CRT-D implantation, with 11.8% experiencing a cardiovascular death and 18.2% having an appropriate ICD shock. (2) Imaging plays a key role in diagnosis for LVNC. The identification and diagnosis of LVNC is evaluated using 2D echocardiography. The initial proposed method by Chin et al., evaluated the size of the trabeculation in the center. (3) The most commonly used criteria, Jenni et al. (4), entail the following four finding: Two-layer structure, with a thin compacted layer and a thick non-compacted layer measure at end-systole at the parasternal short-axis view. LVNC is defined by a ratio of N/C > 2 Absence of co-existing cardiac structural abnormalities Prominent, excessive trabeculations and deep intra-trabecular recesses Recesses supplied by intraventricular blood on color doppler Cardiac MRI has increased the diagnostic accuracy in the diagnosis of LVNC. It has been suggested that a NC/C ratio of > 2.3 in diastole distinguished pathological non-compaction, with sensitivity of 86% and a specificity of 99%, respectively. Although studies have shown an increase specificity with cardiac MRI, caution is needed as it may overestimate the presence of LVNC. Late gadolinium enhancement which suggests myocardial fibrosis or scar has been shown to have some prognostic value in LVNC patients. (5) Management for LVNC is multifaceted. As above,LVNC has a variety of presentations and prevailing manifestations will differ among patients. Therefore, the diagnostic and management approach much be personalized for a given patient. Heart failure with reduced ejection fraction is the most common presentation, thus treatment follows guided directed medical therapy, including ACEi/ARB/ARNi, beta-blockers, MRA, SGLT2i, etc. The risk for thromboembolism in patients with LVNC has not been well-established although case-series have noted an increase in clot formation due to the increase in intertrabecular recesses. Although no definitive criteria for anticoagulation have been suggestive in patients with LVNC and atrial fibrillation who meet current recommendations. There is a weak recommendation for anticoagulation in patients with LVNC and LVEF < 40% with or without atrial fibrillation. (6) Arrhythmias in LVNC is frequent. Ambulatory rhythm monitoring may be used to detect atrial fibrillation and ventricular arrhythmias. As with our patient, individuals with LVNC who survive an episode of sustained ventricular tachycardiac or sudden card

CardioNerds (Dan Ambinder), episode lead Dr. Sarah Fahnhorst (ACHD Cardiologist at Spectrum Health in Grand Rapids, Michigan), and series co-chair Dr. Agnes Koczo (fellow at UPMC) learn about ASD from Dr. Richard Krasuski (ACHD Cardiologist and Director of ACHD at Duke University). Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares An atrial septal defect (ASD) is a common congenital heart disease most often diagnosed in childhood, but initial presentation can be in adulthood. ASDs are abnormal communications between the left and the right atrium.  There are four types of ASDs with different embryologic origins. If the defects are large, they will require percutaneous or surgical closure. Unrepaired defects can lead to symptoms of shortness of breath, exercise intolerance, recurrent chest infections, or pulmonary hypertension. This episode of CardioNerds will review the natural history, embryologic origin, diagnostic modalities/findings, indication for closure and long term complications of repaired and unrepaired atrial septal defects.  Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls – Atrial Septal Defects It’s a CLASSIC! – On physical exam a wide fixed split S2 along with a systolic ejection murmur due to increased blood flow across the pulmonary valve and potentially a diastolic rumble across the tricuspid valve are CLASSIC findings with atrial septal defects.  Atrial septal defects are not all the same. There are four types of atrial septal defects: secundum ASD, primum ASD, sinus venosus and coronary sinus defects (NOTE – the latter are atrial level defects which actually do not involve the interatrial septum). The different types warrant a different approach to closure.  Use your tools and if your suspicion is high for an atrial septal defect, keep looking. Sinus venosus defects can easily be missed since the superior vena cava is difficult to image in adults. Diagnostic tools include: history and physical exam (USE the stethoscope), ECG, echocardiogram, cardiac MRI, cardiac CT, and cardiac catheterization. Not all defects NEED to be closed immediately. Moderate-large defects with a shunt greater than 1.5:1 should be closed due to increased risk of pulmonary hypertension and arrhythmias, barring contraindications.  Surgery was previously the gold standard for closure of ASDs, but many defects especially secundum atrial septal defects are closed in the cath lab.    Show notes – Atrial Septal Defects Notes (developed by Dr. Sarah Fahnhorst What are the four different types of atrial level defects? Secundum atrial septal defect Most common type of atrial septal defect (75%) Located in the center of the atrial septum (fossa ovalis) Hole in the primum septum due to deficiency of the septum secundum Primum atrial septal defect Accounts for 15-20% of ASD Located at the inferior portion of the atrial septum In the spectrum of atrioventricular septal defects/endocardial cushion defects Defect in the development of the septum primum Associated with cleft left AV valve, ventricular septal defects, and subaortic stenosis Sinus venosus defect Accounts for 5-10% of atrial level defect Not a “septal” defect! Located near the superior vena cava-right atrial junction or very rarely at the mouth of the inferior vena cava 80-90% of sinus venosus defects are associated with partial anomalous pulmonary venous return Coronary sinus defect Least common <1% of all ASD Not a “septal” defect! Communication between the coronary sinus and left atrium (“unroofed” coronary sinus)  Not often seen in isolation but are associated with complex congenital heart disease such as heterotaxy syndrome What are the presenting signs, symptoms and diagnostic findings associated with atrial level defects? If small, then asymptomatic Moderate to large defects: shortness of br

CardioNerds Cofounder Dr. Amit Goyal is joined by an esteemed group of UCLA cardiology fellows – Dr. Patrick Zakka (CardioNerds Academy Chief), Dr. Negeen Shehandeh (Chief Fellow), and Dr. Adrian Castillo – to discuss a case of primary cardiac angiosarcoma. An expert commentary is provided by Dr. Eric Yang, beloved educator, associate clinical professor of medicine, assistant fellowship program director, and founder of the Cardio-Oncology program at UCLA. Case synopsis: A female in her 40s presents to the ED for fatigue that had been ongoing for approximately 1 month. She also developed night sweats and diffuse joint pains, for which she has been taking NSAIDs. She was seen by her PCP and after bloodwork was done, was told she had iron deficiency so was on iron replacement therapy. Vital signs were within normal limits. She was in no acute distress. Her pulmonary and cardiac exams were unremarkable. Her lab studies showed a Hb of 6.6 (MCV 59) and platelet count of 686k. CXR was without significant abnormality, and EKG showed normal sinus rhythm. She was admitted to medicine and received IV iron (had not consented to receiving RBC transfusion). GI was consulted for anemia work-up. Meanwhile, she developed a new-onset atrial fibrillation with rapid ventricular response seen on telemetry, for which Cardiology was consulted. A TTE was ordered in part of her evaluation, and surprisingly noted a moderate pericardial effusion circumferential to the heart. Within the pericardial space, posterior to the heart and abutting the RA/RV was a large mass measuring approximately 5.5×5.9 cm. After further imaging work-up with CMR and PET-CT, the mass was surgically resected, and patient established care with outpatient oncology for chemotherapy. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media – primary cardiac angiosarcoma Episode Schematics & Teaching Pearls – primary cardiac angiosarcoma The pericardium is composed of an outer fibrous sac, and an inner serous sac with visceral and parietal layers.   Pericardial masses can be primary (benign or malignant) or metastatic. There are other miscellaneous pericardial masses.  Imaging modalities for the pericardium include echocardiography, cardiac CT and cardiac MRI. There is also role for PET-CT in pericardial imaging for further characterization of pericardial masses.   Cardiac angiosarcomas are extremely rare but are the most common cardiac primary malignant tumors.  Evidence-based management if lacking because of paucity of clinical data given the rarity of cardiac angiosarcomas. Surgery is the mainstay of therapy. Radiotherapy and chemotherapy are often used as well.  Notes – primary cardiac angiosarcoma Pericardial Anatomy  The pericardium is a fibroelastic sac composed of two layers.   Outer layer: fibrous pericardium (<2 mm thick)  Inner layer: serous pericardium, two-layered sac.  Visceral pericardium: adherent to underlying myocardium  Parietal pericardium: lines fibrous sac.  Between the serous layers, there is the pericardial cavity which normally contains up to 50 cc pericardial fluid.  Pericardial Masses  Benign  Lipoma: slow-growing, collection of adipose cells, thought to arise in AV groove  Teratoma: benign germ cell tumors, often right sided. Can cause compressive symptoms of RA, SVC, PA, aortic root.   Fibroma: solid mass of connective tissue  Hemangioma: vascular mass, often arising from visceral pericardium  Malignant  Sarcoma: various types including angiosarcoma and liposarcoma.   Lymphoma: usually non-Hodgkin B-cell lymphoma, often in immunocompromised patients  Mesothelioma: no apparent association with asbestos. Pericardial effusions with nodules/plaques are seen.  Metastatic  Often associated with hemorrhagic pericardial effusions  Breast cancer, lung cancer, melanoma and renal cell carcinoma are most common  Pericardial Imaging  Echocardiography  Advantages:   widely available  low cost   safe  can be performed in multiple settings (e.g., HD unstable)  Disadvantages:   limited view/windows  operator dependent  technical difficulties (lung disease, obesity, surgical bandages)  limited tissue characterization  Cardiac Computed Tomography  Advantages:  Superior tissue characterization compared to echocardiography  Can identify extra-cardiac disease  Identification of calcification  Pre-operative planning  High spatial resolution   Disadvantages:   Use of ionizing radiati

It’s another session of CardioNerds Rounds! In these rounds, Dr. Priya Kothapalli (Interventional FIT at University of Texas at Auston, Dell Medical School) joins Dr. Deepak Bhatt (Dr. Valentin Fuster Professor of Medicine and Director of Mount Sinai Heart) to discuss the nuances of antithrombotic therapy. As one of the most prolific cardiovascular researchers, clinicians, and educators, CardioNerds is honored to have Dr. Bhatt on Rounds, especially given that Dr. Bhatt has led numerous breakthroughs in antithrombotic therapy. Come round with us today by listening to the episodes of #CardsRounds! Audio editing by CardioNerds Academy Intern, Dr. Christian Faaborg-Andersen. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes.  Speaker disclosures: None Challenging Cases – Atrial Fibrillation with Dr. Hugh Calkins CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes – Antithrombotic Management with Dr. Deepak Bhatt Case #1 Synopsis: A woman in her early 70s with a history of hypertension, hyperlipidemia, and paroxysmal atrial fibrillation presented with sudden-onset chest pressure and diaphoresis while at rest and was found to have an acute thrombotic 99% mid-LAD occlusion. The patient received OCT-guided PCI with a single drug-eluting stent. We discussed what the appropriate antithrombotic strategy would be for a patient with recent acute coronary syndrome and atrial fibrillation. Case #1Takeaways According to the recent 2021 revascularization guidelines, in patients with atrial fibrillation undergoing PCI and taking oral anticoagulant therapy, it is recommended to discontinue aspirin after 1 to 4 weeks while maintaining P2Y12 inhibitors in addition to a non-vitamin K oral anticoagulant or warfarin. There are two recent trials – AUGUSTUS and the ENTRUST-AF PCI trial – that evaluated regimens of apixaban and edoxaban, respectively, that support earlier findings reporting lower bleeding rates in patients maintained on oral anticoagulant plus a P2Y12 inhibitor compared to triple therapy. Of note, none of these trials were specifically powered for ischemic endpoints, but when pooling data from these trials, rates of death, MI and stent thrombosis with dual therapy were similar to those seen in patients on triple therapy. Additionally, all of these patients enrolled in these trials were briefly treated with triple therapy after PCI before the aspirin was discontinued. In the 2021 guidelines, it is noted that analyses of stent thrombosis suggest that 80% of events occur within 30 days of PCI. Thus, it is reasonable to consider extending triply therapy to 1 month after PCI in high risk patients to reduce risk of stent thromboses. In AUGUSTUS, 90% of patients received clopidogrel as their P2Y12 inhibitor Case #2 Synopsis: A man in his mid-50s with a history of peripheral vascular disease with prior SFA stent for chronic limb ischemia, hyperlipidemia, tobacco use, diabetes, and chronic kidney disease presented with a two day history of “reflux” that was worse with exertion and that improved with rest and associated with diaphoresis. He was diagnosed with an NSTEMI. His LHC revealed 99% mid-RCA thrombotic occlusion with moderate disease in the LAD. He underwent thrombectomy and PCI with a single drug-eluting stent to the RCA. We discussed his short-term and long-term antithrombotic therapy Case #2 Takeaways There were several things discussed regarding the management of this patient’s “poly-vascular disease.” One of the aspects was what to do with his antithrombotic therapy after one year and specifically how the COMPASS trial may apply to this patient. In the COMPASS trial, more than 27,000 patients with stable CAD or peripheral arterial disease (PAD) were randomly assigned to rivaroxaban plus aspirin, rivaroxaban alone, or aspirin alone with a mean follow-up of about 23 months. Of note, the dose of rivaroxaban in the combination arm was 2.5 mg orally twice per day. The patients on combination therapy compared to aspirin alone had a 23% relative risk reduction in CV mortality (1.7 vs. 2.2%; HR 0.78 [95% CI 0.64-0.96]) and nearly 50% reduction in ischemic stroke. As expected, there was high rates of major bleeding in the combination arm (3.1 vs. 1.9%; HR 1.7 [95% CI 1.4-2.05]). As with most decisions in medicine, each clinician wou

CardioNerd (Daniel Ambinder) and series co-chairs Mark Belkin (AHFT Fellow, University of Chicago) and Karan Desai (Cardiologist, Johns Hopkins), join fellow lead, Dr. Pablo Sanchez (FIT, Stanford) for a discussion with Dr. Ryan Tedford (Professor of Medicine at the Medical University of South Carolina) about Right Ventricular (RV) predominant cardiogenic shock. In this episode we explore risk factors, pathophysiology, hemodynamics, and treatment strategies in this common and complex problem. We dissect three cases that epitomize the range of diagnostic dilemmas and management decisions in RV predominant shock, as Dr. Tedford expertly weaves us through the pathophysiology and decision-making involved in managing the “people’s ventricle.” Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds internship program, CardioNerds academy fellow, and IM resident at Brigham and Women’s Hospital). The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – RV Predominant Cardiogenic Shock The degree of RV dysfunction and failure are modulated by stretching its capacity to tolerate insults from deranged afterload, preload, and contractility. Afterload insults are MUCH LESS tolerated than other insults and broadly comprise the most common pathophysiologic cause of both acute and chronic RV failure. RV and left ventricular (LV) function are anatomically and physiologically connected.  Progressive derangements in RV function can lead to the deadly “RV spiral,” in which poor RV function causes lower LV preload, leading to hypotension, and thus worsening RV perfusion and function. In RV failure/shock, some basic tenets including treating reversible causes, optimizing preload and afterload, and using inotropes and/or temporary MCS for as limited time as possible. Many acute RV failure patients can recover, but multiorgan injury plays an important role. Therefore, thoughtful and expeditious use of mechanical circulatory support is important. Show notes – RV Predominant Cardiogenic Shock Notes drafted by Dr. Pablo Sanchez. What is the basic difference between RV dysfunction and failure? Dysfunction: Abnormalities in systolic/diastolic function of the RV, but not necessarily to the point of leading to end-organ perfusion defects. RV dysfunction leads to poor outcomes regardless of mechanism.1 Failure: Clinical syndrome of inability of RV to maintain adequate output despite adequate preload. 1 How is the RV different from the LV and what impact does it have on pathophysiology and hemodynamics? The LV and RV originate from different embryologic “heart fields.”1,2 The RV wall is thinner and more compliant and has only two layers (instead of 3 like the LV).3 Furthermore, unlike the LV which has a significant proportion of endocardial and epicardial transverse myocardial fibers, the RV myocardial fibers are aligned in a longitudinal plane for the most part. Thus, a more significant proportion of RV systolic contraction is longitudinal – base of the ventricle moving towards the apex. The RV is crescent-shaped and has a large surface-to-volume ratio meaning smaller inward motion ejects the same stroke volume. 1 Hemodynamically, the RV takes blood from a low-pressure venous system and gives it to a distensible system with low impedance (the normal pulmonary circuit at baseline typically has a resistance one-tenth of the systemic resistance). Therefore, volume loads (preload) are much better handled than pressure (afterload).1 What is RV-PA coupling? As Dr. Tedford noted, RV-PA coupling describes “the interaction of RV contractility and afterload (resistive and pulsatile components). It is the most comprehensive description of RV function and therefore the Gold Standard.” Whether we are referring to the LV or RV, the basic concept of coupling describes the energy transfer between ventricular contractility and arterial afterload. RV-PA coupling has typically been assessed by pressure-volume loops, with ventricular contractility assessed by end-systolic elastance (a load-independent measure of systolic function) and arterial afterload by effective arterial elastance. MODUS OPERANDI: RV dysfunction and eventual failure is modulated by stretching its capacity to tolerate insults from afterload, preload, and contractility. What leads to ACUTE right heart failure? Most commonly

CardioNerds (Dr. Patrick Azcarate, Dr. Teodora Donisan, and Amit Goyal) discuss Radiation-Associated Cardiovascular Disease (RACD) with Dr. Eric Yang, cardio-oncologist, assistant professor of medicine, and associate fellowship program director at UCLA. RACD is a consequence of radiation treatment for various mediastinal tumors (breast, lung, lymphoma). It is the second most common cause of morbidity and mortality in patients treated with mediastinal radiation for cancer. While novel techniques decrease radiation exposure during cancer treatment, the incidence is expected to increase because of historical practices and delayed onset of symptoms. The prevalence of RACD is difficult to estimate given under-recognition. Additionally, most of the data comes from patients treated with radiation techniques from decades ago. In this discussion we review every nook and cranny of RACD to help guide you the next time you see a patient with a history of chest radiation. Review this CardioNerds Case Report of radiation associated cardiovascular disease for more: Episode #169. Chest pain in a Young Man – “A Gray (Gy) Area” – UC San Diego. Audio editing by CardioNerds Academy Intern, student doctor Yousif Arif. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan.  Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Pearls • Notes • References • Production Team CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – Radiation-Associated cardiovascular disease Due to the legacy effect, the incidence of RACD will continue to increase in the next few years. When treating patients with a history of mediastinal radiation, we should remember to ask: How much radiation was given? Could the heart have been exposed? Radiation can affect every part of the heart by causing coronary artery disease (CAD), valvulopathy, myocardial disease, conduction disease, and pericardial disease. Exposure to ~25-30 Gy or more significantly increases the risk but RACD can occur at lower doses. Try to delay surgery as much as possible and do all you can in one operation to avoid re-operation in the future. For revascularization, percutaneous coronary intervention (PCI) is typically preferred over coronary artery bypass grafting (CABG) but the choice should be individualized in consultation with a multidisciplinary heart team experienced in the management of RACD. In general, for aortic valve disease, transcatheter replacement is recommended over surgical aortic valve replacement. For mitral valve disease, surgical replacement is recommended over repair. Every decision should be made with a heart team approach and made unique to that specific patient. Show notes – Radiation-Associated cardiovascular disease Notes were drafted by Dr. Patrick Azkarate. 1. Understand the pathophysiology of RACD Ionizing radiation has the potential to damage DNA. Both normal cells and cancer cells get damaged, but cancer has less effective DNA repair mechanisms and therefore malignant cells are more vulnerable to radiation therapy. After radiation causes acute damage, this sets off an inflammatory cascade leading to myofibroblast activation, fibrosis and collagen deposition, and subsequent stiffening of the myocardium and vessels. 2. What may increase one’s risk of developing RACD? Young age (<50 years-old) at the time of radiation High cumulative dose (>30 Gy) or high dose of radiation fractions (>2 Gy/day) Anterior or left chest radiation (breast cancer, lung cancer, lymphoma) Pre-existing cardiovascular disease Tumor in or next to the heart Concomitant chemotherapy (e.g. anthracyclines) 3. What are some techniques being used to reduce radiation exposure? Shielding Respiratory gating techniques (e.g. deep inspiratory breath-hold, activated breathing control) Smaller repeated fractions Narrow tangential beams Proton therapy 4. What are prevention and screening strategies for RACD? Annual history and physical examinationTreat pre-existing conditionsScreen for RACD (myocardial, valvular, pericardial, CAD, or conduction system disease)5 years post-exposure, screen for CAD and consider stress test every 2 years10 years post-exposure, screen for valvular heart disease with an echocardiogram every 2 years1 5. Discuss diagnosis and management of specific complications of RACD CAD The risk of radiation induced CAD (RICAD) is 7.5% per Grey Unit (Gy). The risk is roughly constant, begins several years after exposure,

Cardiogenic shock (CS) remains a complex, multifactorial syndrome associated with significant morbidity and mortality. The CardioNerds Critical Care Cardiology Series tackles this important syndrome in a series of several episodes including: LV-predominant Shock, RV-predominant Shock, and Bi-ventricular Shock. In this episode, we review the definitions, pathophysiology, evaluation, and contemporary management, including use of inotropes and mechanical circulatory support, of left ventricular (LV) predominant CS. Series co-chairs Dr. Eunice Dugan and Dr. Karan Desai along with CardioNerds Co-founders Dr. Amit Goyal and Dr. Daniel Ambinder were joined by FIT lead, Dr. Vanessa Blumer, the recipient of the AHA 2021 Laennec Fellow in Training Clinician Award and currently pursuing Advanced Heart Failure and Transplant fellowship at the Cleveland Clinic. Our episode expert is Dr. Shashank Sinha, an Advanced Heart Failure, Mechanical Circulatory Support, and Cardiac Transplant cardiologist, Medical Director of the Cardiac Intensive Care Unit, and Director of the Cardiovascular Critical Care Research Program at INOVA Fairfax Hospital. His illustrious career accomplishments include being a Steering Committee member and site Principal Investigator for the multicenter Cardiogenic Shock Working Group and Critical Care Cardiology Trials Network. Audio editing by CardioNerds academy intern, Anusha Gandhi. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – LV Predominant Cardiogenic Shock LV-CS is complex! It is important to recognize that the pathophysiology of heart failure-related cardiogenic shock (HF-CS) is distinct from that of acute myocardial infarction (AMI-CS), and also crucial to differentiate between LV-dominant, right ventricular (RV)-dominant and biventricular (BiV)-shock. The SCAI SHOCK Stage Classification provides a unified and standardized vocabulary when assessing severity of CS, and facilitates communication about the diagnosis, presentation, and evolving nature of CS. Norepinephrine is considered the initial vasopressor of choice in most CS patients; the initial inotrope choice is a bit more nuanced! When considering mechanical circulatory support (MCS) for LV shock, high-quality data to guide therapy is lacking but one must always consider “the right patient, for the right device, at the right time” and remember that “pumps pump blood, decisions save lives”. Multidisciplinary, team-based care is paramount to improving survival of the critically ill patient with CS. Show notes – LV Predominant Cardiogenic Shock Notes drafted by Dr. Vanessa Blumer. 1. What tools do you use to define LV CS? CS is a hemodynamically complex and multifactorial syndrome, one of the most common indications for admission to a cardiac intensive care unit, with short-term mortality ranging from 35-50%. It is defined by systemic hypoperfusion and tissue hypoxia due to a primary cardiac insult or dysfunction. Clinical criteria used to define CS typically include evidence of hypotension (classically defined as SBP < 90 mmHg for 30 minutes and/or use of vasopressors, inotropes, or MCS to maintain systolic blood pressure > 90 mmHg) AND evidence of end-organ hypoperfusion (for example, serum lactic acid > 2 mmol/L, acute kidney injury, acute liver injury, altered mental status) in the setting of acute coronary syndrome or acute decompensated heart failure. Laboratory markers, including serum lactic acid, liver function tests, kidney function, and biomarkers including troponin and natriuretic peptides may be helpful. An echocardiogram is an excellent point of care tool to help demonstrate and confirm evidence of LV systolic dysfunction and/or valvular abnormalities.  Finally, a right heart catheterization (demonstrating an abnormally low cardiac output and index with elevated filling pressures) may be useful in facilitating the diagnosis and subsequent management. 2. How do HF-CS and AMI-CS lead to different phenotypes? It is important to recognize that HF-CS is now the predominant cause of CS, accounting for more than half of all CS. AMI-CS is characterized by an abrupt presentation due to a primary myocardial ischemic insult leading to necrosis (occurring in 5-10% of AMI patients) and can occur after STEMI or NSTEMI. The canonical clinical course

It’s another session of CardioNerds Rounds! In these rounds, Dr. Natalie Stokes (Formerly FIT at University of Pittsburgh and now General Cardiology Faculty at University of Pittsburgh) and Dr. Karan Desai (formerly FIT at University of Maryland and now General Cardiology faculty at Johns Hopkins) join Dr. Rick Nishimura (Professor of Medicine at Mayo Clinic) to discuss the nuances of managing mitral regurgitation through real cases. Dr. Nishimura has been an author or Chair of the ACC/AHA valve guidelines going back 20 years and has been recognized internationally as one of the world’s best educators, so you don’t want to miss the #NishFactor on these #CardsRounds! Audio editing by CardioNerds academy intern, Pace Wetstein. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes.  Speaker disclosures: None Challenging Cases – Atrial Fibrillation with Dr. Hugh Calkins CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes – Mitral Regurgitation with Dr. Rick Nishimura Case #1 Synopsis: A man in his 70s with a history of non-ischemic cardiomyopathy (last known LVEF 15-20%) and atrial fibrillation, presented with decompensated heart failure in the setting of moderate to severe mitral regurgitation. He was diuresed, transitioned to GDMT, and referred to cardiac rehabilitation. Over the next 6 months, he continued to have debilitating dyspnea (NHYA Class IIIa) and his outpatient physicians were limited on titrating GDMT further due to hypotension. A TEE was done which demonstrated EF 15%, severe MR by color and quantitation (EROA of 0.5 cm2; Regurgitant Volume of 65 mL), systolic flow reversal in the pulmonary vein and severe tricuspid regurgitation. We were asked how we would approach this case Case #1Takeaways In attempting to keep the evaluation of chronic mitral regurgitation relatively simple, we should ask ourselves three primary questions: (1) What is causing the MR; (2) How much MR is there; and (3) What is the hemodynamic consequence of the MR. To the first question of what is the etiology of the MR – a simple framework is to think of the etiology as an issue of the valve (primary) or an issue of the ventricle/atria (secondary). There is further classification that can be made based on the Carpentier Classification which speaks to the valve leaflet movement and position (normal leaflet motion, excessive leaflet motion [e.g., prolapse], or restricted in systole and/or diastole [e.g., rheumatic heart disease]). During rounds, Dr. Nishimura provided some historical context in that the original valve guidelines had recommendations for intervention on primary mitral regurgitation and not secondary – given that it is considered a disease of the ventricle. Trials like the COAPT trial have greatly shifted our practice in treating secondary mitral regurgitation. Though, we have to be familiar with which patients with secondary MR would truly derive benefit from mitral valve intervention In regards to the COAPT trial, patients with moderate to severe (3+) or severe (4+) mitral regurgitation who remained symptomatic despite maximally tolerated guideline-directed medical therapy (GDMT) were included. Dr. Nishimura makes the point that about one-third of patients intended to be enrolled in the trial were not included because they improved so much on GDMT. And thus, when evaluating patients for consideration of mitral valve intervention in secondary MR – and specifically transcatheter edge to edge repair (TEER) – every effort to optimize GDMT should be made first before intervening. Other important inclusion and exclusion criteria included that patients had LVEF between 20-50%, LV end-systolic diameter less than or equal to 70 mm, and absence of severe pulmonary hypertension (defined as pulmonary artery systolic pressure > 70 mmHg despite vasodilator therapy) or moderate to severe right ventricular failure. Dr. Nishimura asks our audience if the patient is truly on optimal GDMT and/or optimized? There are basic tools that clue us into optimization including chest x-ray (e.g., is there still pulmonary vascular congestion) and physical examination (e.g., what is the venous pressure). Dr. Nishimura makes an interesting point in correlating our examination with the echocardiographic findings. In patients with largely se

In this episode, Dr. Carly Fabrizio (Advanced Heart Failure and Transplant Cardiology Physician at Christiana Care Hospital), CardioNerds Critical Care Series Co-Chair Dr. Mark Belkin (Advanced Heart Failure and Transplant Fellow at University of Chicago) and CardioNerds Co-Founder Dr. Amit Goyal (Cleveland Clinic) join Dr. Gavin Hickey (Director of the AHFTC Fellowship and medical director of the left ventricular assist device program at UPMC) and Dr. David Kaczorowski (Surgical Director for the Advanced Heart Failure center, Department of Cardiothoracic Surgery at UPMC) for a discussion on post-cardiotomy shock. Audio editing by CardioNerds Academy Intern, student doctor, Shivani Reddy. Post-cardiotomy shock is characterized by heart failure that results in the inability to wean from cardiopulmonary bypass or develops post cardiac surgery. Patients who develop post-cardiotomy shock typically require inotropic support and may ultimately require temporary mechanical circulatory support. Post-cardiotomy shock carries a high mortality rate. However, early recognition and prevention strategies can help mitigate the risk for developing post-cardiotomy shock. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. This episode is supported by the 5th Annual Going Back to the Heart of Cardiology (A MedscapeLIVE Conference). Join co-chairs Dr. Robert Harrington and Dr. Fatima Rodriguez January 24-26, 2025 at the Fontainebleau Hotel in Miami Beach, Florida. The agenda will explore the latest advancements in cardiology including cardiovascular prevention, atherosclerosis and thrombosis, cardiovascular dysfunction, arrhythmias, and valvular heart disease. Network, attend engaging presentations by renowned cardiologists, visit the exhibit and poster hall, participate in an exclusive immersive experience, and earn up to 13 CME/CE credits. Register today with code CARDIONERDS for 30% OFF your registration. Click here for more information. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – Post-cardiotomy Shock Weaning from cardiopulmonary bypass is an intricate process that includes: rewarming the patient, de-airing the cardiac chambers, ensuring a perfusing heart rhythm, confirming adequate ventilation and oxygenation, removing the intracardiac catheters and cannulas and slowly reducing the blood diverted to the cardiopulmonary circuit and returning it small aliquots to the patient. Much to monitor during the process! Assessing the risk for post-cardiotomy shock prior to going to the OR is important. Consider left ventricular, right ventricular, and valvular function, and don’t forget about the value of hemodynamic assessments (pulmonary artery catheter evaluations) to ensure patients are adequately compensated. Close peri-operative monitoring of hemodynamics, hemo-metabolic derangements, and acid/base status can help identify patients who are failing therapy and may require upgrade to temporary MCS. RV assessment is challenging. Utilizing both imaging and hemodynamic evaluations can help understand which RV’s will require more support. Multi-disciplinary discussions with a heart team approach prior to cardiac surgery are valuable in identifying high risk patients for post cardiotomy shock and discussing contingency plans if issues arise. Show notes – Post-cardiotomy Shock (drafted by Dr. Carly Fabrizio) How can we diagnose post cardiotomy shock? We can diagnose post cardiotomy shock as patients who are undergoing cardiac surgery that develop hypotension and or tachycardia with hypoperfusion and end organ dysfunction. How can assess the risk of developing postcardiotomy shock prior to going to the OR? LV systolic function is not the only evaluation of cardiac function Don’t ignore the RV! Valvular function must be evaluated in conjunction with LV/RV function Hemodynamics can be helpful prior to going to the OR Filling pressures and CO/CI evaluation –> the more normal range – the less risk of post cardiotomy shock If going in more deranged –> more complications are likely to occur Think about what options are available post operatively if issues arise Include a multi-disciplinary discussions and planning prior to going to the OR Are there any specific pre-operative or intra-operative risk factors that may predispose someone to developing post cardiotomy shock? Many factors can lead to postc

In this episode, Daniel Ambinder and Amit Goyal (CardioNerds co-founders), Dr. Gurleen Kaur (medicine resident at Brigham and Women’s Hospital and Director of CardioNerds Internship), student doctor Adriana Mares (medical student at the University of Texas El Paso/Texas Tech University Health Sciences Center El Paso, CardioNerds Academy Intern), and Dr. Teodora Donisan (general cardiology fellow at the Mayo Clinic and CardioNerds Academy Chief) discuss with Dr. Mayra Guerrero (Interventional Cardiologist and Professor of Medicine at the Mayo Clinic) about challenges with diagnosing and treating valve disease in women, as well as ideas on how to increase recruitment for women in cardiology including interventional and structural cardiology. Dr. Guerrero shares her inspiring personal journey and advice for how to navigate becoming a structural cardiologist as an international medical graduate, woman, and mother. Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • Production Team The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version – Structural Heart Disease and LatinX Representation in Cardiology with Dr. Mayra Guerrero https://youtu.be/KvKADqUwUHQ Quoatables – Structural Heart Disease and LatinX Representation in Cardiology with Dr. Mayra Guerrero “Work hard, give it your best, and your work will speak for itself. Don’t be afraid to work hard and you’ll be able to achieve anything you want.” “I’m very fortunate to have had the opportunities that I’ve had, but now it’s my responsibility and the responsibility of many to make sure that we create those opportunities and that we provide mentorship for others who may want to follow the same steps into this field.” “I get angry, it’s normal to have emotions, but what I’ve learned is to transform my anger into something good – think of a project, find a paper, do something good for your career…channel that energy to do something good.” “It’s important that even at young ages you start thinking about how to pay it forward.” “Don’t wait too long to have kids. There’s never a perfect time to be a parent. Once you decide to have a family don’t put a pause on your personal life for your career.” Notes – Structural Heart Disease and LatinX Representation in Cardiology with Dr. Mayra Guerrero Notes (by Dr. Teodora Donisan) Structural valve disease in women and valve care in the global setting Heart disease is the leading cause of death for women. However, the awareness regarding this major public health concern has been declining over the past decade. Valve disease awareness is one of the lowest, at less than 3%. Women have higher mortality than men when they undergo surgical aortic or mitral interventions, mainly because of a higher risk profile. For example, women with severe aortic stenosis usually present at older ages and have many associated comorbidities, however the outcomes are good when they are treated with transcatheter aortic valve replacement (TAVR). Despite this, women are less likely to be referred for aortic valve replacement (AVR) than men. Once women are referred for therapy, they are more likely to be treated with TAVR than surgical aortic valve replacement (SAVR). There is a deficiency in trial enrollment for women which we need to address in order to generate the knowledge we require with regards to treatment. We also need to identify whether there are referral biases when it comes to AVR. Another hypothesis for the disparities in valve disease treatment for women when compared with men might be the decreased number of women in cardiology, especially in interventional cardiology (<10% of interventional cardiologists are women). Of note, <3% of TAVR operators are women (1.5% are surgeons and 1.5% are interventional cardiologists). Diversity and inclusion in interventional cardiology About 8% of interventional cardiologists are women and only 4.2% of cardiologists are Latinx. In order to i

CardioNerds (Amit Goyal and Dan Ambinder), Series Co-Chair Dr. Dinu Balanescu (Academy House Faculty and Chief Resident at Beaumont Hospital), and Episode Lead Dr. Manu Mysore (Former CardioNerds Ambassador and Cardiologist at the University of Maryland) discuss The Need for Cardio-Oncology with Expert Faculty Dr. Bonnie Ky, Director of Penn Cardio-Oncology Translation Center of Excellence and Editor-in-Chief of JACC CardioOncology. Audio editing by CardioNerds Academy Intern, student doctor Yousif Arif. This episode is supported by a grant from Pfizer Inc. Cardio-Oncology is a burgeoning field. There is a need for cardiologists and oncologists to work together in a multidisciplinary fashion using multi-modality imaging and personalized medicine. Cardiologists in particular need to understand basic oncology, anti-cancer therapies, and address risk factors which play an important role in oncologic progression and/or adverse cardiovascular events. The field can only be furthered by research with a focus on specificity of endpoints and multidisciplinary collaboration. The future of the field is in the hands of investigators and clinicians alike. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan.  Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. This episode is supported by the 5th Annual Going Back to the Heart of Cardiology (A MedscapeLIVE Conference). Join co-chairs Dr. Robert Harrington and Dr. Fatima Rodriguez January 24-26, 2025 at the Fontainebleau Hotel in Miami Beach, Florida. The agenda will explore the latest advancements in cardiology including cardiovascular prevention, atherosclerosis and thrombosis, cardiovascular dysfunction, arrhythmias, and valvular heart disease. Network, attend engaging presentations by renowned cardiologists, visit the exhibit and poster hall, participate in an exclusive immersive experience, and earn up to 13 CME/CE credits. Register today with code CARDIONERDS for 30% OFF your registration. Click here for more information. Pearls • Notes • References • Production Team CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – The Need for Cardio-Oncology with Dr. Bonnie Ky Over 20 million new cancer cases are expected to be added annually to the global burden as novel therapies have improved cancer survivorship. These therapies may be directly associated with cardiotoxicity or may prolong life to allow time for cardiovascular disease to develop in cancer survivors. Hypertension, hyperlipidemia, and obesity are modifiable risk factors that portend a poor prognosis from both an oncologic and cardiovascular perspective. Multi-modality imaging is useful in risk assessment within oncology, with echocardiography (including strain imaging) having a class I indication prior to treatment with many chemotherapeutics. Diverse trial enrollment is essential for furthering the science within Cardio-Oncology to translate clinically into personalized management. There is a need to strengthen a pipeline of young physicians and scientists to further the field of Cardio-Oncology. Show notes – The Need for Cardio-Oncology with Dr. Bonnie Ky Why should cardiologists have familiarity with cancer therapies? By 2030, 23.6 million new cancer cases are expected to be added annually to the global burden.1 Novel therapies and/or combination therapies have improved cancer survivorship but are associated with cardiovascular complications, especially in the elderly and those with pre-existing cardiovascular comorbidities.2 Cardiologists currently lack an understanding of oncologic treatments, with poor knowledge of dosing protocols and cardiotoxicities. This can lead to less aggressive protocols administered, as well as early discontinuation of important treatments for both oncologic and cardiovascular conditions.3 A multidisciplinary collaboration between pharmacists, cardiologists, oncologists, and nurse navigators is needed to improve treatment decision-making for the benefit of cancer patients. Cardiologists should have basic knowledge and understanding of some of the commonly used chemotherapeutic drugs and any adverse events during treatment courses based on clinical trials, FDA reporting, and epidemiological data. JACC Cardio-Oncology seeks to disseminate knowledge through live courses such as Advancing the Care of the Oncology Patient and journal-associated podcasts, with plans to develop a “how-to” series to educate both cardiologists and oncologists. What is the impact of cardiovascular risk

CardioNerds (Daniel Ambinder and Amit Goyal) join Dr. Arielle Schwartz (Emory University cardiology fellow), Dr. Joshua Zuniga (former Emory vascular medicine fellow and now USC cardiology fellow), and Dr. Patrick Zakka (UCLA cardiology fellow) from the Emory University School of Medicine. They discuss a case of a young woman with new onset hypertension refractory to 3 antihypertensive agents who is ultimately diagnosed renovascular hypertension due to fibromuscular dysplasia complicated by saccular aneurysm. Dr. Bryan Wells (Director of Vascular Medicine at Emory University) provides the ECPR for this episode. Audio editing by CardioNerds Academy intern, Dr. Christian Faaborg-Andersen. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media References Gornik HL, Persu A, Adlam D, Aparicio LS, Azizi M, Boulanger M, Bruno RM, de Leeuw P, Fendrikova-Mahlay N, Froehlich J, Ganesh SK, Gray BH, Jamison C, Januszewicz A, Jeunemaitre X, Kadian-Dodov D, Kim ES, Kovacic JC, Mace P, Morganti A, Sharma A, Southerland AM, Touzé E, van der Niepen P, Wang J, Weinberg I, Wilson S, Olin JW, Plouin PF. First International Consensus on the diagnosis and management of fibromuscular dysplasia. Vasc Med. 2019 Apr;24(2):164-189. doi: 10.1177/1358863X18821816. Epub 2019 Jan 16. Erratum in: Vasc Med. 2019 Oct;24(5):475. Erratum in: Vasc Med. 2021 Aug;26(4):NP1. PMID: 30648921. Olin, Circulation. 2014;129:1048-1078. Fibromuscular Dysplasia: State of the Science and Critical Unanswered Questions A Scientific Statement From the American Heart Association S.H.KimMD, MPH†Jeffrey W.OlinDO‡James B.FroehlichMD, MPH§XiaokuiGuMA§J. MichaelBacharachMD‖Bruce H.GrayDO¶Michael R.JaffDO#Barry T.KatzenMD∗∗EvaKline-RogersMS, RN, NP§Pamela D.MaceRN††Alan H.MatsumotoMD‡‡Robert D.McBaneMD§§Christopher J.WhiteMD‖‖Heather L.GornikMD, MHS†. Clinical Manifestations of Fibromuscular Dysplasia Vary by Patient Sex: A Report of the United States Registry for Fibromuscular Dysplasia. JACC. Volume 62, Issue 21, 19–26 November 2013, Pages 2026-2028

CardioNerds Dr. Josh Saef, Dan Ambinder, join Dr. Jim Kimber and interview experts Dr. Adrienne Kovacs, and Dr. Lauren Lastinger and discuss behavioral health needs and psychosocial wellbeing in the congenital heart disease population. In this episode, our experts tackle issues surrounding mental and behavioral health including anxiety/depression, ADHD, neurodevelopmental disabilities, psychosocial challenges, stressors unique to patients with ACHD and their families, and how the healthcare system can better optimize mental health care for the CHD patient population. Audio editing by CardioNerds Academy Intern, Pace Wetstein. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None This episode is supported by the 5th Annual Going Back to the Heart of Cardiology (A MedscapeLIVE Conference). Join co-chairs Dr. Robert Harrington and Dr. Fatima Rodriguez January 24-26, 2025 at the Fontainebleau Hotel in Miami Beach, Florida. The agenda will explore the latest advancements in cardiology including cardiovascular prevention, atherosclerosis and thrombosis, cardiovascular dysfunction, arrhythmias, and valvular heart disease. Network, attend engaging presentations by renowned cardiologists, visit the exhibit and poster hall, participate in an exclusive immersive experience, and earn up to 13 CME/CE credits. Register today with code CARDIONERDS for 30% OFF your registration. Click here for more information. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls – Congenital Heart Disease and Psychosocial Wellbeing Among patients with congenital heart disease, symptoms of anxiety are more common than symptoms of depression. “Heart-focused anxiety” relates to symptoms attributable to a heart condition including fear of appointments, surgery, or health-uncertainty. It is important to differentiate this from generalized anxiety. Predictors of depression and anxiety include patient-reported physical health status. Defect severity (mild, moderate, great complexity) and physician-diagnosed NYHA class were NOT associated with rates of depression/anxiety [2]. Despite CHD, patient self-reported Quality of Life (QoL) is relatively high. Predictors of decreased QoL include older age, lack of employment, never having married, and worse self-reported NYHA functional class Important treatment strategies include: education for patients and caregivers, early identification and referral to mental health providers, incorporation of providers into CHD teams, and encouraging physical activity and peer-interaction. Show notes – Congenital Heart Disease and Psychosocial Wellbeing Notes (developed by Dr. Jim Kimber) Mental Health Terminology: Adults with CHD face the same mental health challenges as people who don’t have a heart condition. Symptoms of depression and anxiety are the most common: Approximately 1/4 – 1/3 of CHD patients will struggle with clinically significant depression or anxiety at any one point. Up to ½ will meet lifetime diagnostic criteria for these conditions Mood and anxiety disorders differ in that they have separate diagnostic criteria. Importantly, research often uses self-reported symptoms, rather than patients who have formally met diagnostic criteria. Historically, the focus has been on depression.  However, elevated symptoms of anxiety are much more common than elevated symptoms of depression. It is important to make the distinction between “Generalized Anxiety,” and “Heart-Focused Anxiety.” Heart-Focused Anxiety: symptoms of anxiety directly related to having a heart condition, such as fear of appointments / worry about a decline in health status, getting an ICD, preparing for surgery, transplants, or having a shortened life expectancy, etc. This may also include a significant component of health uncertainty – the idea that patients are aware of need for a likely intervention but without ability to prognosticate timelines (e.g. need for valve replacemen

CardioNerds (Amit Goyal and Dan Ambinder) join Dr. Radi Zinoviev, Dr. Josh Cohen, and Dr. Tiffany Dong (CardioNerds Ambassador) from the Cleveland Clinic for a day on Edgewater beach. They discuss the following case of the evaluation and management of prosthetic tricuspid valve stenosis in a patient with a history of Ebstein Anomaly. The expert commentary and review (ECPR) is provided by Dr. Jay Ramchand, staff cardiologist with expertise in multimodality cardiovascular imaging at the Cleveland Clinic. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. This episode is supported by the 5th Annual Going Back to the Heart of Cardiology (A MedscapeLIVE Conference). Join co-chairs Dr. Robert Harrington and Dr. Fatima Rodriguez January 24-26, 2025 at the Fontainebleau Hotel in Miami Beach, Florida. The agenda will explore the latest advancements in cardiology including cardiovascular prevention, atherosclerosis and thrombosis, cardiovascular dysfunction, arrhythmias, and valvular heart disease. Network, attend engaging presentations by renowned cardiologists, visit the exhibit and poster hall, participate in an exclusive immersive experience, and earn up to 13 CME/CE credits. Register today with code CARDIONERDS for 30% OFF your registration. Click here for more information. Jump to: Case media – Case teaching – References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media CXR ECG TTE RHC Final TTE TTE 1 TTE 2 TTE 3 Follow up TTE 1 Follow up TTE 2 Episode Schematics & Teaching Pearls – Tricuspid Valve Stenosis Tricuspid stenosis is uncommon (<1% of the US population) and thus we have a lack of evidence as well as guideline recommendations. While there are no official diagnostic criteria for severe tricuspid stenosis, some echocardiographic features include flow acceleration across the valve, a mean pressure gradient of ≥ 5mmHg and an inflow VTI of > 60cm. Structural findings that support the presence of severe tricuspid stenosis include a moderately dilated RA and a dilated IVC, though these are not specific. Right heart catheterization hemodynamics that support tricuspid stenosis include a high right atrial pressure and gradual “y” descent. Bioprosthetic tricuspid valves are generally favored over mechanical valves due to risk of thrombosis and longevity of these valves in the tricuspid position. Notes – Tricuspid Valve Stenosis What are causes of tricuspid stenosis? Causes of tricuspid stenosis can be divided into congenital and acquired causes. Congenital causes include tricuspid atresia or stenosis. Acquired causes include rheumatic heart disease, carcinoid syndrome, endocarditis, prior radiation, or fibrosis from endomyocardial procedures or placement of electrical leads. Rheumatic heart disease is the most common cause of tricuspid stenosis and is usually associated with mitral valvulopathy. What are the symptoms and physical exam findings of tricuspid stenosis? Findings revolve around right sided congestion or heart failure symptoms such as peripheral edema, abdominal distension with ascites, hepatomegaly, and jugular venous distension. When examining the jugular vein, you may see prominent a-waves and an almost absent or slow y descent reflective of delayed emptying of the right atrium (in the absence of tricuspid regurgitation). The murmur of tricuspid stenosis includes an opening snap and low diastolic murmur at the left lower sternal border with inspiratory accentuation. Patients may also report fatigue due to decreased cardiac output from obstruction. On echocardiography, what are the features supportive of severe tricuspid stenosis? Qualitatively, the leaflets may be thickened with reduced mobility and there may be diastolic dooming of the valve. Doppler may show high gradients of ≥ 5 mmHg, which may be elevated if there is coexisting tricuspid regurgitation and lower with decreased cardiac output. Associated structural changes include dilated right atrium and inferior vena cava. What is expected on right heart catheterization for tricuspid stenosis? Assuming the patient remains in sinus rhythm, patients with tricuspid stenosis would display high right atrial pressures and a gradual “y” descent. A diastolic gradient may be measured with dual catheters in the right atrium and the right ventricle. What are the treatment options for tricuspid stenosis? Medical management of tricuspid stenosis includes diuretics and addressing the underlying cause. Intervention is indicated for symptomatic severe tricuspid stenosis although the current 2020 ACC/AHA Valve Guidelines do not address tricuspid stenosis. The 2014 ACC/AHA guidelines give a class I indication for tricuspid stenosis surgery during left sided surgery while there is a class

It’s another session of CardioNerds Rounds! In these rounds, Dr. Stephanie Fuentes (EP FIT at Houston Methodist) joins Dr. Hugh Calkins (Professor of Medicine and Director of the Electrophysiology Laboratory and Arrhythmia Service at Johns Hopkins Hospital) to discuss the nuances of atrial fibrillation (AF) management through challenging cases. As an author of several guideline and expert consensus statements in the management of AF and renowned clinician, educator, and researcher, Dr. Calkins gives us many pearls on the management of AF, so don’t miss these #CardsRounds!  This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes.  Speaker disclosures: None Challenging Cases – Atrial Fibrillation with Dr. Hugh Calkins CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes – Challenging Cases – Atrial Fibrillation with Dr. Hugh Calkins Case #1 Synopsis: A woman in her mid-60s presents with symptomatic paroxysmal atrial fibrillation (AF). An echocardiogram has demonstrated that she has a structurally normal heart. Her primary care doctor had started Metoprolol 50 mg twice a day but she has remained symptomatic. In office, an EKG confirms AF, but she converts to sinus while there. She is seeking advice to prevent further episodes and in general wants to avoid additional medications Case #2 Takeaways We discussed several potential options for treatment. Amongst the first things we discussed was amiodarone. In a patient of this nature without structural heart disease and under the age of 70, Dr. Calkins discussed that he would probably consider amiodarone as a 2nd line option. While amiodarone may be effective in maintaining sinus rhythm in comparison to other antiarrhythmic medications like sotalol, flecainide, and propafenone, it does have significant toxicity. If antiarrhythmic drugs (AAD) were to be considered, we also discussed the options of dofetilide versus sotalol. Dofetilide typically requires inpatient initiation due to the risk of QT prolongation and Torsades. Since women tend to have longer corrected QT (QTc) intervals, high dose dofetilide may be more proarrhythmogenic in women. Though, Dr. Calkins noted that many patients don’t tolerate sotalol due to fatigue and generally dofetilide is well tolerated. When it comes to the “pill in the pocket” approach, Dr. Calkins noted that its utility is more so in patients with persistent AF that is known to not stop on its own. For instance, an individual who has AF a few times a year that is persistent may benefit from flecainide or propafenone (“in the pocket”) instead of being brought in for an electrical cardioversion. In this scenario, the first time one of these agents is used, the patient ought to be closely monitored. For our patient, her episodes were too frequent and self-terminating for a “pill in the pocket” approach to be effective. Current guideline recommendations for catheter ablation include a Class IA recommendation for patients with paroxysmal AF refractory to AADs, and a Class IIA recommendation as first-line therapy for patients with paroxysmal AF. In the 2020 ESC Atrial Fibrillation Guidelines, catheter ablation is given a Class IA recommendation to improve symptoms of AF recurrences in patients who have failed or are intolerant of one Class I or III AADs. For patients who have failed or have been intolerant of beta blocker alone for rhythm control, catheter ablation is given a Class IIA recommendation. As first-line therapy in paroxysmal AF, catheter ablation is given a Class IIA recommendation as well. Of note, three recent trials have demonstrated catheter ablation as first line therapy is reasonable and newer guidelines will reflect this. Specifically, EARLY-AF compared ablation (cryoablation) vs AAD (mainly with flecainide/propafenone) as a first line therapy. The cryoablation arm showed significantly less recurrence of AF at one year The guidelines clearly state that aligning the treatment plan with the patient’s goals and risk tolerance are paramount. Catheter ablation does have potential complications such as pericardial effusion or access-related issues, though these are rare. Furthermore, as time has passed, catheter ablation success rates have improved. Up and coming techniques such as electroporation may be game-changing with regards to success rate and safety. Waiting times for a procedure may be an issue, so one could consider an AAD, such

In this episode, Daniel Ambinder (CardioNerds Co-Founder), Dr. Gurleen Kaur (Director of CardioNerds Internship and medicine resident at Brigham and Women’s Hospital), Dr. Eunice Dugan (Cardiology fellow at Cleveland Clinic) and Dr. Zarina Sharalaya (Interventional and Structural Cardiologist at North Texas Heart) learn from the Dr. Sheila Sahni (Interventional Cardiologist and Director of The Women’s Heart Program at The Sahni Heart Center) regarding radiation safety in the cath lab and methods of reducing radiation exposure to the operator. She also discusses radiation safety for the pregnant interventional cardiologist and how to safely manage pregnancy during the gestational period. We hear her inspirational journey as a female interventional cardiologist and her experience in starting the Women’s Heart Program at Sahni Heart Center. Special message by Dr. Jeff Lander, New Jersey ACC Chapter Governor. Audio editing by CardioNerds Academy Intern, Pace Wetstein. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version – Radiation Safety & Women in Interventional Cardiology with Dr. Sheila Sahni https://youtu.be/iIwnsu6qJ4k Tweetorial – Radiation Safety & Women in Interventional Cardiology with Dr. Sheila Sahni https://twitter.com/gurleen_kaur96/status/1563608232211296256?s=21&t=iay5zosSBDjPBLWJ4kWIAw Quoatables – Radiation Safety & Women in Interventional Cardiology with Dr. Sheila Sahni “Having anyone who can believe in you when you are really passionate about something is really all you need… the passion is what’s going to carry you through. It’s not about being male or female or pregnant or not pregnant, it’s about what you love to do and how can you master it.” “Our careers can wait, but family planning cannot. If you are fortunate enough to have the opportunity to start a family even if it’s during your training, you should”. Notes – Radiation Safety & Women in Interventional Cardiology with Dr. Sheila Sahni What are procedural techniques to utilize during a heart catheterization to reduce radiation exposure to the operator? Decrease number and length of cine acquisitions and fluoroscopy time Decrease the frame rate – halving the frame rate reduces radiation dose by 50% Decrease the distance between the image intensifier and the patient Limit steep LAO angulations Apply collimation as much as possible which reduces overall patient dose and scatter radiation Limit digital magnification which can increase skin dose exposure by 50% What are the important dose limits to consider for a pregnant female and her fetus in the cath lab? The US Nuclear Regulatory Commission (NRC) regulatory equivalent dose limit is 5mSv during the entire pregnancy of the declared pregnant woman. The annual natural background radiation dose in the US is 3mSv. The average under-lead dose to a working pregnant interventionalist over the entire gestation is ~0.3mSv. The fetus of a working pregnant interventionalist is estimated to receive ~0.09mSv over an entire gestation. What are the ways in which pregnant women can protect themselves and the fetus from radiation exposure in the cath lab? Disclose (confidentially if desired) pregnancy to the radiation safety office to ensure fetal protection Wear an additional dosimeter underneath the lead apron at waist level to track fetal radiation dose Decrease occupational exposure via radiation protection measures as summarized below What are important considerations for lead apron use in the cath lab to maximize radiation protection? Make sure your lead fits! Do not sit in your lead- sitting in lead can lead to cracks which can decrease protection Hang up your lead when not being used Consider shoulder pads/arm sleeve addition to lead apron to protect breast tissue Ensure that your lead apron is undergoing periodic screening to monitor for defects Consider lead thickness – 0.5mm thickness attenuates 98-99.5% of scattered r

The modern CICU has evolved to include patients with complex pulmonary mechanics requiring more non-invasive and mechanical ventilation. Series co-chairs Dr. Eunice Dugan and Dr. Karan Desai along with CardioNerds Co-founder Dr. Amit Goyal were joined by FIT lead, Dr. Sam Brusca, who has completed his NIH Critical Care and UCSF Cardiology fellow and currently faculty at USCF. We were fortunate enough to have two expert discussants: Dr. Burton Lee, Head of Medical Education and Global Critical Care within the National Institutes of Health Critical Care Medicine Department and master clinician educator with the ATS Scholar’s Critical Care for Non-Intensivists program, and Dr. Chris Barnett, ACC Critical Care Cardiology council member and Section Chair of Critical Care Cardiology at UCSF.  In this episode, these experts discuss the basics of mechanical ventilation, including the physiology/pathophysiology of negative and positive pressure breathing, a review of ventilator modes, and a framework for outlining the goals of mechanical ventilation. They proceed to apply these principles to patients in the CICU, specifically focusing on patients with RV predominant failure due to pulmonary hypertension and patients with LV predominant failure. Audio editing by CardioNerds Academy Intern, student doctor, Shivani Reddy. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – Positive Pressure Ventilation in the CICU Respiratory distress, during spontaneous negative pressure breathing can lead to high transpulmonary pressures and potentially large tidal volumes. This will increase both RV afterload (by increasing pulmonary vascular resistance) and LV afterload (by increasing LV wall stress). An analogy for the impact of negative pleural pressure during spontaneous respiration on LV function is that of a person jumping over a hurdle. The height of the hurdle does not increase, but the ground starts to sink, so it is still harder to jump over. Intubation in patients with right ventricular failure is a tenuous situation, especially in patients with chronic RV failure and remodeling (increased RV thickness, perfusion predominantly during diastole, RV pressure near or higher than systemic pressure). The key tenant to safe intubation is avoiding hypotension, utilizing induction agents such as ketamine or etomidate, infusing pressors, and potentially even performing awake intubations. Non-invasive positive pressure ventilation in HFrEF has hemodynamic effects similar to a cocktail of IV inotropes, dilators, and diuretics. CPAP decreases pulmonary capillary wedge pressure (LV preload), decreases systemic vascular resistance (afterload), and increases cardiac output. Airway pressure during mechanical ventilation is based on the “equation of motion”: Pressure = Volume/Compliance + Flow*Resistance + PEEP. Our goals of oxygenation on mechanical ventilation include achieving acceptable PaO2/Sat with the lowest FiO2 possible (avoiding oxygen toxicity) and optimal PEEP (which increases oxygenation but can have detrimental impact on cardiac output) Our goals of ventilation on mechanical ventilation include achieving acceptable pH and PaCO2 while preventing ventilator induced lung injury and avoiding auto-PEEP. We prevent lung injury by reducing tidal volume (ideally <8cc/kg, plateau pressure < 30 cmH20, driving pressure < 15 cmH20) and auto-peep by reducing respiratory rate (and allowing for full expiration). No ventilator mode is “superior” to the others. What is most important is that providers are comfortable with the applied mode and able to appropriately respond to active changes in patient effort and mechanics. Show notes – Positive Pressure Ventilation in the CICU 1. What are the hemodynamic effects of Negative Pressure breathing in the RV and LV? RV – Negative pleural pressure is transmitted to pericardium and RV – Negative pleural pressure is also transmitted to the pulmonary vasculature – Thus, the pressure drop is net neutral across the RV-PA circuit and does not affect afterload – However, large negative pleural pressure swings still lead to increased transpulmonary pressure, increased lung volumes, and associated increased PVR (RV afterload). LV – Negative pleural pressure is transmitted to the pericardium and LV – Negative pleural pressure is NOT transmitted to the extra-thoracic aorta – Transmural pressure across the L

CardioNerds (Amit and Dan) join join Dr. Andrew Dicks (Vascular medicine physician at Prisma Health, former fellow at Mass General Vascular) and Dr. Prateek Sharma (Vascular interventional & medicine fellow at MGH) for an ice-cold drinks at the Esplanade in Boston, MA to discuss a case about a patient who developed a pulmonary embolism and masterfully discuss the diagnosis and management of of pulmonary emboli. Dr. Ido Weinberg (Director, Vascular Medicine Fellowship at MGH) provides the ECPR for this episode. Case Abstract: A 59-year-old Spanish-speaking man with no significant past medical history presents after falling 15-20 feet from a ladder and landing on his back. He was found to have an L1 fracture and left radial fracture and underwent T12-L2 fusion with neurosurgery on hospital day 1 and ORIF of left radial fracture with orthopedic surgery on hospital day 2. On hospital day 5, he develops acute onset tachycardia with HR in the 130s bpm with new O2 requirement associated with mild shortness of breath at rest without any chest discomfort. His labs were notable for an elevated troponin and proBNP. He underwent CTPA which demonstrated acute bilateral occlusive pulmonary emboli (PE) extending in the right and left main pulmonary arteries. TTE demonstrated right ventricle dilation. The patient was started on a heparin infusion and a PE response team (PERT) meeting was held to discuss treatment options. Given recent surgery, use of thrombolytic therapy was felt to be too risky and thus he was taken for percutaneous thrombectomy in the cath lab. PA pressure prior to intervention was 51/21 mmHg. The patient underwent suction thromboembelectomy with the Flow Triever device with extraction of thrombus and improvement in PA pressure to 19/11 mmHg. He was treated with anticoagulation thereafter and discharged home two days after the procedure. Jump to: Case media – Case teaching – References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media Acute bilateral occlusive and nonocclusive pulmonary emboli extending from the right and left main pulmonary arteries to the lobar and segmental arteries of all the lobes.  Moderate right heart strain including the right atrium and the right ventricle. RV/LV ratio > 1.0. Right ventricular cavity is dilated (RV size at the base measures to 45mm). Right ventricular systolic function is moderately decreased. Right ventricular free wall is hypokinetic with sparing of the right ventricular apex consistent with acute right ventricular strain Pulmonary angiography demonstrated extensive proximal bilateral PEs Caption: Post-procedure TTE demonstrated resolution of RV strain with normalization of RV size and function. Episode Schematics & Teaching Pearls While there are markers to suggest PE, such as ECG findings or evidence of RV dilatation, a PE cannot be confirmed without imaging. Elevation of cardiac biomarkers and evidence of RV dysfunction are used to risk stratify PE, not the degree of thrombus burden or locale of thrombus. Enoxaparin is the preferred anticoagulant to initiate at time of PE diagnosis if comorbidities allow. Optimal treatment of intermediate risk PE remains uncertain as there is little data about long-term outcomes. Aggressive treatment should be used judiciously and chosen on a case-by-case basis. PE response teams (PERT) allow for multidisciplinary expert opinion in the face of scarce evidence to determine what is felt to be the best management strategy. Notes 1. What is a PERT team and why is it helpful? We have several tools and approaches for the management of PE. There are also many subspecialities involved in the care of patients with PE, including vascular medicine, intervention cardiology, hematology, pulmonology, cardiac surgery, radiology, emergency department, intensive care, and more. As such, the best treatment plan for a given patient with PE can be challenging, especially if the services involved in treatment of the PE function in silos. PERT, or PE Response Team, was built to address this concern. It is a multidisciplinary team that originated at MGH whose goal is to coordinate care for high-risk PE patients and advance PE-related care in the institution. PERT allows for multidisciplinary expert opinion in the face of scarce evidence to determine what is felt to be the best management strategy. 2. How do we risk stratify patients with PE? Risk stratification is largely dependent on the hemodynamic significance caused by the PE. In addition to vital sign derangement, patients with PE should also be evaluated for evidence of cardiac strain due to PE by checking for evidence of RV dilatation on CT or TTE and for elevation of cardiac biomarkers. The combination of this information is used to risk stratify patients. Additionally, risk stratifi

CardioNerds (Daniel Ambinder) and ACHD series co-chair Dr. Dan Clark discuss advanced heart failure therapies including mechanical circulatory support (MCS) and heart transplantation (HT) in patients with adult congenital heart disease (ACHD) with Dr. Rafael Alonso-Gonzalez, cardiologist and director of Adult Congenital Heart Disease program at the University of Toronto and ACHD fellow Dr. Andy Pistner (University of Washington). They cover epidemiology of heart failure in ACHD, outcomes after HT, unique challenges of HT in this population, impact of allocation policies on access to transplantation, and regionalization of advanced heart failure care. They also discuss a practical approach to advanced heart failure therapy evaluation in ACHD. Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None This episode is made possible with support from Medmastery. At Medmastery you can learn some of the most important clinical skills like echo, advanced EKG, coronary angiography, PCI basics, pacemaker- and ICD troubleshooting and so much more. CardioNerds listeners can get an exclusive 15% discount on a lifetime subscription. Click HERE for details. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls – Advanced Heart Failure Therapies (MCS/HT) Among ACHD Patients Heart failure is a major comorbidity and the leading cause of death in adults with congenital heart disease. Identification of advanced heart failure in ACHD is challenging. ACHD patients do not always self-identify exercise limitations or exertional dyspnea. Cardiopulmonary exercise testing is a useful tool in evaluating these patients. Patients with ACHD awaiting heart transplantation are less likely than non-ACHD patients to receive a heart transplant, and ACHD patients have an increased risk of death or delisting while awaiting heart transplantation. Evaluation of transplant candidacy and potential need for multi-organ transplantation in complex congenital heart disease (i.e., Fontan palliation) requires a multidisciplinary approach. Regionalization of care improves outcomes for ACHD patients with advanced heart failure. High volume transplant centers have better early survival for ACHD patients after heart transplant, and the highest volume ACHD transplant centers in each UNOS region have better early survival. Show notes – Advanced Heart Failure Therapies (MCS/HT) Among ACHD Patients 1. How many ACHD patients have heart failure? Patients with ACHD are a large and heterogeneous group. The signs and symptoms of heart failure vary widely depending on the underlying congenital heart disease. Patients with D-transposition of the great arteries repaired with an arterial switch operation have low rates of heart failure (~3%)1 compared to those patients Fontan palliation for single ventricle physiology (40%)2. Heart failure is the leading cause of death in patients with ACHD3,4. 2. How many patients with ACHD end up receiving a heart transplant or mechanical circulatory support? Heart transplantation for congenital heart disease in adults has been increasing in frequency since the late 1980s. Between 2010 and 2012, this accounted for 4% of all adult heart transplants in the United States5. This represents a small fraction compared to the number of adults who die due to complications of heart failure related to congenital heart disease. In a recent study of the INTERMACs registry, 126 patients with ACHD from a total of 16,000 patients over a 10-year period underwent placement of durable mechanical support devices (ventricular assist device)6. 3. Why are these numbers low relative to the number of ACHD patients with heart failure? Identification of those patients with ACHD who are at risk for adverse outcomes related to heart failure is challenging. The symptoms of heart failure reported in these patients is often different from what is described in patients with acquired heart failure. Similarly, having grown up with reduced aerobic capacity, many of these pa

CardioNerds (Amit Goyal), Dr. Colin Blumenthal (CardioNerds Academy House Faculty Leader and FIT at the University of Pennsylvania), and Dr. Anjali Wagle (CardioNerds Ambassador and FIT at Johns Hopkins University), discuss the baseline assessment of stroke and bleeding risk in patients with atrial fibrillation (AF) with Dr. Elaine Hylek. Dr. Hylek is a professor of medicine at the Boston University School of Medicine and is the Director of the Thrombosis and Anticoagulation Service at Boston Medical Center. Stroke is a potentially devastating and preventable complication of AF. Understanding the balance between stroke and bleeding risk is crucial in determining who should be on anticoagulation. Join us to discuss this topic! In the next episode of the series, we will discuss situational risk assessment in the context of peri-cardioversion, peri-procedural status, triggered atrial fibrillation, and more. Audio editing by CardioNerds Academy Intern, Pace Wetstein. This CardioNerds Atrial Fibrillation series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Kelly Arps and Dr. Colin Blumenthal. This series is supported by an educational grant from the Bristol Myers Squibb and Pfizer Alliance. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. We have collaborated with VCU Health to provide CME. Claim free CME here! Disclosures: Dr. Hylek discloses grant and research support from Medtronic and Janssen, and honoraria and/or consulting fees from Boehringer Ingelheim, and Bayer. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – Atrial Fibrillation: Assessment of Stroke & Bleeding Risk The CHA2DS2-VASc should be used to determine stroke risk in all patients. It was updated from the CHADS2 score to better separate patients into high and low risk and a score of 0 has a very low risk of a stroke. Understanding a given model’s derivation is key to application for any risk model. Understanding who was and was not included when a risk score was derived helps determine how to clinically use it. For example, mechanical valves, hypertrophic cardiomyopathy, cardiac amyloidosis, and moderate to severe MS were all excluded or poorly represented and should receive AC in AF regardless of CV. The HAS-BLED score should be used to identify modifiable risk factors for bleeding and address them. It is less useful to determine when we should stop AC. Factors that go into the score are dynamic and the intention was to alert the provider of potentially modifiable factors that could be addressed to lower bleeding risk (such as better BP control). Fear the clot. Patients should be on AC unless there is a serious contraindication as embolic strokes can be devastating with a high mortality (~24% mortality at 30 days) “What am I saying by not writing the prescription… I am saying that it’s OK to have an ischemic stroke.” Survey data shows that patients are willing to experience 3.5 GI bleeds on average before 1 stroke, so favoring AC is often a patient centered approach Notes – Atrial Fibrillation: Assessment of Stroke & Bleeding Risk Notes drafted by Dr. Anjali Wagle 1. Why do strokes happen in atrial fibrillation? Why is reducing stroke risk so important? Atrial fibrillation is associated with a significantly increased risk of stroke. The mortality of strokes related to AF have been estimated to be around 25% at 30 days in early studies which included either persistent or permanent AF, though of note, these studied were biased towards larger strokes since the diagnosis was based on physical exam and not high resolution imaging. AF promotes thrombogenesis through Virchow’s triad which includes: Abnormal blood flow Endothelial damage Hypercoagulability In atrial fibrillation, patients usually have a dilated left atrium and decreased blood flow through the atrial appendage which contribute to thrombogenesis. Multiple risk scores have been derived (i.e., CHA2DS2VASc) for estimation of stroke risk in patient with AF to identify whom to treat with anticoagulation to reduce the stroke risk. 2. How were CHADS2 and CHA2DS2VASc (CV) created and validated? The CHADS2 score was derived in 2001 by Gage et al from data including hospitalized patients with nonrheumatic AF who were not prescribed warfarin at hospitalized discharge. The CHADS2 score assigns one point to congestive heart failure, hypertension, age ≥ 75 years, and diabetes mellitus and two points to a previous history of stroke or transient ischemic attack (TIA) for a total of 6 points. Stroke

With the advent and rapid evolution of contemporary percutaneous coronary intervention (PCI), the early invasive management of acute myocardial infarction (AMI) has become a mainstay in therapy with significant impact on patient outcomes. However, despite modern advances in technology and system-based practices, AMI presenting with cardiogenic shock (CS) continues to portend a high risk of morbidity and mortality. Few randomized controlled clinical trials are available to guide decision-making in this uniquely challenging patient population. Understanding the pathophysiologic mechanism by which injury occurs and propagates the shock cycle can be instrumental in selecting an appropriate strategy for revascularization and left ventricular unloading. In this episode we are joined by Dr. Venu Menon, The Mehdi Razavi Endowed Chair and Professor of Medicine at the Cleveland Clinic Lerner College of Medicine,  section head of clinical cardiology, fellowship program director, and director of the Cardiac intensive care unit at the Cleveland Clinic. Dr. Menon shares his wealth of knowledge and experience to help us review the contemporary data available for AMI CS management in a case-based discussion. We are also joined by Dr. Priya Kothapalli, star chief fellow and future interventionalist from University of Texas at Austin, series co-chair Dr. Yoav Karpenshif, and CardioNerds Co-founders Amit Goyal and Daniel Ambinder. Audio editing by CardioNerds Academy Intern, Dr. Christian Faaborg-Andersen. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. This episode is made possible with support from Medmastery. At Medmastery you can learn some of the most important clinical skills like echo, advanced EKG, coronary angiography, PCI basics, pacemaker- and ICD troubleshooting and so much more. CardioNerds listeners can get an exclusive 15% discount on a lifetime subscription. Click HERE for details. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon The H&P does matter! Age, location of infarction, heart rate, systolic blood pressure, and heart failure symptoms all carry weight in determining prognosis and risk of mortality. Define functional status, comorbid conditions, and life expectancy to help guide clinical decision-making. Do a quick bedside echocardiogram if possible to elucidate the predominant mechanism driving CS and rule out mechanical complications. Act with urgency! Get to the catheterization lab to characterize coronary anatomy and revascularize the culprit vessel as soon as possible. Minimize/avoid the use of vasopressors; if needed, wean as quickly as possible to avoid worsening myocardial ischemia. Consider mechanical circulatory support early! Despite dramatic advances in AMI management, data is limited in AMI CS management. Ask the important questions, get involved in the scientific inquiry as a trainee! Show notes – Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon 1. Why is it important to recognize AMI complicated by CS? AMI CS occurs in 7-10% of patients presenting with AMI and has a higher prevalence among elderly patients. The SHOCK trial (1999) showed significant survival benefit at 6 months with early revascularization with balloon angioplasty compared to medical therapy alone in AMI CS. Registry data suggests that early revascularization is beneficial in AMI CS even in elderly patients. Decision-making should be guided using a holistic view of the patient’s overall biology. Despite advances in revascularization techniques and availability of mechanical support, AMI CS portends a 40-45% risk of 30-day mortality in the modern era. Significant variation in management strategy exists between centers and data to guide decision-making is limited. The Society for Cardiovascular Angiography and Intervention (SCAI) classification system of shock stage may be helpful in characterizing patient risk and guiding clinical decision-making. 2.     Which patients with AMI CS should undergo invasive monitoring and revascularization? What should be the timing of any intervention? In viable patients presenting with AMI CS, the primary goal should be to get to the catheterization laboratory to characterize the anatomy and revascularize the culprit vessel as soon as possible. Patient history, physical exam, laboratory exam, and echocardiography, if available, ar

It’s another session of CardioNerds Rounds! In these rounds, Co-Chair, Dr. Karan Desai (previous FIT at the University of Maryland Medical Center, and now faculty at Johns Hopkins) joins Dr. Ryan Tedford (Professor of Medicine and Chief of Heart Failure and Medical Directory of Cardiac Transplantation at the Medical University of South Carolina in Charleston, SC) to discuss the nuances of managing pulmonary hypertension in the setting of left-sided heart disease. Dr. Tedford is an internationally-recognized clinical researcher, educator, clinician and mentor, with research focuses that include the hemodynamic assessment of the right ventricle and its interaction with the pulmonary circulation and left heart. This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes.  Speaker disclosures: None Cases discussed and Show Notes • References • Production Team CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes – Challenging Cases – Nuances in Pulmonary Hypertension Management with Dr. Ryan Tedford Case #1 Synopsis: A woman in her late 30s presented to the hospital with 4 weeks of worsening dyspnea. Her history includes dilated non-ischemic cardiomyopathy diagnosed in the setting of a VT arrest around 10 years prior. Over the past 10 years she has been on guideline-directed medical therapy with symptoms that had been relatively controlled (characterized as NYHA Class II), but without objective improvement in her LV dimensions or ejection fraction (LVEF 15-20% by TTE and CMR and LVIDd at 6.8 cm). Over the past few months she had been noting decreased exercise tolerance, worsening orthopnea, and episodes of symptomatic hypotension at home. When she arrived to the hospital, she presented with BP 95/70 mmHg, increased respiratory effort, congestion and an overall profile consistent with SCAI Stage C-HF shock. In the case, we go through the hemodynamics at various points during her hospitalization and discuss options for management including medical therapy and mechanical support. The patient was eventually bridged to transplant with an Impella 5.5. Initial Hemodynamics Right Atrium (RA) Pressure Tracing: Right Ventricle (RV) Pressure Tracing: Pulmonary Artery (PA) Pressure Tracing: Pulmonary Capillary Wedge Pressure (PCWP) Tracing: Case 1 Rounding Pearls One of the first points that Dr. Tedford made was thinking about our classic frameworks of characterizing acute decompensated heart failure, specifically the “Stevenson” classification developed by Dr. Lynne Stevenson that phenotypes patients along two axes: congestion (wet or dry) and perfusion (warm or cold). Dr. Tedford cautioned that young patients may not fit into these classic boxes well, and that a normal lactate should not re-assure the clinician that perfusion is normal. In reviewing the waveforms, Dr. Tedford took a moment to note that besides just recording the absolute values of the pressures transduced in each chamber or vessel, it is critical to understand the morphology of the tracings themselves. For instance, with the RA pressure tracing above, there is no respiratory variation in the mean pressure. This is essentially a “resting Kussmaul’s sign,” which is typically indicative of significant RV dysfunction. Thus, even though our echocardiogram in this case did not necessarily show a significantly dilated RV with mildly reduced longitudinal function (TAPSE), hemodynamically the patient is demonstrating significant RV compromise. If we compare the RA pressure tracing to the PCWP, we see that there is respiratory variation in the PCWP tracing. We typically think of pronounced respiratory variation in the RA or PCWP tracing in the setting of obesity or lung disease, but loading conditions can also lead to significant respiratory variation. As was noted during the case discussion, irreversible pulmonary hypertension is considered an absolute contraindication to heart transplantation though there is variation on the absolute threshold above which transplantation is contraindicated. Generally, a pulmonary vascular resistance (PVR) of 3 Woods Units is considered a contraindication to isolated cardiac transplantation. Testing for reversibility of an elevated PVR with a vasodilator like nitroprusside is common in this patient population. In a study by Dr. Steven Hsu and colleagues, Pulmonary Artery Pulsatility Index (PAPi) was shown to be the hemodynamic factor that best correlated with int

The following question refers to Section 6.2 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Christian Faaborg-Andersen, answered first by Houston Methodist medicine resident Dr. Najah Khan, and then by expert faculty Dr. Jaideep Patel. Dr. Patel recently graduated from Virginia Commonwealth University cardiology fellowship and is now a preventive cardiologist at the Johns Hopkins Hospital. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #18 A 60-year-old Black woman with a history of hypertension and heart failure with reduced ejection fraction (EF 40%) presents to clinic for follow-up. She is currently doing well with NYHA class II symptoms. She is taking carvedilol 25 mg BID, sacubitril/valsartan 97/103 mg BID, and spironolactone 25 mg daily, all of which have been well tolerated. In clinic, her BP is 125/80 mmHg, and her HR is 55 bpm. Routine labs are within normal limits including Cr of 1.0, K of 4.0, and HbA1c of 6.0. What is the most appropriate next step in her management? A. No change in management B. Reduce beta blocker C. Add an SGLT2 inhibitor (dapagliflozin or empagliflozin) D. Add vericiguat E. Add hydralazine/isosorbide dinitrate Answer #18 The correct answer is C – Add an SGLT2 inhibitor (dapagliflozin or empagliflozin) For patients with symptomatic HFrEF, neurohormonal antagonists (ACEi, ARB, ARNI; BB; MRA) improve survival and reduce the risk of HF hospitalization. This patient is already on these agents. The addition of an SGLT2 inhibitor on top of neurohormonal blockade reduces the risk of CV death and worsening HF in patients with symptomatic HFrEF and is the next best step for this patient (Class I, LOE A). Vericiguat may be considered in patients with symptomatic HFrEF with HF worsening despite already being on maximally tolerated neurohormonal blockade (Class IIb, LOE B), but first-line therapies should be started first. Hydralazine/Isosorbide dinitrate should be considered in self-identified Black patients or people who have EF ≤ 35% or <45% with dilated LV with class III-IV symptoms despite maximally tolerated neurohormonal blockade (Class IIa, LOE B), but is not the next best step here. She is tolerating the beta blocker without adverse effects so there is no reason to decrease the dosage. Main Takeaway In patients with symptomatic HFrEF (EF ≤ 40%), SGLT2 inhibitors are considered first line therapy in addition to ACE-I/ARB/ARNI, BB, and MRAs to reduce the risk of HF hospitalization and death. Importantly this is irrespective of presence of diabetes. Guideline Location Section 6.2, page 3295-3296 Figure 13 page 3278; recommendation table page 3279. CardioNerds Decipher the Guidelines – 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

The following question refers to Section 4.9 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Christian Faaborg-Andersen, answered first by UCSD fellow Dr. Patrick Azcarate, and then by expert faculty Dr. Melissa Tracy. Dr. Tracy is a preventive cardiologist, former Director of the Echocardiography Lab, Director of Cardiac Rehabilitation, and solid organ transplant cardiologist at Rush University. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #17 A 74-year-old man with a history of hypertension, chronic kidney disease, and gastroesophageal reflux presents with chest pain and is found to have an NSTEMI due to an obstructive lesion in the proximal LAD. One drug-eluting stent is placed, and he is started on dual antiplatelet therapy with aspirin and clopidogrel. He is concerned about the risk of bleeding from his gastrointestinal tract. What would you recommend to reduce his risk of bleeding? A. Lansoprazole, a proton pump inhibitor B. Famotidine, a histamine-2 blocker C. Calcium carbonate, an antacid D. None, proton pump inhibitors are contraindicated. Answer #17 The correct answer is A. The ESC recommends that patients at high risk for GI bleeding who are receiving antiplatelet therapy take proton pump inhibitors (Class I, LOE A). High risk for bleeding includes patients who are age ≥65, history of peptic ulcer disease, Helicobacter pylori infection, dyspepsia or GERD symptoms, chronic renal failure, diabetes mellitus, and concomitant use of other antiplatelet agents, anticoagulants, nonsteroidal anti-inflammatory drugs, or steroids. Coadministration of proton pump inhibitors that specifically inhibit CYP2C19 (omeprazole or esomeprazole) may reduce the pharmacodynamic response to clopidogrel. Although this interaction has not been shown to affect the risk of ischemic events, coadministration of omeprazole or esomeprazole with clopidogrel is not recommended. Main Takeaway In patients with high gastrointestinal bleeding risk who are receiving antiplatelet therapy, proton pump inhibitors are recommended. Omeprazole and esomeprazole may reduce the efficacy of clopidogrel and should not be used concomitantly with clopidogrel. Guideline Location Section 4.9.3, Page 3291 Figure 13 page 3278; recommendation table page 3279. CardioNerds Decipher the Guidelines – 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

The following question refers to Section 4.6 and Figure 13 of the 2021 ESC CV Prevention Guidelines. The question is asked by student doctor Shivani Reddy, answered first by NP Carol Patrick, and then by expert faculty Dr. Roger Blumenthal. Dr. Roger Blumenthal is professor of medicine at Johns Hopkins where he is Director of the Ciccarone Center for the Prevention of Cardiovascular Disease. He was instrumental in developing the 2018 ACC/AHA CV Prevention Guidelines. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #16 True or False: For patients with established ASCVD, secondary prevention entails adding a PCSK9 inhibitor if goal LDL is not met on maximum tolerated doses of a statin and ezetimibe. Answer #16 The correct answer is True. The ultimate on-treatment LDL-C goal of <55 mg/dL (<1.4 mmol/L) and a reduction of at least ≥50% from baseline should be considered for primary prevention of persons <70 years of age at very high risk (Class IIa) and in those with established ASCVD (Class I). It is recommended that a high-intensity statin is prescribed up to the highest tolerated dose to reach these LDL-C goals (Class I). The combination of statin with ezetimibe brings a benefit that is in line with meta-analyses showing that LDL-C reduction has benefits independent of the approach used.  The beneficial effect of ezetimibe is also supported by genetic studies. Together, these data support the position that ezetimibe should be considered as second-line therapy, either on top of statins when the therapeutic goal is not achieved (Class I), or when a statin cannot be prescribed (Class IIa). PCSK9 inhibitors (monoclonal antibodies to PCSK9) decrease LDL-C by up to 60%, either as monotherapy or in addition to the maximum tolerated dose of statin and/or other lipid-lowering therapies, such as ezetimibe. Their efficacy appears to be largely independent of background therapy. Among patients in whom statins cannot be prescribed, PCSK9 inhibition reduced LDL-C levels when administered in combination with ezetimibe. Both alirocumab and evolocumab effectively lower LDL-C levels in patients who are at high or very high CVD risk, including those with DM, with a large reduction in future ASCVD events. Therefore, for those who do not meet LDL-C goals with maximally tolerated doses of both a statin and ezetimibe, combination therapy including a PCSK9 inhibitor may be considered for primary prevention of patients at very high risk but without familial hypercholesterolemia (Class IIa) and is recommended for secondary prevention for those with established ASCVD (Class I). In addition, for very-high-risk FH patients (that is, with ASCVD or with another major risk factor) who do not achieve their goals on a maximum tolerated dose of a statin and ezetimibe, combination therapy including a PCSK9 inhibitor is recommended (Class I). Main Takeaway Statins, ezetimibe, and PCSK9 inhibitors should be used in a stepwise approach to achieve target lipid lowering goals in accordance with their risk profile. Guideline Location Page 3279, Sections 4.6.3.1.4, 4.6.3.1.5 Figure 13 page 3278; recommendation table page 3279. CardioNerds Decipher the Guidelines – 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

The following question refers to Section 4.3 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern Dr. Maryam Barkhordarian, answered first by pharmacy resident Dr. Anushka Tandon and then by expert faculty Dr. Kim Williams. Dr. Williams is Chief of the Division of Cardiology and is Professor of Medicine and Cardiology at Rush University Medical Center. He has served as President of ASNC, Chairman of the Board of the Association of Black Cardiologists (ABC, 2008-2010), and President of the American College of Cardiology (ACC, 2015-2016). The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #15 Your patient mentions that she drinks “several” cups of coffee during the day. She also describes having a soda daily with lunch and occasionally a glass of wine with dinner. Which of the following recommendations is appropriate?  A. Coffee consumption is not harmful and may even be beneficial, regardless of the number of drinks per day. B. Drinking two glasses of wine/day is safe from a cardiovascular prevention standpoint. C. Soft drinks (and other sugar-sweetened beverages) must be discouraged. D. None of the above Listen to this podcast episode!  Answer #15 The correct answer is C.  Soft drinks (and other sugar-sweetened beverages) must be discouraged. Sugar-sweetened beverages have been associated with a higher risk of CAD and all-cause mortality. The ESC guidelines give a class I recommendation for restriction of free sugar consumption (in particular sugar-sweetened beverages) to a maximum of 10% of energy intake. This is a class IIa recommendation in the ACC/AHA guidelines. Choice A is incorrect because: the consumption of nine or more drinks a day of non-filtered coffee (such as boiled, Greek, and Turkish coffee and some espresso coffees) may be associated with an up to 25% increased risk of ASCVD mortality. Moderate coffee consumption (3-4 cups per day) is probably not harmful, and perhaps even moderately beneficial. Choice B is incorrect: It is a class I recommendation to restrict alcohol consumption to a maximum of 100 g per week. The standard drink in the US contains 14 g of alcohol, so 100 mg of alcohol translate to: o   84 ounces of beer (5% alcohol) o   Or 56 – 63 ounces of malt liquor (75% alcohol) or o   Or 35 ounces of wine (12% alcohol) or ONE 5 fl oz glass of wine/day. o   Or 31.5 ounces of distilled spirits (40% alcohol). The ACC/AHA guidelines recommended limiting alcohol consumption only for the management of hypertension to: ≤2 drinks daily for men and: ≤1 drink daily for women. Main Takeaway The main takeaway: ASCVD risk reduction can be achieved by restricting sugar-sweetened beverages to a maximum of 10% of energy intake. Guideline Location Section 4.3.2, Page 3271 CardioNerds Decipher the Guidelines – 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

The following question refers to Sections 3.3-3.4 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Adriana Mares, answered first by early career preventive cardiologist Dr. Dipika Gopal, and then by expert faculty Dr. Allison Bailey. Dr. Bailey is a cardiologist at Centennial Heart. She is the editor-in-chief of the American College of Cardiology’s Extended Learning (ACCEL) editorial board and was a member of the writing group for the 2018 American Lipid Guidelines.  The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #14 Ms. Soya M. Alone is a 70-year-old woman of Bangladeshi ethnicity with a history of anxiety and depression. She currently lives at home by herself, does not have many friends and family that live nearby, and has had a tough year emotionally after the passing of her husband. She spends most of her time in bed with low daily physical activity and has experienced more weakness and exhaustion over the past year along with loss of muscle mass. Which of the following are potential risk modifiers in this patient when considering her risk for CVD? A. Bangladeshi ethnicity B. Psychosocial factorsC. Frailty D. History of anxiety and depressionE. All of the above Answer #14 The correct answer is E – All of the above. Traditional 10-year CVD risk scores do not perform adequately in all ethnicities. Therefore, multiplication of calculated risk by relative risk for specific ethnic subgroups should be considered (Class IIa, LOE B). Individuals from South Asia have higher CVD rates. The ESC guidelines recommend using a correction factor by multiplying the predicted risk by 1.3 for Indians and Bangladeshis, and 1.7 for Pakistanis. These correction factors are derived from data from QRISK3. In the UK, the QRISK calculator algorithm has been derived and validated in 2.3 million people to estimate CVD risk in different ethnic groups and unlike other calculators, it counts South Asian origins as an additional risk factor. The reasons for such differences remain inadequately studied, as do the risks associated with other ethnic backgrounds. Barriers to developing accurate risk prediction tools include the wide heterogeneity amongst the population. The 2019 ACC/AHA guidelines also list high-risk race/ethnicities such as South Asian ancestry as a risk-enhancing factor. However, there is no separate pooled cohort equation for different ethnicities, and consideration should be given that the pooled cohort equations will underestimate ASCVD risk in South Asians. Psychosocial stress including loneliness and critical life events are associated, in a dose-response pattern, with the development and progression of ASCVD, with relative risks between 1.2 and 2.0. Conversely, indicators of mental health, such as optimism and a strong sense of purpose, are associated with lower risk. While there is not a specific way proposed by the guidelines for psychosocial factors to improve risk classification, it is important to screen patients with ASCVD for psychological stress, and clinicians should attend to somatic and emotional causes of symptoms as well. The ESC guidelines give a Class IIa (LOE B) recommendation for assessment of stress symptoms and psychosocial stressors. This patient should also be formally screened for frailty, which is not the same as aging but includes factors such as slowness, weakness, low physical activity, exhaustion and shrinking, and makes her more vulnerable to the effect of stressors and is a risk factor for both high CV and non-CV morbidity and mortality. However, the ability of frailty measures to improve CVD risk prediction has not been formally assessed, so the guidelines do not recommend integrating it into formal CVD risk assessment. Frailty may however, influence treatment as it can help build an individualized care plan. Mental disorders such as anxiety and depression are associated with the development of CVD as well. Detrimental effects may be potentially caused by unhealthy lifestyle, increased exposure to socioeconomic stressors, and cardiometabolic side-effects of medications. The ESC guidelines give a Class 1 (LOE C) recommendation that mental disorders with either significant functional impairment or decreased use of healthcare systems be considered as influencing total CVD risk. Main Takeaway Psychosocial stress and frailty are associated with risk of ASCVD and should be assessed in patients when considering CVD risk. In addition, current risk scores may under-or over-estimate CVD risk in different ethnic minority groups. Guideline Location Section 3.3.1, 3.3.2, 3.3.4, 3.4.10, page 3258 – 3259, 3265 – 3266 CardioNerds Decipher the Guidelines – 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNer

The following question refers to Section 3.2 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Hirsh Elhence, answered first by Mayo Clinic Fellow Dr. Teodora Donisan, and then by expert faculty Dr. Eugene Yang. Dr. Yang is professor of medicine of the University of Washington where he is medical director of the Eastside Specialty Center and the co-Director of the Cardiovascular Wellness and Prevention Program. Dr. Yang is former Governor of the ACC Washington Chapter and current chair of the ACC Prevention of CVD Section. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #13 You are seeing a 45-year-old woman with a past medical history of hypertension, overweight status, hyperlipidemia, and active tobacco use disorder. Her BMI is 27 kg/m2, BP is 150/75, HbA1C is 5.8%, total cholesterol is 234 mg/dL, HDL is 59 mg/dL, and LDL is 155 mg/dL. She is from Romania, a country with very high CVD risk. Which of the following statements is CORRECT? A. LDL-C needs to be decreased by at least 50%, as small absolute LDL-C reductions would not provide clinical benefit B. Hypertension is not an important CVD risk factor in our patient, as she is young. C. Prediabetes is not a significant CV risk factor for our patient, as she is not yet diabetic. D. Smoking confers a higher CVD risk for women than for men. E. Her weight does not increase her CVD risk, as she is overweight rather than obese Answer #13 The correct answer is D – Smoking confers a higher CVD risk for women than for men. Prolonged smoking increases the CVD risk more in women than in men. Our patient is 45 years old. CVD risk in smokers < 50 years-old is 5x higher than in non-smokers. Of note, smoking is responsible for 50% of all avoidable deaths in smokers and a lifetime smoker will lose 10 years of life, on average. Secondhand smoke and smokeless tobacco can also increase the CVD risk. Option A is incorrect. The SCORE2 risk chart for populations at very high CVD risk places her at a 14% (very high) 10-year risk for myocardial infarction, stroke, or cardiovascular death. She would derive benefit even from incremental reductions in LDL-C values. The absolute benefit of lowering LDL-C depends on both the absolute risk of ASCVD and the absolute reduction in LDL-C, so even a small absolute reduction in LDL-C may be beneficial in high- or very-high-risk patients. Furthermore, the reduction in CVD risk is proportional to the decrease in LDL-C, irrespective of the medications used to achieve such change. This remains true even when lowering LDL-C values to < 55 mg/dl. Option B is incorrect. Hypertension is a major cause of CVD regardless of age, and the risk of death from either CAD or stroke increases linearly from BP levels as low as 90 mmHg systolic and 75 mmHg diastolic upwards. Particularly relevant for our patient, lifetime BP evolution differs in women compared to men, potentially resulting in an increased CVD risk at lower BP thresholds. Option C is incorrect. Type 1 DM, type 2 DM, and prediabetes are all independent risk factors for ASCVD. Of note, it would be important to address this risk factor with our patient, as women who develop type 2 diabetes have a particularly high risk for stroke. Option E is incorrect. All-cause mortality is lowest at a BMI on 20-25 kg/m2 in apparently healthy patients. Even overweight patients are at increased CVD risk. There is a linear relationship between BMI and mortality in non-smokers and a J-shaped relationship in ever-smokers. In patients with heart failure, a lower mortality risk has been observed with higher BMI – the “obesity paradox.” It would be important to evaluate the waist circumference in our patient, as both BMI and waist circumference are associated with ASCVD risk. Main Takeaway The main ASCVD risk factors are hyperlipidemia (elevated apolipoprotein-B-containing lipoproteins, of which LDL-C is most abundant), hypertension, cigarette smoking, diabetes, and adiposity. Identifying patients who will benefit most from ASCVD risk factor treatment is central to ASCVD prevention efforts. In general, the higher the absolute CVD risk, the higher the absolute benefit of risk factor treatment, and thus the lower the number needed to treat to prevent one CVD event during a period of time. Guideline Location Section 3.2.1., pages 3236, 3242, 3243. CardioNerds Decipher the Guidelines – 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

CardioNerds (Dr. Kelly Arps, Dr. Colin Blumenthal, Dr. Dan Ambinder, and Dr. Teodora Donisan) discuss the screening, detection, and diagnosis of atrial fibrillation (AF) with Dr. Ben Freedman. AF is frequently undiagnosed and its first manifestation can be a debilitating stroke. European and American guidelines differ slightly with regards to guidelines for AF screening in asymptomatic individuals. There are multiple methods available to screen for AF; the setting and the clinical scenario can help guide the choice. Consumer-led screening has its own challenges, as it can detect AF in a younger population where we should prioritize aggressive management of risk factors and comorbidities. There is uncertainty regarding the minimum AF burden that increases thromboembolic risk, however a high CHAD2S2-VASc score remains the strongest predictor of stroke risk independent of AF burden. Perioperative AF associated with non-cardiac surgery has increased risk of future stroke and adverse cardiac outcomes and should likely be treated as a new diagnosis of chronic AF.    This CardioNerds Atrial Fibrillation series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Kelly Arps and Dr. Colin Blumenthal. This series is supported by an educational grant from the Bristol Myers Squibb and Pfizer Alliance. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. We have collaborated with VCU Health to provide CME. Claim free CME here! Disclosures: Dr. Ben Freedman disclosed that he has received grant or research support from Pfizer. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – Screening, Detection, and Diagnosis of Atrial Fibrillation “Stroke is a poor early sign of AF.”   AF remains frequently undiagnosed and there remains uncertainty about the optimal target population and screening methodology.   “We have to tailor AF screening to the purpose we’re using it for”   If in a primary care setting, check the pulse. If the goal is to exclude high-risk AF –  handheld ECG for heart rhythm snapshots are appropriate. If the goal is to identify or exclude AF with a high level of certainty, continuous monitors are necessary for greater sensitivity.  Consumer-led screening is performed by (mostly young) individuals using commercial monitors and smart watches, facilitating earlier recognition of paroxysmal AF in this population. In these cases, we should prioritize aggressive management of risk factors and comorbidities to reduce the risk of progression to persistent AF.  There is no specific cutoff for AF duration which has been identified to predict elevated stroke risk; AF is likely both a risk factor and a risk marker for stroke, suggesting an underlying atrial myopathy.  Non-cardiac surgeries and procedures can be considered “AF stress tests.” If AF occurs in these settings, it is usually more clinically significant and has a higher risk of stroke and death than AF associated with cardiac surgeries.  Notes – Screening, Detection, and Diagnosis of Atrial Fibrillation Notes drafted by Dr. Teodora Donisan and reviewed by Dr. Kelly Arps 1. Why is it important to screen for AF and who should be screened?  AF is frequently undiagnosed and its first manifestation can be a debilitating stroke or death. Let’s go over a few numbers:  15% of people with AF are currently undiagnosed and 75% of those individuals would be eligible for anticoagulation.1    10-38% of individuals with ischemic strokes are found to have AF as a plausible cause, and the true proportion may be even higher, given difficulties in detecting intermittent AF.2  Current guideline recommendations:   European guidelines: opportunistic screening for AF is recommended for individuals ≥65 years old.3  American guidelines: AF screening is recommended in patients with cryptogenic strokes and those with device-recorded atrial high-rate episodes.4  Opportunistic screening for AF can be done by checking the pulse or noticing the irregular heart rate on blood pressure monitors. When AF is found by opportunistic screening at a single time point, it is usually persistent AF. Continuous ambulatory heart rhythm monitoring can identify shorter episodes of paroxysmal AF, perhaps earlier in the AF disease course.   In patients with unexplained stroke we have different ways to search for occult AF:  In the hospital: all patients should have 72h of ECG monitoring. There is evidence that nurse-led ECG surveillance detects more paroxysmal AF

CardioNerds Tommy Das (Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic), Rick Ferraro (cardiology fellow at the Johns Hopkins Hospital), and Dr. Xiaoming Jia (Cardiology Fellow at Baylor College Medicine) take a closer look at the mechanism of icosapent ethyl in triglyceride lowering and ASCVD risk reduction with Dr. Michael Shapiro, the Fred M. Parrish professor of cardiology at Wake Forest University and Director of the Center for Preventative Cardiology at Wake Forest Baptist Health. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. This episode is part of the CardioNerds Lipids Series which is a comprehensive series lead by co-chairs Dr. Rick Ferraro and Dr. Tommy Das and is developed in collaboration with the American Society For Preventive Cardiology (ASPC). Relevant disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiovascular Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls – Icosapent Ethyl Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are two major Omega-3 fatty acids found in fish oil. While both have been shown to lower triglycerides, only purified EPA formulations have been shown to reduce ASCVD risk. Mechanisms of triglyceride (TG) lowering by icosapent ethyl are multiple and include reduction of hepatic VLDL production, stimulation of lipoprotein lipase activity, increased chylomicron clearance, reduced lipogenesis, increased beta oxidation, and reduced delivery of fatty acids to the liver. There was only modest reduction of triglycerides in REDUCE-IT and JELIS despite association with significant reduction in cardiovascular outcome events, suggesting likely mechanisms outside of triglyceride lowering that may contribute to ASCVD reduction. While there was an increased signal for peripheral edema and atrial fibrillation associated with icosapent ethyl in prior trials, overall side effect rates were very low. Icosapent ethyl is considered to be cost-effective based on cost-effective analysis. Show notes – Icosapent Ethyl EPA and DHA have differing biological properties that may explain differences in ASCVD risk reduction observed in cardiovascular outcome trials 1. The REDUCE-IT trial, which enrolled secondary prevention and high-risk primary prevention patients with elevated triglycerides who were on statin therapy, showed significant reduction of major adverse cardiovascular events in the icosapent ethyl group compared with a mineral oil placebo2.  Only modest reductions of TG were seen in the REDUCE-IT and JELIS trials despite association with significant reduction in events 2,3.  Potential mechanisms contributing favorable effects of EPA on ASCVD risk reduction include inhibition of cholesterol crystal formation, stabilization of membrane structures, reversal of endothelial dysfunction, inhibition of lipoprotein and membrane lipid oxidation 4. Pleotropic effects of EPA include influence on platelet aggregation, lower thromboxane activity, increased prostaglandin level, and effects on blood pressure, insulin resistance and inflammation. Triglycerides are a surrogate for triglycerides-rich lipoproteins, which are likely causally associated with ASCVD 5. There is increased signal for bleeding, lower extremity edema, and atrial fibrillation with icosapent ethyl but overall side effect rates are very low 2. In order to ensure higher rates of medication access and adherence, clinicians must be cognizant of the cost to the patient. In practice, it is important to have a structured approach to improve insurance approval rate for medications that require prior authorizations With icosapent ethyl, cost effectiveness analyses have shown the medication is cost-effect for ASCVD risk reduction in secondary prevention patients and high-risk diabetic patients6. While moderate hypertriglyceridemia (150-499mg/dL) is likely a marker for increased residual risk for ASCVD, those with severe hypertriglyceridemia (>=500mg/dL) are also at risk for acute pancreatitis. Remember that these are fasting levels and post-prandial levels are likely much higher (i.e., in the thousands). In most scenarios, hypertriglyceridemia is driven by a combination of environmental and genetic factors. Environmental factors to consider when treating these patients include diet, alcohol intake, metabolic syndrome, diabetes, hypothyroidism, nephrotic syndrome, CKD, medications (ie. anti-rejection medications, steroids, thiazides). Hypertriglyceridemia is very amenable to lifestyle modification – diet, weight loss, exercise, diabetes control, etc. Equations for estimating LDL-C are generally not accurate when TG is severely elevated. In these circumstances we can instead use direct LDL-C, non-HDL-C, or apoB. We are

CardioNerd (Amit Goyal), ACHD series co-chair Dr. Agnes Koczo (UPMC), and episode FIT lead, Dr. Logan Eberly (Emory University, incoming ACHD fellow at Boston Adult Congenital Heart) join Dr. Peter Ermis (Program Director of the Adult Congenital Heart Disease Program at Texas Children’s Heart Center), and Dr. Scott Cohen (Associate Professor and Director of the Adult Congenital Heart Disease Program at the Medical College of Wisconsin) for a discussion about transitions of care in congenital heart disease. Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship and CardioNerds Academy Fellow). Congenital heart disease (CHD) is the most common clinically significant congenital defect, occurring in approximately 1 in 100 live births. With modern advances in pediatric cardiology and cardiac surgery, over 90% of children born in the developed world with CHD will now survive into adulthood, and there are currently more adults than children living with CHD in the United States1. As these children become adults, they will need to transition their care from pediatric to adult-centered care. Unfortunately, during this transition period, there is often delayed or inappropriate care, improper timing of the transfer of care, and undue emotional and financial stress on the patients, their families, and the healthcare system. At its worst, patients are lost to appropriate follow-up. In this episode, we review the current climate in transitions of care for CHD patients from child-centered to adult-centered care, discuss the difficulties that can occur during the transitions process. We further discuss how to mitigate them, and highlight the key elements to the successful transitions of care. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls – Transitions of Care in Congenital Heart Disease There is a clear distinction between the TRANSFER of care and TRANSITION of care. Transfer is merely moving from a pediatric to adult provider. Transition involves the continuing education of the patient with regards to their congenital heart disease, the importance of longitudinal follow up, and leading patients toward more autonomous medical care. Transition begins in the pediatric cardiology clinic prior to the transfer of care and is an ongoing process that continues well after the physical transfer of care. A critical aspect of the transition and transfer of care is cultivating trust—that is, the new adult congenital heart disease (ACHD) provider must earn the trust of the patient and family. A failure to do so will inevitably prevent an optimal transition of care. During transition, parents are transitioning along with their children. With transition to adult care, there is also a goal to transition responsibility for medical care from the parent to the child. Setting goals and expectations can help both the parents and the child effectively make this transition. Loss to follow up is one of the most concerning complications of poor transition. Interestingly, there does not appear to be a strong association between complexity of congenital heart disease and the likelihood of loss to follow up. ACHD providers should not assume that patients with complex ACHD are less likely to be lost to follow up. For example, approximately 25-30% of Fontan patients have lapses or gaps in care. Effective transition of care is essential for all severity levels of ACHD. It is recommended in the 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease2, as well as in the 2011 AHA Scientific Statement on Best Practices in Managing Transition to Adulthood for Adolescents With Congenital Heart Disease3. Show notes – Transitions of Care in Congenital Heart Disease 1. What is the current climate in transitions of care for patients from child-centered to adult-centered care, and what are some of the difficulties on the side of the provider as well as the patient during this process? Transition is a complex process, and there

CardioNerds (Amit Goyal and Daniel Ambinder), join  Dr. Gurleen Kaur (Director of CardioNerds Internship and medicine resident at Brigham and Women’s Hospital),  Dr. Victoria Thomas (Cardionerds Ambassador, Vanderbilt University Medical Center) Dr. Katie Berlacher (Cardiology program director, University of Pittsburgh Medical Center), and Dr. Julie Damp (Vanderbilt University Medical Center Cardiovascular disease fellowship program director) to discuss becoming & thriving as a fellowship program director and more in this installment of the Narratives in Cardiology Series. Special message by Tennessee ACC State Chapter Governor, Dr. John L Jefferies. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Tweetorial – Becoming & Thriving as a Fellowship Program Director with Dr. Katie Berlacher and Dr. Julie Damp https://twitter.com/gurleen_kaur96/status/1542620967733805056?s=21&t=AMSKElEz4oZZTA9nVbWBCA Video version – Becoming & Thriving as a Fellowship Program Director with Dr. Katie Berlacher and Dr. Julie Damp https://youtu.be/E-C-SSV7LZg Notes – Becoming & Thriving as a Fellowship Program Director with Dr. Katie Berlacher and Dr. Julie Damp Drafted by Dr. Victoria Thomas. 1. What does it mean to be a big “E” when people say they are a clinician Educator? It can mean teaching students directly at bedside.  However, it is also a sacrifice of daily mentoring and listening to students’ challenges and difficulties. Being a clinician educator is just as much of a calling as is serving in medicine. Clinician Educators focus on medicine but also the science and best practices of teaching the art of doctoring. 2. What is physician burnout? Why is this important for to CardioNerds? Physician burnout is a syndrome of chronic workplace stress that leads to emotional exhaustion and a sense of dissatisfaction and disconnection personally and professionally.  30-45% of cardiologists have reported physician burnout. 3. What factors affect physician burnout? Emotional and physical exhaustion often lead to physician burnout. First year of training as an intern or fellow and first year of serving as an attending are particularly high-risk periods. This is largely due to learning a new system and responsibilities mixed with a sense of decreased accomplishment. The sense of decreased accomplishment can lead to physicians suffering from impostor syndrome. Grit can be defined as a perseverance for long-term goals.  The level of grit was not associated with burnout among first-year Internal Medicine residents. 4. What are some of the solutions to prevent or address physician burnout? Physicians need to feel a sense of belonging and should be supported and celebrated when they have accomplished something by their colleagues and administrators. Fellows and attendings want to feel listened to and supported. Destigmatizing this idea of “perfection in medicine”. Physician should share with each other their accomplishments but also their mistakes to create a community of personal and professional connection and acceptance. Practicing mini acts of gratitude such as exercise or therapy can help with burnout. Delegation of work tasks and taking breaks have been shown to improve mental well-being. 5. What support do program directors have to help prevent burnout for themselves? Many local graduate medical education (GME) offices will have some resources for program directors depending on the size and funding.  The Accreditation Council for Graduate medical Education (ACGME) had developed an on-line series to help new program directors understand their new roles.  It is also recommended to network and create community of program directors to work with and bounce ideas from. 6. What are some of the differences found among cardiology program directors regarding support fro

CardioNerds (Amit and Dan) join Dr. Omid Amidi (CardioNerds Academy Graduate) and Dr. Marwah Shahid from the UCLA Cardiology Fellowship program along with Dr. Evelyn Song (CardioNerds Academy House Faculty and Heart Failure Hospitalist at UCSF) to discuss a complex case focused on management of severe coronary artery disease in a patient with Glanzmann thrombasthenia. Dr. Rushi Parikh (Interventional cardiologist, UCLA) provides the ECPR for this episode. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. Glanzmann Thrombasthenia is a bleeding disorder due to impairment of platelet aggregation secondary to a mutation in the GPIIB/IIIA receptor. This case is focused on work up of stable coronary artery disease followed by a discussion on duration of dual antiplatelet therapy post percutaneous coronary intervention in a patient with Glanzmann thrombasthenia.   Check out this published case in JACC: Case Reports Jump to: Case media – Case teaching – References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media See the published case in JACC: Case Reports Episode Schematics & Teaching Pearls 1. Patients with Glanzmann thrombocytopenia (GT) may have a higher risk of bleeding, depending on their disease phenotype. 2. It is unclear whether the mechanism of GT protects patient against stent thrombosis in the setting of PCI. Additionally, there is little data on the use of antiplatelet agents in patients with GT. 3. Short-term DAPT may be a reasonably safe option for patients with GT undergoing PCI. 4. We report a successful case of percutaneous coronary intervention in a patient with GT with no complications at a 1 year follow up. Notes 1. What is Glanzmann thrombasthenia? GT is an inherited platelet disorder that is characterized by spontaneous bleeding with phenotypic variability ranging from minimal bruising to potentially fatal hemorrhaging.  GT is caused by autosomal recessive inheritance of quantitative or qualitative deficiencies of functional αIIbβ3 integrin coded by ITGA2B or ITGB3 genes for αIIb and β3, respectively. As a result, platelets may be stimulated, but the platelet glycoprotein IIb/IIIa receptor is unable to bind fibrinogen to cross-link platelets, rending them potentially ineffective. In platelet aggregation studies, there is lack of response to collagen, epinephrine, arachidonic acid, and ADP stimulation. Thus, platelet aggregation is impaired.  2. What is known about PCI and antiplatelet therapy in the setting of Glanzmann thrombasthenia? To the best of our knowledge, this is the first case report of percutaneous coronary intervention in the setting of GT. It is unclear if the mechanism of GT alone provides sufficient antiplatelet activity and whether antiplatelet therapy leads to significantly increased bleeding risk. The use of antiplatelet therapy is not well studied in the GT population. What we do know is that the mechanism of GT prevents platelet aggregation—the final step in platelet-related thrombosis—while oral antiplatelet therapy affects platelet activation, thus, in our patient we felt that short term DAPT was reasonable. It is important to note that in the event of an active bleed requiring platelet transfusion, donor platelets possess functional glycoprotein IIb/IIIa receptors and thus exponentially increase the risk of stent thrombosis. Therefore, unlike our case, if a patient is not maintained on chronic oral antiplatelet therapy, initiation of oral or intravenous antiplatelet therapy should be considered to prevent stent thrombosis at the time of platelet transfusion. Like any other patient with a high bleeding risk, it is important to have clear indications to conduct a coronary angiogram in patients with GT. Shared decision making is vital in regard to the benefits and risk of an angiogram in relation to the patient’s presentation, symptoms and history. The same is true in regard to coronary revascularization in these patients. Besides functional stress testing, coronary CTA is a viable option to evaluate coronary anatomy to identify high risk anatomy in these patients. References Truong Katie P., Zhang Jessica J., Shahid Marwah, et al. Management of high-grade coronary artery disease and concomitant glanzmann thrombasthenia. JACC: Case Reports. 2021;3(14):1625-1629. Lawton Jennifer S., Tamis-Holland Jacqueline E., et al. 2021 acc/aha/scai guideline for coronary artery revascularization. Journal of the American College of Cardiology. 2022;79(2):e21-e129. Gulati Martha, Levy Phillip D., et al. 2021 aha/acc/ase/chest/saem/scct/scmr guideline for the evaluation and diagnosis of chest pain. Journal of the American College of Cardiology. 2021;78(22):e187-e285.

CardioNerds (Amit Goyal and Daniel Ambinder), Dr. Ahmed Ghoneem (CardioNerds Academy Chief of House Taussig and medicine resident at Lahey Hospital), and Dr. Gurleen Kaur (Director of CardioNerds Internship and medicine resident at Brigham and Women’s Hospital) discuss family history of premature ASCVD with Dr. Ann Marie Navar, Preventive Cardiologist and Associate Professor in the Departments of Internal Medicine and Population and Data Sciences at UT Southwestern Medical Center. They discuss the art of soliciting a nuanced family history, refining cardiovascular risk using risk models and novel markers, counseling patients with elevated risk, and more. Show notes were drafted by Dr. Ahmed Ghoneem and reviewed by Dr. Gurleen Kaur. Audio editing was performed by CardioNerds Intern, student Dr. Adriana Mares. For related teaching, check out this Tweetorial about CAC by Dr. Gurleen Kaur, the Family History of Premature ASCVD Infographic by Dr. Ahmed Ghoneem, and the CardioNerds Cardiovascular Prevention Series. CardioNerds Cardiovascular Prevention PageCardioNerds Episode Page Show notes – Family History of Premature ASCVD with Dr. Ann Marie Navar Patient summary: Mr. B is a 51-year-old gentleman who is referred to CardioNerds Prevention Clinic by his PCP. He does not have a significant past medical history. He is a former smoker but quit 2 years ago. His BP in clinic today is 138/84; he is not on any antihypertensives. His most recent lipid profile 2 weeks prior showed a total cholesterol level of 250 mg/dL, a TG level of 230 mg/dL, an LDL cholesterol of 174 mg/dL, and an HDL cholesterol of 30 mg/dL. He tells us that his father had a “heart attack” at the age of 52, and he would like to further understand his own risk. We calculate his ASCVD risk score, and it is 9.8%. 1. What constitutes a positive family history (FHx) of premature ASCVD? What is an approach to the art of soliciting the FHx from our patients? Definition of family history of premature ASCVD: the history of an atherosclerotic event (e.g., myocardial infarction or stroke) in a male first degree relative before the age of 55 or a female first degree relative before the age of 65. Dr. Navar’s approach to soliciting a family history: Lead with a general question such as “what do you know about any medical conditions that run in your family?”. Then ask more specific questions about the parents and siblings, such as “Is your mother still alive? How long did she live? Has she ever had a heart attack or stroke?” If the answer is yes, ask about how old they were at the time of the event. A challenging aspect of the FHx can be eliciting the difference between atherosclerotic events and sudden cardiac death. While atherosclerotic diseases are a much more common cause of unexplained sudden death, it’s important that we don’t miss the opportunity to identify inherited cardiomyopathies, channelopathies, inherited aortopathies or other heritable SCD syndromes. 2. Is the “dose” of family history important (for example: the number of affected relatives, the closeness of those relationships, the age of onset)? While conducting studies to test this may be difficult, the few studies that have looked at the number of affected relatives have found a dose-response type relationship, where increasing number of relatives affected increases the risk of heart disease.1,2 3. How does a family history affect cardiovascular risk stratification? FHx of premature ASCVD does not improve the predictive ability of the Pooled Cohort Equations (PCE) at a population level. Therefore, it does not factor into the ASCVD risk calculation utilizing the PCE. However, it enhances the patient’s risk at an individual level. The ACC/AHA guidelines recognize FHx of premature ASCVD as a risk-enhancing factor [together with CKD, chronic inflammatory conditions such as psoriasis, primary hypercholesterolemia, high-risk ethnicity such as South Asian ancestry, metabolic syndrome, history of premature menopause (before age 40 y) and history of pregnancy-associated conditions that increase later ASCVD risk, such as preeclampsia].3 Dr. Navar’s advice is to think of the PCE as a starting point during risk assessment, followed by searching for the other risk-enhancing factors, to come up with a more tailored risk assessment for that individual patient. 4. After we explained to our patient the enhanced risk, he tells us that he feels like his fate is sealed and that nothing he can do would improve his outcomes because it’s in his genes. We have data though, that shows that healthy lifestyles reduce the risk of coronary artery disease and individuals at high genetic risk of CAD.4 How would you handle this challenging conversation and counsel our patient? We should always think about how risk conversations can affect our patients emotionally. Many patients come to CV prevention clinic because they want to know what they can do about their risk. A “scared straight” approach can be

It’s another session of CardioNerds Rounds! In these rounds, Co-Chairs, Dr. Karan Desai and Dr. Natalie Stokes and Dr. Tiffany Dong (FIT at Cleveland Clinic) joins Dr. Randall Starling (Professor of Medicine and Director of Heart Transplant and Mechanical Circulatory Support at Cleveland Clinic) to discuss the nuances of guideline directed medical therapy (GDMT) through real cases. As a past president of the Heart Failure Society of America (HFSA) and author on several guidelines, Dr. Starling gives us man pearls on GDMT. Come round with us today by listening to the episodes and joining future sessions of #CardsRounds! This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes.  Speaker disclosures: None Cases discussed and Show Notes • References • Production Team CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes – CardioNerds Rounds: Challenging Cases – Modern Guideline Directed Therapy in Heart Failure with Dr. Randall Starling Case #1 Synopsis: A man in his 60s with known genetic MYPBC3 cardiomyopathy and heart failure with a reduced ejection fraction of 30% presents with worsening dyspnea on exertion over the past 6 months. His past medical history also included atrial fibrillation with prior ablation and sick sinus syndrome with pacemaker implantation. Medications are listed below. He underwent an elective right heart catheterization prior to defibrillator upgrade for primary prevention. At the time of right heart catheterization, his blood pressure was 153/99 with a heart rate of 60. His RHC demonstrated a RA pressure of 15mmHg, RV 52/16, PA 59/32 (mean 41), and PCWP 28 with Fick CO/CI of 2.8 L/min and index of 1.2 L/min/m2. His SVR  was 1900 dynes/s/cm-5. He was admitted to the cardiac ICU and started on nitroprusside that was transitioned to a regimen of Sacubitril-Valsartan and Eplerenone. His final RHC numbers were RA 7, PA 46/18/29, PCWP 16 and Fick CO/CI 6.1/2.6. His discharge medications are shown below. Takeaways from Case #1 Unless there are contraindications (cardiogenic shock or AV block), continue a patient’s home beta blocker to maintain the neurohormonal blockade benefits. A low cardiac index should be interpreted in the full context of the patient, including their symptoms, other markers of perfusion (e.g., urine output, mentation, serum lactate), and mean arterial pressure before holding or stopping beta blockade. Carvedilol, metoprolol succinate and bisoprolol are all evidence-based options for beta blockers in heart failure with reduced ejection fraction. If there is concern of lowering blood pressure too much with Sacubitril/Valsartan, one method is to trial low dose of valsartan first and then transition to Sac/Val. Note, in the PARADIGM-HF trial, the initial exclusion criteria for starting Sac/Val included no symptomatic hypotension and SBP ≥ 100. At subsequent up-titration visits, the blood pressure criteria was decreased to SBP ≥ 95. In multiple studies, protocol-driven titration of GDMT has shown to improve clinical outcomes, yet titration remains poor. The following image from Greene et al. in JACC shows that in contemporary US outpatient practices that GDMT titration is poor with few patients reaching target dosing. Case #2 Synopsis: A 43 year-old male with a past medical history of familial dilated cardiomyopathy requiring HVAD placement two years prior now comes in with low flow alarms. He is feeling well otherwise with chronic dyspnea on exertion. A CT chest and abdomen with contrast for showed outflow graft occlusion. Given a TTE showed LV recovery that correlated with invasive hemodynamics, his LVAD was decommissioned. He was tried on a low dose Sacubitril/Valsartan but was unable to tolerate it due to hypotension. He was discharged on carvedilol 3.125mg BID and lisinopril 5mg daily. Over the next 10 months in clinic, his GDMT was titrated to carvedilol 25mg BID, spironolactone 25mg daily and Sacubitril/Valsartan 49-51mg BID.  Takeaways Case #2 In patients with ventricular assist devices, the differential for low flow alarms includes hypovolemia, arrhythmias, RV failure, cardiac tamponade and inflow cannula obstruction. A careful history, exam (with particular attention to the JVD), and bedside echocardiogram can help differentiate the cause. EF recovery occurs in about 5% of patients in large LVAD registries. Favorable prognostic factors for EF recovery include female sex and nonischemic

Atrial fibrillation may reach pandemic proportions in the next 2-3 decades. Factors that drive this phenomenon have been studied in predominantly White populations, leading to a significant underrepresentation of certain racial/ethnic groups in atrial fibrillation epidemiological studies. Most atrial fibrillation epidemiology studies suggest that the non-Hispanic Black population has a lower incidence/prevalence of atrial fibrillation, despite a higher risk factor burden (“Afib paradox”). At the same time, non-Hispanic Blacks have worse outcomes compared to the White population and underrepresented populations and women are less likely than White men to receive optimal guideline-based therapies for atrial fibrillation. In this episode, CardioNerds Dr. Kelly Arps (Co-Chair Atrial Fibrillation series, Cardiology fellow at Duke University), Dr. Colin Blumenthal (Co-Chair Atrial Fibrillation series, CardioNerds Academy House Faculty Leader for House Jones, Cardiology fellow at the University of Pennsylvania), and Dr. Dinu-Valentin Balanescu (CardioNerds Academy Faculty for House Jones, rising internal medicine chief resident at Beaumont Hospital), discuss with Dr. Larry Jackson (cardiac electrophysiologist and Vice Chief of Diversity, Equity, and Inclusion in the Division of Cardiology at Duke University) about atrial fibrillation epidemiology and health equity, challenges and possible solutions to improving diversity in clinical trials, and race/ethnicity/sex/gender differences in the detection, management, and outcomes of atrial fibrillation. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. This CardioNerds Atrial Fibrillation series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Kelly Arps and Dr. Colin Blumenthal. This series is supported by an educational grant from the Bristol Myers Squibb and Pfizer Alliance. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. We have collaborated with VCU Health to provide CME. Claim free CME here! Disclosure: Larry R. Jackson II, MD, MHs, has the following relevant financial relationships:Advisor or consultant for: Biosense Webster Inc.Speaker or a member of a speakers bureau for: Biotronik Inc.; Medtronic Inc. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – Atrial Fibrillation: Epidemiology, Health Equity, & The Double Paradox Atrial fibrillation confers an enormous public health burden. It is estimated that it will reach pandemic proportions over the next 30 years, with potentially 100-180 million people worldwide suffering from this condition. Large epidemiological atrial fibrillation registries have very small populations of underrepresented groups. More diverse enrollment in clinical trials is essential and may be obtained by increasing diversity among research staff, principal investigators, and steering committees, and use of mobile/telehealth technologies to remove bias related to differences in presentation. The CardioNerds Clinical Trials Network specifically aims pair equitable trial enrollment with trainee personal and professional development. Most atrial fibrillation epidemiology studies suggest that the non-Hispanic Black population has lower incidence/prevalence of atrial fibrillation, despite higher risk factor burden. This “paradox” is likely due to a multifactorial process, with clinical differences, socioeconomic factors, and genetic factors contributing. Underrepresented populations are less likely than White patients to receive optimal guideline-based management of atrial fibrillation. Though there is a higher incidence of intracranial bleeding on vitamin K antagonists in this population, they are less likely to receive optimal anticoagulation for stroke prevention with direct oral anticoagulants. Also, despite overall worse outcomes, they are less likely to be prescribed rhythm control strategies or offered catheter-based ablation despite known data with improved outcomes with early rhythm control. Gender-based differences in atrial fibrillation epidemiology, management, and outcomes also exist. Compared to men, women have a lower incidence/prevalence of atrial fibrillation but are more likely to be symptomatic. They are also more likely to receive rate instead of rhythm control strategies and suboptimal stroke reduction therapies Overall, women have worse outcomes than men.  “I want to differentiate [equitable care] from equal care. I think this idea of equity means that we have to take into account the myriad of differences that we see between people of different races, ethnicities, ge

CardioNerds Tommy Das (Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic), Rick Ferraro (cardiology fellow at the Johns Hopkins Hospital), and Dr. Aliza Hussain (cardiology fellow at Baylor College Medicine) take a deep dive on the REDUCE-IT trial with Dr. Peter Toth, director of preventive cardiology at the CGH medical center in Sterling, Illinois, clinical professor in family and community medicine at the University of Illinois School of Medicine, and past president of the National Lipid Association and the American Board of Clinical Lipidology. Special introduction to CardioNerds Clinical Trialist Dr. Jeff Wang (Emory University). Audio editing by CardioNerds academy intern, Shivani Reddy. This episode is part of the CardioNerds Lipids Series which is a comprehensive series lead by co-chairs Dr. Rick Ferraro and Dr. Tommy Das and is developed in collaboration with the American Society For Preventive Cardiology (ASPC). Relevant disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiovascular Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls – REDUCE-IT The Reduction of Cardiovascular Events with EPA-Intervention Trial (REDUCE-IT) trial was a large randomized controlled trial that showed a significant reduction in atherosclerotic cardiovascular disease (ASCVD) events with use of icosapent ethyl ester in secondary prevention patients and high risk primary prevention patients with diabetes and residual elevated triglycerides between 135 to 499 mg/dL on top of maximally tolerated statin therapy1. Despite the use of high intensity statin therapy, considerable residual risk for future atherosclerotic cardiovascular disease exists in patients with ASCVD. Elevated triglycerides (TGs) are an important marker of increased residual ASCVD risk2. There are two primary types of Omega-3 fish oils: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Omege-3 fish oils have been shown to lower triglyceride levels. Low-dose combination EPA and DHA has not exhibited incremental cardiovascular benefit in either primary prevention and secondary prevention patients on top of statin therapy3-5. REDUCE-IT showed the use of high dose EPA in patients with either ASCVD or DM and one additional risk factor, and relatively well-controlled LDL-C levels on maximally tolerated statin therapy and residual hypertriglyceridemia (TG 135-499 mg/dL) results in significant reductions in cardiovascular events over a median follow-up period of 4.9 years1. Show notes – REDUCE-IT Multiple epidemiologic and Mendelian randomization studies have established elevated triglyceride (TG) levels as an important risk factor for atherosclerotic cardiovascular events6-8. However previous clinical trials using TG-lowering medication such as niacin, fibrates and low dose omega-3 fish oil have not shown to reduce cardiovascular events when added to statin therapy in patients with or without ASCVD,9,10. The JELIS trial first demonstrated a significant reduction in cardiovascular events when 1.8g daily of eicosapentaenoic acid (EPA) was added to low-intensity statin therapy in patients with ASCVD and hypercholesterolemia, However, the trial was limited due to open label design without placebo, use of low doses of background statin therapy, and geographic/demographic limitations to participants in Japan11. In a large international multicenter randomized controlled trial, the Reduction of Cardiovascular Events with Icosapent Ethyl–Intervention Trial (REDUCE-IT) randomized 8,179 patients with established atherosclerotic heart disease or diabetes and an additional risk factor, on maximally tolerated statin therapy, to 4 gm/day of icosapent ethyl (a highly purified and stable EPA ethyl ester) or mineral oil1.  Over a median follow up of 4.9 years, the use of icosapent ethyl ester was associated with significant reductions in major cardiovascular events (cardiovascular death, nonfatal MI, nonfatal stroke, coronary revascularization, or unstable angina) compared to placebo, with an absolute risk reduction of 4.8% and NNT of 21. There were similar reductions in the key components of the primary endpoint, including a 20% relative risk reduction in cardiovascular death with icosapent ethyl. Median TG levels were reduced by 18% in the icosapent ethyl group and rose by 2.2% in the placebo group. LDL levels increased in both groups, although to a lesser degree in the icosapent ethyl group. There was a trend towards increased bleeding (2.7% with icosapent ethyl versus 2.1% with placebo, p=0.06) and a modest but significant increase in hospitalizations for atrial fibrillation or flutter with icosapent ethyl (3.1% versus 2.1%). Since the publication of REDUCE-IT, several clinical practice guidelines, including tho

The following question refers to Section 4.11 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Christian Faaborg-Andersen, answered first by UCSF resident Dr. Jessie Holtzman, and then by expert faculty Dr. Laurence Sperling. Dr. Laurence Sperling is the Katz Professor in Preventive Cardiology at the Emory University School of Medicine and Founder of Preventive Cardiology at the Emory Clinic. Dr. Sperling was a member of the writing group for the 2018 Cholesterol Guidelines, serves as Co-Chair for the ACC’s Cardiometabolic and Diabetes working group, and is Co-Chair of the WHF Roadmap for Cardiovascular Prevention in Diabetes. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #12 Medically supervised cardiac rehabilitation programs after ASCVD events and for patient with heart failure carries a Class I recommendation. However, placement of referrals, uptake and enrollment after referral, and rigor of rehabilitation all remain inconsistent. What minimum cumulative duration of cardiac rehabilitation has been chosen as a threshold of effectiveness for cardiac rehabilitation by the European Society of Cardiology? A. 100-300 minutes, 10 sessions B. 300-500 minutes, 16 sessions C. 500-700 minutes, 22 sessions D. 700-1000 minutes, 28 sessions E. >1000 minutes, 36 sessions Answer #12 The correct answer is E: >1000 minutes across 36 sessions. Cardiac rehabilitation is a comprehensive, multidisciplinary intervention not just including exercise training and physical activity counselling, but also education, risk factor modification, diet/nutritional counselling, and vocational and psychosocial support. A broad evidence base demonstrates that multidisciplinary cardiac rehabilitation and prevention programs after ASCVD events or revascularization reduce recurrent cardiovascular hospitalizations, myocardial infarction, and cardiovascular mortality. In patients with chronic HF (mainly HFrEF), exercise based cardiac rehabilitation (EBCR) may improve all-cause mortality, reduce hospital admissions, and improve exercise capacity and quality of life. Such programs include a wide array of activities including physical activity, risk factor modification, psychosocial support, nutrition counseling, and more. Despite the heterogenous design of clinical trials, cardiac rehabilitation has been shown to be a cost-effective intervention. Based upon the available review data, the European Association of Preventive Cardiology and the European Society of Cardiology proposed minimum standards for secondary prevention cardiac rehabilitation programs. Based upon a comprehensive review of the literature, ESC recommends that cardiac rehabilitation be multidisciplinary, supervised by health professionals, and start as soon as possible after a cardiovascular event. Cardiac rehabilitation should include both aerobic and muscular resistance tailored to the fitness level of the participant, should carry a duration of >1000 minutes in total, and should exceed 36 sessions total. While uptake remains limited, electronic prompts within the medical record and automatic referrals should be considered to enhance referral and participation. Future research should continue to explore the benefit of home-based cardiac rehabilitation with or without telemonitoring. Lastly, studies have shown that uptake remains lower among women, and targeted programs should be undertaken to address such disparities. Main Takeaway Current European Society of Cardiology guidelines provide a Class I (LOE A) recommendation for the participation in multidisciplinary cardiac rehabilitation programs for the secondary prevention of ASCVD events including revascularization and in individuals with heart failure (mainly HFrEF) to improve patient outcomes. Guideline Location Section 4.11, Page 3292. CardioNerds Decipher the Guidelines – 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

The following question refers to Section 6.1 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Christian Faaborg-Andersen, answered first by UCSD cardiology fellow Dr. Harpreet Bhatia, and then by expert faculty Dr. Eugenia Gianos. Dr. Gianos specializes in preventive cardiology, lipidology, cardiovascular imaging, and women’s heart disease; she is the director of the Women’s Heart Program at Lenox Hill Hospital and director of Cardiovascular Prevention for Northwell Health. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #11 A 70-year-old man with a history of hypertension, diabetes, hyperlipidemia, peptic ulcer disease with a prior upper GI bleed, as well as coronary artery disease presents to clinic. About one year ago he suffered an NSTEMI treated with percutaneous coronary intervention to the mid LAD. He is feeling well and able to walk 1 mile daily with no anginal symptoms. He is currently taking aspirin 81 mg daily, ticagrelor 90 mg BID, atorvastatin 40 mg daily, metoprolol 25 mg BID, lisinopril 5 mg daily, and lansoprazole 15mg daily. He has a preserved ejection fraction. His BP in clinic is 110/70 and HR is 65 bpm. His LDL is 50 mg/dL. What do you recommend for his further management? A. Switch ticagrelor to clopidogrel, continue indefinitelyB. Stop ticagrelor, continue aspirin indefinitelyC. Continue aspirin + ticagrelor indefinitelyD. Stop ticagrelor, start rivaroxaban 2.5 mg BID Listen to the podcast episode! Answer #11 The correct answer is B – stop ticagrelor, continue aspirin indefinitely. Twelve months of DAPT is recommended for acute coronary syndromes (Class I, LOE A). Long-term secondary prevention with dual anti-thrombotic therapy (DAPT > 12 months with a P2Y12 inhibitor and low-dose aspirin or low-dose rivaroxaban 2.5mg BID with low-dose aspirin) may be considered for patients who are at high ischemic risk without high risk of bleeding (Class IIa, LOE A). However, this patient is at increased bleeding risk (peptic ulcer disease with prior GI bleeding) and has no ischemic symptoms, and so neither would be recommended. Main Takeaway In summary, 12 months of DAPT is recommended after ACS. Prolonged DAPT or low-dose rivaroxaban may be considered with high ischemic risk and low bleeding risk. Guideline Location Section 6.1, Pages 3294-3295. CardioNerds Decipher the Guidelines – 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

The following question refers to Section 4.6 of the  2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Shivani Reddy, answered first by NP Carol Patrick, and then by expert faculty Dr. Eileen Handberg. Dr. Handberg is an Adult Nurse Practitioner, Professor of Medicine, and Director of the Cardiovascular Clinical Trials Program in the Division of Cardiovascular Medicine at the University of Florida. She has served as Chair of the Cardiovascular Team Section and the Board of Trustees with the ACC and is the President Elect for the PCNA. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #10 Ms. DW is a 67-year-old woman with a history of coronary artery disease and prior percutaneous coronary intervention in 2019 with a drug-eluting stent to the proximal left anterior descending artery. They have transitioned to your clinic from a previous provider, and their LDL is 134 mg/dL. What would be the ESC recommended goal LDL-C level for this patient?  A. <30 mg/dL B. <55 mg/dL C. <70 mg/dL D. <100 mg/dL Answer #10 The correct answer is B. The ESC guidelines outline a robust LDL-C reduction goal of <55mg/dL (<1.4mmol/L) and ≥50% reduction from baseline in those with known atherosclerotic cardiovascular disease, with the highest possible Class I (LOE A) recommendation for this goal. A goal LDL-C <55mg/dL with ≥50% reduction from baseline should also be considered in apparently healthy persons <70 years of age who are at very high risk (Class IIa, LOE C).  To achieve these goals, the guidelines recommend a stepwise approach to treatment including dietary, lifestyle, and medical management. Recognizing that lower LDL-C is better, the guidelines recommend liberal intensification of treatment especially if using submaximal doses of generic or low-cost statins and side effects are not apparent. High-intensity statin is recommended to be prescribed to the highest tolerated dose to reach LDL-C goals set for each specific risk group (Class I, LOE A). If these goals are not achieved with the maximum tolerated dose of a statin, combination therapy with ezetimibe is recommended (Class I, LOE B). Choice A is incorrect. An LDL-C <30mg/dL is a more significant reduction than that recommended by the guidelines, even for patients with known ASCVD. Notably, for patients with ASCVD who experience a second vascular event within 2 years while taking maximum tolerated statin-based therapy, an LDL-C goal of <1.0 mmol/L (40 mg/dL) may be considered. Choice C is incorrect. The ESC prevention guidelines recommend considering a goal of <70mg/dL for patients in the primary prevention setting at high risk who are <70 years of age (Class IIa, LOE C). (Recall again that for those at very high risk the primary prevention recommendation is target LDL-C <55 mg/dL). Choice D is incorrect. LDL-C <100mg/dL was a frequently cited goal in older iterations of various prevention and lipid guidelines. As the data has shifted to support lower LDL-C goals, this is not a noted goal within the 2021 ESC prevention guidelines for patients <70 years of age. Main Takeaway Lower is better when it comes to LDL-C For those with known atherosclerotic cardiovascular disease, liberal intensification of lipid lowering treatment is recommended.  Guideline Location Section 4.6.2.1, page 3276-3279, Figure 6 on page 3252, Figure 7 on page 3253 CardioNerds Decipher the Guidelines – 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

The following question refers to Section 4.3 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Maryam Barkhordarian, answered first by pharmacy resident Dr. Anushka Tandon, and then by expert faculty Dr. Noreen Nazir. Dr. Noreen Nazir is Assistant Professor of Clinical Medicine at the University of Illinois at Chicago, where she is the director of cardiac MRI and the preventive cardiology program. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #9 Mr. A is a 28-year-old man who works as an accountant in what he describes as a “desk job” setting. He shares that life got “a little off-track” for him in 2020 between the COVID-19 pandemic and a knee injury. His 2022 New Years’ resolution is to improve his overall cardiovascular and physical health. He has hypertension and a family history of premature ASCVD in his father, who died of a heart attack at age 50. Prior to his knee injury, he went to the gym 3 days a week for 1 hour at a time, split between running on the treadmill and weightlifting. He has not returned to the gym since his injury and has been largely sedentary, although he is trying to incorporate a 20-minute daily walk into his routine. Which of the following exercise-related recommendations is most appropriate? A. A target of 75-150 minutes of vigorous-intensity or 150-300 minutes of moderate-intensity aerobic physical exercise weekly is recommended to reduce all-cause mortality, CV mortality, and morbidity. B. Bouts of exercise less than 30 minutes are not associated with favorable health outcomes. C. Exercise efforts should be focused on aerobic activity, since only this type of activity is associated with mortality and morbidity benefits. D. Light-intensity aerobic activity like walking is expected to have limited health benefits for persons with predominantly sedentary behavior at baseline. Answer #9 The correct answer is A. There is an inverse relationship between moderate-to-vigorous physical activity and CV morbidity/mortality, all-cause mortality, and incidence of type 2 diabetes, with additional benefits accrued for exercise beyond the minimum suggested levels. The recommendation to “strive for at least 150-300 min/week of moderate-intensity, or 75-150 min/week of vigorous-intensity aerobic physical activity, or an equivalent combination thereof” is a Class 1 recommendation per the 2021 ESC guidelines, and a very similar recommendation (at least 75 minutes of vigorous-intensity or 150 minutes of moderate-intensity activity) is also Class 1 recommendation per 2019 ACC/AHA primary prevention guidelines. Both the ESC and ACC/AHA provide examples of activities grouped by absolute intensity (the amount of energy expended per minute of activity), but the ESC guidelines also offer suggestions for measuring the relative intensity of an activity (maximum/peak associated effort) in Table 7, which allows for a more individualized, customizable approach to setting activity goals. Importantly, individuals who are unable to meet minimum weekly activity recommendations should still be encouraged to stay as active as their abilities and health conditions allow to optimize cardiovascular and overall health. Choice B is incorrect, as data suggests physical activity episodes of any duration, including <10 min, are associated with favorable outcomes like all-cause mortality benefit. The duration of a single exercise bout is less correlated with health benefits than the total physical activity time accumulated per week. Choice C is incorrect. Per the ESC guidelines, it is a class 1 recommendation to perform resistance exercise, in addition to aerobic activity, on 2 or more days per week to reduce all-cause mortality. Data indicate that the addition of resistance exercise to aerobic activity is associated with lower risks of total CV events and all-cause mortality, so it’s expected that a combination of weightlifting and aerobic activity may be more beneficial for than either type of activity alone. The 2019 ACC/AHA prevention guidelines do not make a formal recommendation regarding resistance exercise; they do note that it has multiple health benefits (e.g., BP-lowering, improved glycemic control) though state its association with ASCVD risk reduction is unclear.  Choice D is incorrect: sedentary time is independently associated with greater risk for several major chronic diseases and mortality. Reducing sedentary time for inactive adults and adding in light-intensity physical activity (as little as 15 minutes daily) is a class 1 recommendation to reduce all-cause and CV mortality and morbidity. The 2019 ACC/AHA guidelines suggest that reduced sedentary behavior may be “reasonable for ASCVD risk reduction” (Class 2b). Assuming our patient has had pr

This question refers to Sections 3.1 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern, student Dr. Hirsh Elhence, answered first by internal medicine resident at Beaumont Hospital and soon to be Mayo Clinic cardiology fellow and Dr. Teodora Donisan and then by expert faculty Dr. Eugene Yang. Dr. Yang is professor of medicine of the University of Washington where he is medical director of the Eastside Specialty Center and the co-Director of the Cardiovascular Wellness and Prevention Program. Dr. Yang is former Governor of the ACC Washington Chapter and current chair of the ACC Prevention of CVD Section. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #8 Please read the following patient vignettes and choose the FALSE statement. A. A 39-year-old man who comes for a regular physical, has normal vitals and weight, denies any significant past medical or family history – does not need systematic cardiovascular disease (CVD) assessment.B. A 39-year-old woman who comes for a regular physical, has normal vitals and weight, and has a history of radical hysterectomy (no other significant past medical or family history) – could benefit from systematic or opportunistic CVD assessment.C. A 39-year-old woman who comes for a regular physical, has normal vitals except for a BMI of 27 kg/m2 and a family history of hypertension – requires a systematic global CVD assessment.D. A 39-year-old man who comes for a regular physical, has normal vitals and weight, and has a personal history of type I diabetes – requires a systematic global CVD assessment. Answer #8 The correct answer is C. Option A is an accurate statement, as systematic CVD risk assessment is not recommended in men < 40 years-old and women < 50 years-old, if they have no known cardiovascular (CV) risk factors. (Class III, level C) Option B is an accurate statement, as this patient had a radical hysterectomy, which means the ovaries have been removed as well and she is considered postmenopausal. Systematic or opportunistic CV risk assessment can be considered in men > 40 years-old and women > 50 years-old or postmenopausal, even in the absence of known ASCVD risk factors. (Class IIb, level C) Option C is a false statement and thus the correct answer, as the recommendations for global screening in this patient are not as strong and would require shared decision making. Opportunistic screening of blood pressure can be considered in her, as she is at risk for developing hypertension. Blood pressure screening should be considered in adults at risk for the development of hypertension, such as those who are overweight or with a known family history of hypertension. (Class IIa, level B) Option D is an accurate statement, as systematic global CVD risk assessment is recommended in individuals with any major vascular risk factor (i.e., family history of premature CVD, familial hyperlipidemia, CVD risk factors such as smoking, arterial hypertension, DM, raised lipid level, obesity, or comorbidities increasing CVD risk). (Class I, level C) Additional learning points: Do you know the difference between opportunistic and systematic CVD screening? Opportunistic screening refers to screening without a predefined strategy when the patient presents for different reasons. This is an effective and recommended way to screen for ASCVD risk factors, although it is unclear if it leads to benefits in clinical outcomes. Systematic screening can be done following a clear strategy formally evaluating either the general population or targeted subpopulations (i.e., type 2 diabetics or patients with significant family history of CVD). Systematic screening results in improvements in risk factors but has no proven effect on CVD outcomes. Main Takeaway Systematic CVD risk assessment in the general population without CV risk factors does not seem to be cost effective and has unclear benefits on outcomes, although it does lead to increased detection of potentially actionable CV risk factors. Risk assessment is not a one-time event and should be repeated (e.g., every 5 years), but there is no clear data to guide intervals. Guideline Location Section 3.1, page 3236; Table on page 3242. CardioNerds Decipher the Guidelines – 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

The following question refers to Section 3.4 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Adriana Mares, answered first by early career preventive cardiologist Dr. Dipika Gopal, and then by expert faculty Dr. Michael Wesley Milks. Dr. Milks is a staff cardiologist and assistant professor of clinical medicine at the Ohio State University Wexner Medical Center where he serves as the Director of Cardiac Rehabilitation and an associate program director of the cardiovascular fellowship. He specializes in preventive cardiology and is a member of the American College of Cardiology’s Cardiovascular Disease Prevention Leadership Council. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #7 While you are on holiday break visiting your family, your aunt pulls you aside during the family gathering to ask a few questions about your 70-year-old uncle. He has hypertension, hyperlipidemia, type 2 diabetes mellitus, and moderate chronic obstructive pulmonary disease. His medications include Fluticasone/Salmeterol, Tiotropium, Albuterol, Lisinopril, Simvastatin, and Metformin. She is very concerned about his risk for heart disease as he has never had his “heart checked out.” She asks if the presence of COPD increases his chance of having heart disease. Which of the following statements would best answer her question? A. Systemic inflammation and oxidative stress caused by COPD promote vascular remodeling and a paradoxical ‘anticoagulant’ state affecting all vasculature types. B. Although chronic COPD is associated with increased cardiovascular events, individual exacerbations have no impact on risk of cardiovascular events. C. Patients with mild-moderate COPD are 8-10x more likely to die from atherosclerotic cardiovascular disease than respiratory failure. D. Cardiovascular mortality increases proportionally with an increase in forced expiratory volume in 1 second (FEV1) Answer #7 The correct answer is C. Patients with mild-moderate COPD are 8-10x more likely to die from atherosclerotic cardiovascular disease than respiratory failure. Patients with COPD have a 2-3-fold increased risk of CV events compared to age-matched controls even when adjusted for tobacco smoking, a shared risk factor. This can be partly explained by other common risk factors including aging, hypertension, hyperlipidemia, and low physical activity. Interestingly, CVD mortality increases proportionally with a decrease (rather than increase) in FEV1, making answer choice D wrong (28% increase CVD mortality for every 10% decrease in FEV1). Additionally, COPD exacerbations and related infections are associated with a 4x increase in CVD events, making answer choice B incorrect. COPD has several effects on the vasculature which creates a ‘procoagulant’ not ‘anticoagulant’ effect on all vascular beds. This is associated with increased risk of cognitive impairment due to cerebral microvascular damage as well as increased risk of ischemic and hemorrhagic stroke. Main Takeaway The presence of COPD (even mild to moderate) has a significant impact on the incidence of non-fatal coronary events, stroke, and cardiovascular mortality mediated by inherent disease process and progression, risk factors (smoking, aging, hypertension, and hyperlipidemia), and systemic inflammation altering vasculature creating a ‘procoagulant’ effect. The ESC gives a Class I indication (LOE C) to investigate for ASCVD and ASCVD risk factors in patients with COPD. Guideline Location 3.4.5, Page 3264. CardioNerds Decipher the Guidelines – 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

CardioNerds (Amit Goyal, Daniel Ambinder) and special co-host Dr. Mark Belkin, join the Journal of Cardiac Failure Family to discuss the 2022 AHA/ACC/HFSA Guideline for The Management of Heart Failure. The JCF Editor-In-Chief Dr. Robert Mentz, Deputy Editor Dr. Anu Lala, and FIT editors — Dr. Vanessa Bluemer, Dr. Ashish Corrhea, and Dr. Quinton Youmans — share their hot takes and practical takeaways from the guidelines. At JCF, we’re privileged to share this important document that will support improved care for those living with heart failure,” stated Editor-in Chief Dr. Robert J. Mentz and Deputy Editor Anu Lala. “The 2022 guidelines convey patient-centered updates regarding the language we use to communicate disease considerations (e.g., stages of HF) and practice-changing guidance around the diagnosis and management of HF including newer therapeutics (e.g., SGLT2i). There is an emphasis not only on managing HF but also on how to treat important comorbidities as part of the holistic care for patients living with HF.” 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure Executive Summary A Clinician’s Guide to the 2022 ACC/AHA/HFSA Guideline for the Management of Heart Failure by Dr. Michelle Kittleson CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Guideline Top 10 Take-Home Messages – Guideline for The Management of Heart Failure 1. Guideline-directed medical therapy (GDMT) for heart failure (HF) with reduced ejection fraction (HFrEF) now includes 4 medication classes that include sodium-glucose cotransporter-2 inhibitors (SGLT2i). 2. SGLT2i have a Class of Recommendation 2a in HF with mildly reduced ejection fraction (HFmrEF). Weaker recommendations (Class of Recommendation 2b) are made for ARNi, ACEi, ARB, MRA, and beta blockers in this population. 3. New recommendations for HFpEF are made for SGLT2i (Class of Recommendation 2a), MRAs (Class of Recommendation 2b), and ARNi (Class of Recommendation 2b). Several prior recommendations have been renewed including treatment of hypertension (Class of Recommendation 1), treatment of atrial fibrillation (Class of Recommendation 2a), use of ARBs (Class of Recommendation 2b), and avoidance of routine use of nitrates or phosphodiesterase-5 inhibitors (Class of Recommendation 3: No Benefit). 4. Improved LVEF is used to refer to those patients with previous HFrEF who now have an LVEF >40%. These patients should continue their HFrEF treatment. 5.Value statements were created for select recommendations where high-quality, cost-effectiveness studies of the intervention have been published. 6. Amyloid heart disease has new recommendations for treatment including screening for serum and urine monoclonal light chains, bone scintigraphy, genetic sequencing, tetramer stabilizer therapy, and anticoagulation. 7. Evidence supporting increased filling pressures is important for the diagnosis of HF if the LVEF is >40%. Evidence for increased filling pressures can be obtained from noninvasive (e.g., natriuretic peptide, diastolic function on imaging) or invasive testing (e.g., hemodynamic measurement). 8. Patients with advanced HF who wish to prolong survival should be referred to a team specializing in HF. A HF specialty team reviews HF management, assesses suitability for advanced HF therapies, and uses palliative care including palliative inotropes where consistent with the patient’s goals of care. 9. Primary prevention is important for those at risk for HF (stage A) or pre-HF (stage B). Stages of HF were revised to emphasize the new terminologies of “at risk” for HF for stage A and pre-HF for stage B. 10.Recommendations are provided for select patients with HF and iron deficiency, anemia, hypertension, sleep disorders, type 2 diabetes, atrial fibrillation, coronary artery disease, and malignancy.

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Phoo Pwint Nandar (former FIT Ambassador), Dr. Deep Shah (current FIT Ambassador), and Dr. Sugat Wagle from the Summa Health Cardiology Department for an afternoon at Cuyahoga National Valley Park. We discuss a case of a post-partum woman who presented with ventricular fibrillation arrest due to SCAD. She had ongoing advanced cardiac life support (ACLS) for nearly 60 minutes before obtaining return of spontaneous circulation. We discuss the broad differential of VF arrest, including acute coronary syndrome and spontaneous coronary artery dissection (SCAD) – among many others. We also go over the etiology and management of SCAD as well the complications. Pregnancy is a crucial stressor to the cardiovascular system and understanding its hemodynamic changes is crucial to all physicians. The E-CPR segment is provided by Dr. Grace Ayafor, Interventional cardiology faculty, Summa Health. This episode is made possible with support from Medmastery. At Medmastery you can learn some of the most important clinical skills like echo, advanced EKG, coronary angiography, PCI basics, pacemaker- and ICD troubleshooting and so much more. CardioNerds listeners can get an exclusive 15% discount on a lifetime subscription. Click HERE for details. Jump to: Case media – Case teaching – References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media Episode Schematics & Teaching – SCAD Pearls – SCAD SCAD remains underdiagnosed. It has a wide range of clinical presentations, including chest pain, ACS, VT/VF arrest, and cardiogenic shock. Underlying etiologies of SCAD include autoimmune diseases, connective tissue disorders, fibromuscular dysplasia, external stressors, and pregnancy. There are 3 types of SCAD, and coronary angiogram is the gold standard for diagnosis. Common areas of involvement of SCAD include left anterior descending and left circumflex arteries; however, SCAD can manifest in any coronary artery as well as simultaneously in multiple coronary arteries. Left main trunk involvement is rare, more likely to be associated with the peri-partum state, and requires complex management decisions guided by a heart team approach. Most SCAD cases are benign and treated conservatively, however, some require intervention (PCI or CABG) depending on clinical severity and course. Recurrent SCAD has been reported in 10-30% of the patients and aggressive management of hypertension is recommended. Guidelines regarding SCAD management are largely based on expert consensus due to a dearth of high-quality data. Efforts to raise awareness and study this syndrome are of paramount importance. Notes – SCAD 1. What is SCAD and how does it present? Spontaneous coronary artery dissection (SCAD) is defined as an epicardial coronary dissection that is not associated with atherosclerosis or instrumentation. This occurs with hematoma formation within the tunica media,  thereby potentially compressing the arterial true lumen leading to ischemia. There are two proposed mechanisms of hematoma formation: “inside-out” and “outside-in”. The inside-out hypothesis posits that the hematoma arises from the true lumen via a dissection flap – an endothelial-intimal disruption. Conversely the outside-in hypothesis posits that the hematoma arises de novo within the media through disruption of traversing microvessels. There is a wide range of clinical presentation for SCAD varying in severity including asymptomatic / benign presentation, anginal syndromes, acute myocardial infarction, VT/VF arrest, and cardiogenic shock. Our patient presented with VF arrest and ACS. SCAD epidemiology is confounded by a lack of awareness. A high index of suspicion is warranted. Diagnosis can be missed in young or mid-life without CV risk factors who would present with atypical/mild chest pain. 2. What are the etiologies of SCAD? SCAD is associated with the peripartum state (presumed due to combination of hormonal mediated vessel wall integrity changes and hemodynamic stressors), illicit substance use, autoimmune disorders, connective tissue disorders, fibromuscular dysplasia, and vigorous external stressors. Many patients recall extreme physical or emotional stress preceding the event. Men are more likely to present in the setting of a physical stressor whereas women are more likely to report an emotional stressor. Pregnancy-associated SCAD is most common in the first week after delivery like our patient. Genetic evaluation for connective tissue disorders and aortopathy syndromes (i.e., Marfan, Loeys-Dietz, and Ehlers-Danlos) should be considered. Arterial imaging to identify significant extracoronary vascular abnormalities is recommended since there is the association of SCAD with fibromuscular dyspla