Cardionerds: A Cardiology Podcast

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214. Lipids: Review of Icosapent Ethyl with Dr. Michael Shapiro Jun 19, 2022

Show notes

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 authorizationsWith 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 entering an exciting era of preventative cardiology with many new therapeutics in the pipeline. References - Icosapent Ethyl Mozaffarian D, Wu JH. Omega-3 fatty acids and cardiovascular disease: effects on risk factors, molecular pathways, and clinical events. J Am Coll Cardiol. 2011;58(20):2047-2067.Bhatt DL, Steg PG, Miller M, et al. Cardiovascular Risk Reduction with Icosapent Ethyl for Hypertriglyceridemia. N Engl J Med. 2019;380(1):11-22.Yokoyama M, Origasa H, Matsuzaki M, et al. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis. Lancet. 2007;369(9567):1090-1098.Jia X, Koh S, Al Rifai M, Blumenthal RS, Virani SS. Spotlight on Icosapent Ethyl for Cardiovascular Risk Reduction: Evidence to Date. Vasc Health Risk Manag. 2020;16:1-10.Wall R, Ross RP, Fitzgerald GF, Stanton C. Fatty acids from fish: the anti-inflammatory potential of long-chain omega-3 fatty acids. Nutr Rev. 2010;68(5):280-289.Weintraub WS, Bhatt DL, Zhang Z, et al. Cost-effectiveness of Icosapent Ethyl for High-risk Patients With Hypertriglyceridemia Despite Statin Treatment. JAMA Netw Open. 2022;5(2):e2148172. Guest Profiles Dr. Michael Shapiro Dr. Michael Shapiro the Fred M. Parrish professor of cardiology at Wake Forest University and leader in the field of cardiovascular prevention. He is the Director of the Center for Preventative Cardiology at Wake Forest Baptist Health and has published widely in the field of atherosclerosis imaging and cardiovascular health. Dr. Xiaoming Jia Dr. Xiaoming Jia is a cardiology fellow at Baylor College of Medicine CardioNerds Lipids Production Team Tommy Das, MD Dr. Rick Ferraro Amit Goyal, MD Daniel Ambinder, MD

213. ACHD: Transitions of Care in Congenital Heart Disease with Dr. Peter Ermis and Dr. Scott Cohen Jun 15, 2022

Show notes

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 is no “one size fits all” approach to the effective transition of ACHD patients.Many patients live far away from an ACHD centers of excellence.There are also currently not enough ACHD cardiologists to care for ACHD patients.Due to these challenges, there can be anxiety with regards to transferring care to an ACHD provider from the perspective of both the patient and the pediatric cardiologist.This time in a young person’s life is not just a time of transition of medical care; there are many simultaneous immense life transitions as well. There may be a loss of focus on the importance of ongoing follow up in medical care. 2. What topics should be addressed at the first ACHD visit? The ACHD program and its relationship to both the pediatric and adult hospital should be thoroughly explained, and the patient needs to be informed where both inpatient and outpatient care take place.ACHD providers should ask open-ended questions to determine the patient’s understanding of their congenital heart disease and then provide education as needed.The first ACHD visit should focus on laying out a detailed, long-term plan of care for the patient. Patients should be advised what specifically will be monitored going forward (such as valve function, cardiac chamber size, arrhythmias, etc.), as well as what future diagnostic testing (echo, MRI/CT, stress testing, etc.) is to be expected. For female patients, contraception and the safety of pregnancy should be addressed starting in the first visit.One of the primary goals of the first ACHD visit is also to build trust. To this end, an ACHD provider should try to avoid any major changes to medical therapy at the first visit unless deemed absolutely necessary. 3. What are advantages and disadvantages of different models of transitions of care? There is no “one size fits all” model to transition, but there certainly are some guiding principles.Formal transition programs are important. They can help normalize transition and eliminate the sentiment that the patient is being “kicked out” of pediatric cardiology clinic. Additionally, formal transitions programs can reduce unexpected cardiac hospitalizations for ACHD patients2. This decreases the unnecessary utilization of hospital resources.An ACHD program that remains within a children’s hospital has the benefit that the patients are already familiar with the site, and they may also be less likely to be lost to follow up. However, there is the drawback that non-cardiology providers in a children’s hospital are often unfamiliar with the management of adult medical problems, which necessitates forming relationships with adult providers at partner institutions, and this can be challenging.Ultimately, ACHD patients can be cared for effectively at either a children’s hospital-based or adult hospital-based program. The model that is most effective for a particular institution is dependent upon the resources available and the investment of a supportive multi-disciplinary team. 4. What is the role of the parents in the transition process? Parents play a vital role in the transition process. They are often quite informed of their child’s history, so the new ACHD provider needs to carefully review the patient’s history prior to the first visit. Having thorough knowledge of a patient's medical history will help build trust with patients and their families.ACHD providers should involve the parents in the transition process and should set goals and expectations. They should ask the parents to empower their child with regards to their medical care (such as encouraging them to manage their own medications, schedule their own medical appointments, etc.)ACHD providers need to have patience when working with parents during the transition process. Providers need to acknowledge that the parents have been the primary manager of their child’s medical care for many years, and it is often difficult to give up this role and to allow their child to be autonomous.It’s important to remember that parents are also transitioning. They transition from being the primary manager of their child’s health to being co-managers, before ultimately relinquishing the responsibility to their child. 5. What are some negative sequelae of a poor transition of care? The worst possible outcome is loss to follow up. This can result in potentially preventable medical complications.Inadequate or poor transition can lead to parental and/or patient distrust of the ACHD provider, which in turn increases the risk of being lost to follow up.Suboptimal transition increases the risk that the patient will engage in high-risk behaviors that can be harmful to their health.Patients who are not transitioned properly tend to utilize more hospital resources. 6. How should female ACHD patients be counseled on women’s health issues? In general, cardiologists are not well trained in addressing issues such as sexual health and contraception....

212. Narratives in Cardiology: Becoming & Thriving as a Fellowship Program Director with Dr. Katie Berlacher and Dr. Julie Damp – Tennessee Chapter Jun 03, 2022

Show notes

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 from leadership? 45% of men versus 29% of women program directors felt adequate support from leadership. 56% of late-career versus 35% mid-career and early-career program directors felt adequate support from leadership.There is no evidence to support this, however, but contributing factors may include the documented history of gender bias, wage inequality, and program size. References Team Cullen, M. W., Damp, J. B., Soukoulis, V., Keating, F. K., Abudayyeh, I., Auseon, A., ... & Weissman, G. (2021). Burnout and well-being among cardiology fellowship program directors. Journal of the American College of Cardiology, 78(17), 1717-1726.Mehta, L. S., Lewis, S. J., Duvernoy, C. S., Rzeszut, A. K., Walsh, M. N., Harrington, R. A., ... & American College of Cardiology Women in Cardiology Leadership Council. (2019). Burnout and career satisfaction among US cardiologists. Journal of the American College of Cardiology, 73(25), 3345-3348.Peckham C. Physician burnout: it just keeps getting worse. Medscape; 2015.Klein, A. J., Grau, T., Spagnoletti, C. L., Rothenberger, S. D., & Berlacher, K. (2021). Grit Does Not Predict Burnout among First-Year Internal Medicine Residents. Southern Medical Journal, 114(5), 272-276.Edwards, S. T., Helfrich, C. D., Grembowski, D., Hulen, E., Clinton, W. L., Wood, G. B., ... & Stewart, G. (2018). Task delegation and burnout trade-offs among primary care providers and nurses in Veterans Affairs Patient Aligned Care Teams (VA PACTs). The Journal of the American Board of Family Medicine, 31(1), 83-93.Shanafelt, T. D., & Noseworthy, J. H. (2017, January). Executive leadership and physician well-being: nine organizational strategies to promote engagement and reduce burnout. In Mayo Clinic Proceedings (Vol. 92, No. 1, pp. 129-146). Elsevier. Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

211. Case Report: A Zebra in Polka Dots – Coronary Intervention With Glanzmann Thrombasthenia – UCLA May 29, 2022

Show notes

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.

210. Family History of Premature ASCVD with Dr. Ann Marie Navar May 27, 2022

Show notes

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 de-motivating for these patients.“It's never too late to start cardiovascular prevention. And there are never patients that are too high risk that we can't do anything to lower their risk of heart disease” can be a reassuring beginning to the conversation.Reinforce any work that the patient has already done to lower their risk of heart disease such as quitting smoking. This shows the patients that they have already started making a difference.This can then be followed by discussing the available tools to lower this patient’s risk: diet modification, exercise, weight management, control of diabetes, control of blood pressure, statins, etc. 5. In addition to lifestyle management, would you recommend a statin for Mr. B, who has an intermediate CVD risk and risk enhancing factors such as positive family history? Dr. Navar’s short answer is YES. Even though the patient is at intermediate risk, his actual risk is higher given his family history. “The cornerstone of long-term risk prevention for this patient is going to be a statin”.Dr. Navar usually approaches this conversation using a simple yet effective analogy: “imagine that you're out shopping, and there's a vitamin that will lower your risk of heart disease over your lifetime by 30 to 50%, depending on your cholesterol level and how much your cholesterol is lowered. It's very safe. It has minimal side effects and it's all of $3 a month. But unlike vitamins, we actually have randomized control trial data that show that they make a difference. Would you take it?”.It’s important to identify the LDL goal for each patient before prescribing a statin. 6. Our patient is still uncertain about starting a statin mainly because he's asymptomatic and doesn't feel that his family history is a strong enough reason for him to have to take a daily medication for the rest of his life. The ACC/AHA guidelines highlight the importance of shared decision making with our patients. They also recommend measuring the coronary artery calcium or CAC score in intermediate risk patients to help facilitate a more informed risk discussion. Would a CAC score be of benefit in our patient’s case? The initial step in this decision-making process is to identify what are the patient’s thoughts on taking statins, i.e where they are on the “Statin Spectrum” as Dr. Navar eloquently described. It is important to discuss the current evidence for the benefit of statins, and that the relative risk reduction we see per degree of LDL lowering is actually highest in the youngest and lowest risk groups.Some patients are engaged and interested in taking statins from the beginning. It may not be beneficial to measure CAC scores in these patients.Other patients, like our patient, remain uncertain about statins. These patients are great candidates for CAC score, which acts as a “tie-breaker” in this situation. Being aware of the presence of CAC in their arteries can be a strong motivator for these patients to start statin therapy.In non-smoking patients with CAC=0, it would be reasonable to hold statin therapy and repeat a CAC score in five years (assuming no major change in other risk factors such as diabetes, return to smoking, etc.).5It is important to recognize the caveats of CAC scores:The ACC/AHA guidelines identify some patients whom clinicians should not de-risk despite a CAC=0, such as active smokers.CAC is less prevalent in young people, and less prevalent in women compared to men, raising the possibility of false reassurance.CAC testing involves a small, but not insignificant, amount of radiation exposure.It is often not covered by insurance. 7. There've been a lot of interest in novel lipid biomarkers such as lipoprotein(a) and Apolipoprotein B, and how elevated blood levels of these markers may be associated with ASCVD risk and are recognized as risk enhancing factors. How do you incorporate testing for Lp(a) and ApoB into your practice? Lipoprotein (a)It is a type of cholesterol particle that looks like an LDL particle, but it has an additional protein on it on the surface. It doesn't correlate with LDL levels or any of the traditional risk factors for ASCVD, and Lp(a) levels are very consistent throughout lifetime. Moreover, it is genetically determined, and elevated Lp(a) levels usually run in families.The guidelines recommend measuring Lp(a) in patients with family history of premature ASCVD.3There are no commercially available treatments at this time that lower Lp(a), however a number of novel therapies are currently in clinical trials.Despite that fact, several preventive cardiologists (such as Dr. Navar) may measure Lp(a) to identify patients at increased risk, and subsequently target lower LDL levels in these patients (LDL

209. CardioNerds Rounds: Challenging Cases – Modern Guideline Directed Therapy in Heart Failure with Dr. Randall Starling May 24, 2022

Show notes

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 cardiomyopathy of short duration.In the TRED-HF trial, patients were randomly assigned to phased withdrawal or continuation of GDMT over 6 months. The primary endpoint was relapse defined as a reduction in LVEF of more than 10% and to less than 50%, an increase in LVEDV by more than 10% and to higher than the normal range, a two-fold rise in NT-pro-BNP and to more than 400 ng/L or clinical evidence of heart failure. While a small trial (51 patients were enrolled), over the first 6 months, 44% of patients assigned to treatment withdrawal met the primary endpoint of relapse compared with none assigned to continue treatment (estimated of event rate 45.7% [95% CI 28.5-67.2]; p=0.0001).We still do not have great predictors of relapse, and thus for most patients with HFrecEF, GDMT should continue indefinitely. References - CardioNerds Rounds: Challenging Cases - Modern Guideline Directed Therapy in Heart Failure with Dr. Randall Starling Halliday BP, Wassall R, Lota AS, et al. Withdrawal of pharmacological treatment for heart failure in patients with recovered dilated cardiomyopathy (TRED-HF): an open-label, pilot, randomised trial. Lancet. 2019 Jan 5;393(10166):61-73. doi: 10.1016/S0140-6736(18)32484-X. Epub 2018 Nov 11. PMID: 30429050; PMCID: PMC6319251.Greene SJ, Fonarow GC, DeVore AD, et al. Titration of Medical Therapy for Heart Failure With Reduced Ejection Fraction. J Am Coll Cardiol. 2019 May 21;73(19):2365-2383. doi: 10.1016/j.jacc.2019.02.015. Epub 2019 Mar 4. PMID: 30844480; PMCID: PMC7197490.McMurray JJ, Packer M, Desai AS, et al. Angiotensin-neprilysin inhibition versus enalapril in heart failure. N Engl J Med. 2014 Sep 11;371(11):993-1004. doi: 10.1056/NEJMoa1409077. Epub 2014 Aug 30. PMID: 25176015. Production Team Karan Desai, MD Natalie Stokes, MD Amit Goyal, MD Daniel Ambinder, MD

208. Atrial Fibrillation: Epidemiology, Health Equity, & The Double Paradox with Dr. Larry Jackson May 20, 2022

Show notes

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, genders, sexes, regions, whether they’re citizens or not, whether they’re disabled or not […] and make sure that we’re thinking about those in terms of prescriptions and discussion and communication, and offering our patients therapy, […] it's not [enough] to offer different people the same therapy because they may have different barriers that may prevent them from uptaking that therapy or utilizing that.” Dr. Larry Jackson Notes - Atrial Fibrillation: Epidemiology, Health Equity, & The Double Paradox Drafted by Dr. Dinu-Valentin Balanescu and reviewed by Dr. Colin Blumenthal. 1. What factors contribute to the atrial fibrillation epidemic and where do we expect to be over the next 20-30 years? The current global prevalence of atrial fibrillation is unclear. It is estimated that over the next 30 years, the prevalence of atrial fibrillation may reach pandemic proportions, with potentially 100-180 million people worldwide suffering from this condition.1Factors that drive this increase:Classic: heart failure, coronary artery disease, hypertension, diabetes, tobacco use, obesity.Novel risk factors: obstructive sleep apnea, metabolic syndrome, left ventricular hypertrophy, left atrial enlargement.Novel markers (inflammatory, biochemical): B-type natriuretic peptide, CRP.Many of the above factors have been determined by studying predominantly White populations. 2. There is conflicting data regarding the incidence of atrial fibrillation across race and ethnicity, with most studies suggesting a higher incidence in the non-Hispanic White population compared to non-Hispanic Black or Hispanic individuals, while some suggest a similar prevalence. How is this discrepancy explained? The discrepancy may stem from various rates of clinical detection, rather than incidence or prevalence, of atrial fibrillation between different race/ethnicity groups (“ascertainment bias”).Conflicting data persists even when detection is adjusted for. A cohort of the MESA study showed that the prevalence among race and ethnicity was similar when the diagnosis was made using Holter monitor data.2 Data from the ASSERT trial suggest that when using implantable loop recorders, the incidence of atrial fibrillation among the non-Hispanic Black population was lower than a European White population.3There is a substantial need for further study on the epidemiology of atrial fibrillation across race/ethnicity. 3. Non-Hispanic Black populations have a higher risk factor burden for atrial fibrillation than White patients, but as described above most studies demonstrate a lower incidence – how is this “paradox” explained? The “atrial fibrillation paradox” is a double paradox, as Dr. Jackson explains: despite a higher risk factor burden, non-Hispanic Blacks have a lower incidence/prevalence of atrial fibrillation. At the same time, non-Hispanic blacks have worse outcomes compared to the white population.4This is likely due to a multifactorial process, with clinical differences, socioeconomic factors, and genetic factors contributing.5 Specifically:Ascertainment bias. Certain racial/ethnic groups may have access issues preventing them from seeking medical attention for rhythm assessment and/or may be less likely to be prescribed rhythm monitors for objective assessment. Additionally, it has been shown that the non-Hispanic Black population has more paroxysmal symptoms, which could lead to difficulties in diagnosis.Survival bias. Non-Hispanic Whites have a longer life expectancy compared to underrepresented racial/ethnic groups, which may lead to a greater risk of developing atrial fibrillation over time.Genetic/epigenetic differences. Stronger European ancestry within non-Hispanic Blacks is associated with a higher risk of atrial fibrillation. Genome-wide association studies suggest that non-Hispanic Blacks may have protective genes compared to whites. 4. What are barriers to the diagnosis of atrial fibrillation in understudied populations and how can inclusion in research studies be improved? Large epidemiological registries have traditionally included very small proportions of underrepresented groups. A more diverse enrollment in clinical trials is essential.Clinical trial participation of marginalized populations may be achieved by:Using mobile/telehealth technologies to recruit and follow patients.Increasing diversity and heterogeneity among research staff, principal investigators, steering committees, which has been shown to improve study diversity.From a clinical standpoint, barriers may be removed by:Educating patients on atrial fibrillation, its complications, its treatments, and its outcomes.Involving family and other social communities as part of decision-making support. The CardioNerds Clinical Trials Network specifically aims pair equitable trial enrollment with trainee personal and professional development 5. How are race and ethnicity associated with the workup for atrial fibrillation and t

207. Lipids: REDUCE-IT Versus STRENGTH Trials – EPA in Clinical Practice with Dr. Peter Toth May 16, 2022

Show notes

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 those of the American Diabetes Association (ADA), National Lipid Association (NLA) and the European Society of Cardiology (ESC)/European Atherosclerosis Society (EAS), have endorsed the use of icosapent ethyl in their recommendations to further reduce ASCVD risk in select patients. References - REDUCE-IT Bhatt DL, Steg PG, Miller M, et al. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia. N Engl J Med. 2019;380(1):11-22. doi: 10.1056/NEJMoa1812792. https://www.nejm.org/doi/full/10.1056/nejmoa1812792Libby P. Triglycerides on the rise: Should we swap seats on the seesaw? Eur Heart J. 2015;36(13):774-776. doi: 10.1093/eurheartj/ehu500. https://academic.oup.com/eurheartj/article/36/13/774/475534Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: Results of the GISSI-prevenzione trial. gruppo italiano per lo studio della sopravvivenza nell'infarto miocardico. Lancet. 1999;354(9177):447-455. doi: S0140673699070725. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(99)07072-5/fulltextRisk and Prevention Study Collaborative Group, Roncaglioni MC, Tombesi M, et al. N-3 fatty acids in patients with multiple cardiovascular risk factors. N Engl J Med. 2013;368(19):1800-1808. doi: 10.1056/NEJMoa1205409. https://www.nejm.org/doi/10.1056/NEJMoa1205409?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200www.ncbi.nlm.nih.govASCEND Study Collaborative Group, Bowman L, Mafham M, et al. Effects of n-3 fatty acid supplements in diabetes mellitus. N Engl J Med. 2018;379(16):1540-1550. doi: 10.1056/NEJMoa1804989. https://www.nejm.org/doi/10.1056/NEJMoa1804989?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200www.ncbi.nlm.nih.govTriglyceride Coronary Disease Genetics Consortium and Emerging Risk Factors Collaboration, Sarwar N, Sandhu MS, et al. Triglyceride-mediated pathways and coronary disease: Collaborative analysis of 101 studies. Lancet. 2010;375(9726):1634-1639. doi: 10.1016/S0140-6736(10)60545-4. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)60545-4/fulltextDo R, Willer CJ, Schmidt EM, et al. Common variants associated with plasma triglycerides and risk for coronary artery disease. Nat Genet. 2013;45(11):1345-1352. doi: 10.1038/ng.2795. https://www.nature.com/articles/ng.2795Sarwar N, Danesh J, Eiriksdottir G, et al. Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 western prospective studies. Circulation. 2007;115(4):450-458. doi: CIRCULATIONAHA.106.637793. https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.106.637793?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmedKeech A, Simes RJ, Barter P, et al. Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): Randomised controlled trial. Lancet. 2005;366(9500):1849-1861. doi: S0140-6736(05)67667-2. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(05)67667-2/fulltextACCORD Study Group, Ginsberg HN, Elam MB, et al. Effects of combination lipid therapy in type 2 diabetes mellitus. N Engl J Med. 2010;362(17):1563-1574. doi: 10.1056/NEJMoa1001282. https://www.nejm.org/doi/full/10.1056/nejmoa1001282Yokoyama M, Origasa H, Matsuzaki M, et al. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): A randomised open-label, blinded endpoint analysis. Lancet. 2007;369(9567):1090-1098. doi: S0140-6736(07)60527-3. https://www.thelancet.com/article/S0140-6736(07)60527-3/fulltextNicholls SJ, Lincoff AM, Garcia M, et al. Effect of high-dose omega-3 fatty acids vs corn oil on major adverse cardiovascular events in patients at high cardiovascular risk: The STRENGTH randomized clinical trial. JAMA. 2020;324(22):2268-2280. doi: 10.1001/jama.2020.22258. https://doi.org/10.1001/jama.2020.22258. . Guest Profiles Dr. Peter Toth Dr. Peter Toth is the Director of Preventive Cardiology at CGH Medical Center in Sterling, IL, and Professor of Clinical Family and Community Medicine at the University of Illinois College of Medicine in Peoria, and adjunct associate professor of medicine, Johns Hopkins University School of Medicine. He received his medical degree from Wayne State University School of Medicine in Detroit, MI, and PhD in Biochemistry from Michigan State University in East Lansing. He has written extensively on the topic of lipids and is Co-Editor of twenty textbooks in preventive cardiology, diabetes, hypertension, and lipidology. Additionally, Dr. Toth is the President of the American Society of Preventive Cardiology, past President of the National Lipid Association, as well as incoming chair of the American Heart Association’s Council on Lipoproteins, Lipid Metabolism, and Thrombosis. Dr. Aliza Hussain Dr. Aliza Hussain is a cardiology fellow at Baylor College of Medicine....

206. Guidelines: 2021 ESC Cardiovascular Prevention – Question #12 with Dr. Laurence Sperling May 13, 2022

Show notes

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!

205. Guidelines: 2021 ESC Cardiovascular Prevention – Question #11 with Dr. Eugenia Gianos May 12, 2022

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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 BIDListen 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 TakeawayIn 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 LocationSection 6.1, Pages 3294-3295. CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

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