Cardionerds: A Cardiology Podcast

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204. Guidelines: 2021 ESC Cardiovascular Prevention – Question #10 with Dr. Eileen Handberg May 11, 2022

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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.

203. Guidelines: 2021 ESC Cardiovascular Prevention – Question #9 with Dr. Noreen Nazir May 10, 2022

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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

202. Guidelines: 2021 ESC Cardiovascular Prevention – Question #8 with Dr. Eugene Yang May 09, 2022

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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 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 TakeawaySystematic 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 LocationSection 3.1, page 3236; Table on page 3242. 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!

201. Guidelines: 2021 ESC Cardiovascular Prevention – Question #7 with Dr. Wesley Milks May 08, 2022

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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!

200. 2022 AHA/ACC/HFSA Guideline for The Management of Heart Failure – Hot Takes from The Journal of Cardiac Failure Family May 06, 2022

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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.

199. Case Report: The Perfect Storm of Complications Post-Partum – Summa Health May 04, 2022

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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. 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 dysplasia. 3. What is the gold standard to diagnose SCAD? Coronary angiography performed by an experienced interventional cardiologist is the gold standard to diagnose SCAD. The left anterior descending artery is most commonly affected, and most cases of SCAD occur in the mid-distal arteries.There are 3 angiographic variants SCAD.Type 1 is with evident with the contrast dye staining the arterial wall with multiple radiolucent lumen.Type 2 (majority of the cases including the present case) is diffuse stenosis of varying severity with subtle abrupt changes in arterial caliber (long smooth narrowing).Type 3 mimics atherosclerosis and is often difficult to differentiate from it. 4. What is the management of SCAD in acute setting? Management of SCAD depends on clinical severity. Thrombolytics should be avoided. Most cases are benign and treated conservatively with work up for secondary causes. 95% of conservatively treated patients with mild SCAD such as minimal ongoing ischemia with preserve coronary flow will heal within 30 days. More severe cases of SCAD require intervention such as PCI or CABG. Surgical approaches are preferred in left main involvement, long segments, and with diffuse coronary artery involvement like in our case. Utilizing vein grafts is preferred as most SCAD cases heal with eventual graft closure. Off note, PCI in SCAD is associated with higher complication rates and suboptimal outcomes, including risk of iatrogenic dissection or propagation of hematoma. 5. What is the management of SCAD in pregnant patient? The management strategy of SCAD during pregnancy is similar to that in the nonpregnant state, with additional considerations to optimize maternal and fetal outcomes. After 20 weeks gestation, recommend left lateral recumbent positioning whenever possible to reduce aortocaval compression and optimize venous return. If necessary, consider maternal stabilization and optimization of cardiac status followed by planned delivery under controlled conditions. For more, enjoy Episode #167 – Cardiac Interventions During Pregnancy with Dr. Michael Luna. 5. What is the prognosis of SCAD and long-term management? Recurrent SCAD has been reported in 10-30% of patients. Post-SCAD chest pain is common and may persist for many months. Due to iatrogenic risk from invasive angiography, serial electrocardiography and biomarker assessment, and noninvasive cardiac computed tomography angiography should be considered. Standard heart failure medications are indicated for left ventricular dysfunction, and hypertension should be treated. 6. How to prevent recurrent SCAD? The factors associated with recurrence remain poorly understood. After SCAD, further pregnancy should perhaps be discouraged and contraception should be discussed. Women who strongly desire pregnancy should receive thorough preconception counseling. References Macaya, F., Salinas, P., Gonzalo, N., Fernández-Ortiz, A., Macaya, C., & Escaned, J. (2018). Spontaneous coronary artery dissection: contemporary aspects of diagnosis and patient management. Open Heart, 5(2), e000884. Hayes, S. N., Kim, E. S. H., Saw, J., Adlam, D., Arslanian-Engoren, C., Economy, K. E., Ganesh, S. K., Gulati, R., Lindsay, M. E., Mieres, J. H., Naderi, S., Shah, S., Thaler, D. E., Tweet, M. S., & Wood, M. J. (2018). Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association. Circulation, 137(19). McGrath-Cadell, L., McKenzie, P., Emmanuel, S., Muller, D. W. M., Graham, R. M., & Holloway, C. J. (2016). Outcomes of patients with spontaneous coronary artery dissection. Open Heart, 3(2), e000491. Alonso-Fernández-Gatta, M., Uribarri, A., Diego-Nieto, A., & Sánchez, P. L. (2017). Progressive spontaneous coronary artery dissection secondary to fibromuscular dysplasia requiring mechanical circulatory support. Journal of Cardiology Cases, 16(6), 216–218. Cepas-Guillén, P. L., Flores-Umanzor, E. J., Sabate, M., & Masotti, M. (2019). Multivessel spontaneous coronary artery dissection involving the left main coronary artery: a case report. European Heart Journal - Case Reports, 3(1). Tweet, M. S., Eleid, M. F., Best, P. J. M., Lennon, R. J., Lerman, A., Rihal, C. S., Holmes, D. R., Jr, Hayes, S. N., & Gulati, R. (2014). Spontaneous Coronary Artery Dissection. Circulation: Cardiovascular Interventions, 7(6), 777–786. Hayes SN, Tweet MS, Adlam D, et al. Spontaneous Coronary Artery Dissection: JACC State-of-the-Art Review. J Am Coll Cardiol 2020;76:961-984.

198. ACHD: Cardiovascular Multimodality Imaging in Congenital Heart Disease with Dr. Eric Krieger May 03, 2022

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CardioNerds (Daniel Ambinder), ACHD series co-chairs, Dr. Josh Saef (ACHD fellow, University of Pennsylvania) Dr. Daniel Clark (ACHD fellow, Vanderbilt University), and ACHD FIT lead Dr. Jon Kochav (Columbia University) join Dr. Eric Krieger (Director of the Seattle Adult Congenital Heart Service and the ACHD Fellowship, University of Washington) to discuss multimodality imaging in congenital heart disease. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. Special introduction to CardioNerds Clinical Trialist Dr. Shiva Patlolla (Baylor University Medical Center). In this episode we discuss the strengths and weaknesses of the imaging modalities most commonly utilized in the diagnosis and surveillance of patients with ACHD. Specifically, we discuss transthoracic and transesophageal echocardiography, cardiac MRI and cardiac CT. The principles learned are then applied to the evaluation of two patient cases – a patient status post tetralogy of Fallot repair with a transannular patch, and a patient presenting with right ventricular enlargement of undetermined etiology. 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 - Cardiovascular Multimodality Imaging in Congenital Heart Disease Transthoracic echocardiography (TTE) is the first line diagnostic test for the diagnosis and surveillance of congenital heart disease due to widespread availability, near absent contraindications, and ability to perform near comprehensive structural, functional, and hemodynamic assessments in patients for whom imaging windows allow visualization of anatomic areas of interest.Transesophageal echocardiography (TEE) use in ACHD patients is primarily focused on similar indications as in acquired cardiovascular disease patients: the assessment of endocarditis, valvular regurgitation/stenosis severity and mechanism, assessment of interatrial communications in the context of stroke, evaluation for left atrial appendage thrombus, and for intraprocedural guidance. When CT or MRI are unavailable or contraindicated, TEE can also be used when transthoracic imaging windows are poor, or when posterior structures (e.g. sinus venosus, atrial baffle) need to be better evaluated.Cardiac MRI (CMR) with MR angiography imaging is unencumbered by imaging planes or body habitus and can provide comprehensive high resolution structural and functional imaging of most cardiac and extracardiac structures. Additional key advantages over echocardiography are ability to reproducibly quantify chamber volumes, flow through a region of interest (helpful for quantifying regurgitation or shunt fraction), assess for focal fibrosis via late gadolinium enhancement imaging, and assess the right heart.Cardiac CT has superior spatial resolution in a 3D field of view which makes it useful for clarifying anatomic relationships between structures, visualizing small vessels such as coronary arteries or collateral vessels, and assessing patency of larger vessels (e.g branch pulmonary arteries) through metallic stents which may obscure MR imaging. Downsides relative to CMR include requirement of nephrotoxic contrast for imaging of intracardiac/intravascular structures, and while gated images can be obtained throughout the cardiac cycle similarly to CMR, this is particularly costly from an ionizing radiation standpoint.When working up an unknown congenital lesion, it is critical to communicate the differential diagnosis when ordering a test so that the imager can protocol the study accordingly. Not all echocardiograms, CT or MRI scans are the same. Show notes - Cardiovascular Multimodality Imaging in Congenital Heart Disease What are the key strengths and weaknesses of transthoracic echocardiography? STRENGTHS: (1) “Most important ability is availability”: Transthoracic echocardiography is the first line imaging modality in the assessment of patients with congenital heart disease because it is widely available at significantly lower cost with no contraindications or risks to the patient. (2) Versatility: A wide array of echo approaches can be employed to provide comprehensive structural and physiological data. 2D echo techniques are most useful for visual assessment of cardiac structural abnormalities. Color doppler provides qualitative data regarding flow, and spectral doppler (inclusive of tissue doppler imaging) provides quantitative data defining intracardiac hemodynamics. 3D echo can be applied to optimize imaging planes for valve area planimetry and quantify chamber volumes as well as global contractile function. Strain imaging using 2D speckle tracking techniques can be employed to evaluate regional contractility. (3) High temporal resolution: High temporal resolution makes echocardiography a superior modality for imaging fast-moving structures (e.g., valvular vegetations or intracardiac masses). WEAKNESSES: (1) “You can’t study what you can’t see”: Suboptimal ultrasound penetration can limit transthoracic imaging quality in patients with large body habitus, or patients in the post-operative state. Furthermore, imaging planes are limited by sonographic windows - many anatomic cardiac (e.g., sinus venosus and coronary sinus defects, anomalous coronary arteries) and extracardiac (e.g., aortic dilation/coarctation, anomalous venous return) abnormalities are often incompletely evaluated by echocardiography in adult patients. This is a major limitation as many ACHD conditions are associated with aortopathy and anomalous pulmonary or systemic venous return which may necessitate dedicated cross-sectional imaging. Finally, right ventricular imaging is limited by near field artifact and complex chamber geometry; and similarly anterior structures such as right ventricular to pulmonary arterial conduits are poorly evaluated with transthoracic echocardiography. What differentiates a congenital echocardiogram from a standard adult protocol? Congenital echocardiograms obtain more comprehensive anatomic evaluation to visualize structural anomalies that might not be evident in standard imaging planes. Most congenital echo protocols begin with a subcostal short axis and long axis sweep to determine segmental anatomy, visceral and atrial situs, cardiac position, cardiac looping, and arterial situs. Additional views are attempted from the suprasternal position to better characterize major venous and arterial connections and anatomy (bidirectional Glenn, etc.). Sweeps are often obtained between views within the same window to clarify the relationships between anatomic structures and identify abnormalities (e.g. inter-chamber connections) not apparent in the standard imaging planes. What is the role of transesophageal echocardiography in adult congenital cardiology imaging? In adult patients with acquired cardiovascular disease, transesophageal echocardiography (TEE) is most commonly employed for the assessment of endocarditis, valvular regurgitation/stenosis severity and mechanism, assessment of interatrial communications in the context of stroke, evaluation for left atrial appendage thrombus, and for intraprocedural guidance. Each of these indications are also commonly encountered in an ACHD population. In congenital cardiology, improved spatial resolution of posterior heart structures can similarly be leveraged to image pathology not well visualized by a transthoracic approach such as for identifying sinus venosus defects, characterizing secundum atrial septal defects to determine feasibility of percutaneous closure, or for assessment of baffle leak on Fontan or atrial switch D-TGA patients. Additionally, TEE increasingly plays a critical role in the perioperative setting (e.g., examining physiology pre- and post-bypass) and for monitoring and guidance of percutaneous interventions in the cardiac catheterization lab. What are the key strengths and weaknesses of Cardiac MRI? STRENGTHS: (1) Unencumbered imaging planes: Unlike echocardiography, for which views are limited by echocardiographic windows, cardiac MRI technicians can prescribe unlimited imaging planes for a more complete coverage of both intracardiac and extracardiac anatomy – particularly with addition of MR angiography. This allows for improved assessment of anterior structures (e.g., the RV, RV-PA conduits), posterior structures (e.g., atrial baffles, sinus venosus or coronary sinus defects), and extracardiac anomalies (e.g., anomalous venous return, aortopathies, pulmonary arterial stenoses), which are usually poorly imaged by echocardiography in adults. Additionally, imaging is generally unaffected by body habitus, and may be used as the primary imaging modality for patients with poor transthoracic windows. (2) Reproducible volumetric quantification: Cardiac MRI is the gold standard for chamber volume assessment. Chamber volumes are obtained from endocardial contouring of Cine-CMR short axis stacks, allowing for measurements that are independent of geometric assumpt

197. Narratives in Cardiology: Empowering the LGBTQIA+ Community of Cardiovascular Patients & Professionals with Dr. Stephen Cook & Dr. Katie Berlacher – Indiana Chapter Apr 27, 2022

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CardioNerds (Amit Goyal and Daniel Ambinder), join Dr. Kara Denby (Interventional cardiology fellow, Cleveland Clinic), Dr. Tony Pastor (ACHD fellow, Harvard Medical School), Dr. Katie Berlacher (Cardiology program director, UPMC), and Dr. Stephen Cook (ACHD cardiologist, Indiana University) to discuss empowering the LGBTQIA+ community of cardiovascular patients & professionals and more in this installment of the Narratives in Cardiology Series. This episode features the Indiana ACC Chapter. Episode introduction and audio editing by CardioNerds Academy Intern, Pace Wetstein. This discussion was inspired by this perspective piece on ACC.org titled: Finding Our Voices: Building an LGBTQIA+ Community Within Cardiology. To learn more about diversity and equity among the LGBTQIA+ population, check out this webinar organized by the ACC. 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 - Empowering the LGBTQIA+ Community of Cardiovascular Patients & Professionals https://twitter.com/Gurleen_Kaur96/status/1526334939830034432?s=20&t=wMk75ORn1_KJtMTOY1IAdw Video version - Empowering the LGBTQIA+ Community of Cardiovascular Patients & Professionals Coming soon Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

196. Case Report: What I C, I Remember: A Case of Acute Heart Failure – Lahey Hospital and Medical Center Apr 24, 2022

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CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Sonu Abraham (Cardiology fellow, Lahey Hospital and Medical Center), Dr. Amitoj Singh (Internal Medicine Resident, Lahey Hospital and Medical Center), Dr. Ahmed Ghoneem (Internal Medicine Resident, Lahey Hospital and Medical Center, CardioNerds Academy Chief) and Dr. Aanika Balaji (Internal Medicine Resident, Johns Hopkins) for a scrumptious meal on the Boston Harbor as they discuss a case of a young woman with metastatic melanoma on immune checkpoint inhibitors presenting with dyspnea. The presentation, risk factors, work up and management of patients with immune checkpoint inhibitor induced myocarditis are described. The E-CPR segment is provided by Dr. Sarju Ganatra, the founding director of the cardio-oncology program at Lahey Clinic. CardioNerds Clinical Trialist Dr. Carrie Mahurin (University of Vermont Medical Center) is introduced at the beginning of the episode. A 41-year-old woman presented with mild dyspnea on exertion and non-productive cough. She had a history of Hashimoto thyroiditis, nodular thyroid s/p resection on levothyroxine, and metastatic melanoma on immune checkpoint inhibitor therapy with ipilimumab and nivolumab. She also had a history of obesity and underwent gastric bypass surgery several years prior. Though she lost weight after the surgery, she regained a significant amount and was 244 lbs with a BMI of 42. Her exam findings were remarkable for tachycardia, bilateral pulmonary rales, elevated JVP, and symmetric pedal edema. Investigations revealed a mild troponin elevation, non-specific EKG changes, and TTE with severely reduced left ventricular function (EF 15%) and a low GLS. Cardiac MRI showed patchy delayed myocardial enhancement in a non-ischemic distribution with marked global hypokinesis and EF of 11%. Endomyocardial biopsy confirmed the diagnosis of immune checkpoint inhibitor (ICI) associated myocarditis. The ICI therapy was discontinued and she was treated with high dose intravenous corticosteroids followed by a prolonged oral steroid taper with clinical improvement and complete recovery of left ventricular function. 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 - immune checkpoint inhibitor myocarditis Episode Schematics & Teaching CardioNerds Myocarditis, updated 1.20.21 Pearls - immune checkpoint inhibitor myocarditis ICI-associated myocarditis has a high mortality rate necessitating a high degree of clinical suspicion. When in doubt, check it out! The initial 4 diagnostic pillars include EKG, troponin, BNP and TTE. Cardiac MRI and endomyocardial biopsy help to confirm the diagnosis.Left ventricular function is normal in 50% of these patients with ICI-associated myocarditis, so the ejection fraction is not a sensitive test for ruling this out.Endomyocardial biopsy should be considered in patients with a high clinical suspicion but negative or ambiguous non-invasive imaging.Early initiation of corticosteroids within 24 hours of presentation is associated with better outcomes.ICIs should be discontinued indefinitely in those with Grade 3 or 4 disease. Notes - immune checkpoint inhibitor myocarditis 1. Immune checkpoint inhibitors – What are they and why should we as cardiologists know about them? Immune checkpoint inhibitors (ICI) boost the host immune response against tumor cells by inhibiting the intrinsic brakes of the immune response.There are currently 7 FDA approved drugs in this group: one CTLA-4-blocking antibody called ipilimumab; three PD-1-blocking antibodies [nivolumab, pembrolizumab, and cemiplimab]; and three PD-L1-blocking antibodies [atezolizumab, avelumab, and durvalumab].Like a car, T-cells have an ignition switch, gas pedals, and brakes.T-cells become activated when receptors on the surface of the T-cell bind to an antigen on the surface of the invading cells like cancer cells.Think of the T-cell receptor as the ignition switch and the antigen as the key.Antigen presenting cells patrol the body and pick up evidence of foreign antigens like cancer which they present to T-cells in the lymph nodes via the T-cell receptor.Like gas pedals, there are co-stimulatory signals like CD 28 which interact with proteins on the antigen presenting cells. With these “gas pedal” stimuli, T-cells get activated, multiply, and hunt for the cancer and finally kill the cancer cells.The T-cells also have “breaks” or “checkpoints” to down-regulate the immune response.The Cytotoxic T-lymphocyte antigen 4, also called the CTLA-4, acts to slow down the activation of T-cells.Further down the line, there is another checkpoint called the Programmed cell death 1 or PD-1. PD-1 is a molecule on the surface of T-cells which acts as another set of brakes.When a T cell with PD-1 on its surface interacts with another cell which has a PD-1 ligand (PD-L1), the T-cell activity is down-regulated.Many cancer cells overexpress PD-L1 to fight back against the T cells, by putting a “brake” on their immune response.By removing these brakes, we can augment the T-cells’ immune response against cancer cells.But if the T-cells mount an exaggerated response against normal host cells, then an autoimmune process ensues leading to “immune-related adverse events” (irAEs) like ICI-associated myocarditis. 2. Who are at risk of developing ICI-associated myocarditis? Anti-CTLA 4 therapy is associated with a higher prevalence of cardiotoxicity than the PD-1 and PD-L1 inhibitors.Combination therapy (i.e., when 2 or more ICIs are given together) increase the risk of irAEs.Preexisting diabetes, obesity, and autoimmune disease have been found to be independent risk factors.An association of preexisting cardiovascular risk factors like hypertension and smoking with the development of ICI-induced myocarditis has been suggested. 3. What are the prevalence and prognosis of ICI-associated myocarditis? Immune checkpoint inhibitors have various forms of cardiotoxicities, but ICI-associated myocarditis is the most feared complication.The overall prevalence is 1.2% to 2.4% when using combination ICI therapy. However, the estimated rate of mortality in ICI associated myocarditis is 38 to 46%.Approximately 50% of these patients with myocarditis may develop heart failure, cardiogenic shock, complete heart block, cardiac arrest, and ventricular arrhythmias. 4. What is the differential diagnose for ICI-associated myocarditis? The differential diagnoses are acute coronary syndrome, stress cardiomyopathy, other forms of myocarditis, pericarditis, pneumonitis, viral myocarditis, endocrinopathies, cardiac sarcoidosis and other causes of cardiomyopathy and heart failure including prior cardiotoxic therapy. 5. What are the initial investigations to be done for ICI-associated myocarditis? EKG, troponin, BNP, and TTE (as needed) are the basic 4 pillars of testing in patients with suspected ICI induced myocarditis.Nearly all patients with myocarditis have an abnormal EKG. These are however non-specific findings like sinus tachycardia, QRS or QT prolongation, conduction abnormalities, diffuse T-wave inversion, abnormal Q waves, atrial or ventricular arrhythmias, local or diffuse ST elevation.Troponins are elevated in most cases, up to 94% in one study. The implications of the level of troponin elevation are not completely clear but there is data that suggests that higher levels of troponin elevation are associated with worse cardiovascular outcomes.BNP can be elevated if the patient is in heart failure or volume overloaded. However, it lacks sensitivity and specificity for ICI associated myocarditis and is not always helpful.Even patients with fulminant myocarditis can present with a normal left ventricular function. Around 50% of patients with ICI induced myocarditis have been found to have a normal LV function. Also, among those who had major adverse cardiac events, 38% had a normal EF. 6. How do you grade severity? The American Society of Clinical Oncology broadly categorized the intensity of disease into 4 groups: G1 – Mildly abnormal screening tests and no symptomsG2 – Abnormal screening tests with mild symptomsG3 – Moderately abnormal screening tests (arrhythmia, cardiac biomarker > upper limits of normal and significant echocardiographic findings) and symptoms with mild activity.G4 – Moderate to severe decompensation, hemodynamic instability, cardiac biomarker > 3 upper limit of normal, requiring intravenous medications or interventions. To summarize, G1 and G2 are considered stable and minimally symptomatic and G3 and G4 are very symptomatic or unstable patients and will need to be admitted. 7. What are the treatment options? Prompt initiation of immunosuppressive therapy is critical for these patients.The first line agents are corticosteroids.Start with high dose corticosteroids within 24 hours of presentation. Typically, we start with intravenous methylprednisolone 1000 mg daily for 3 days, followed by oral prednisone 1 mg/kg/day.The steroids should then be tapered slowly over at least 4–6 weeks only after resolution of symptoms, normalization of LVEF or stabilization of arrhythmias.If unresponsive to steroids, tacrolimus, mycophenolate mofetil, anti-thymocyte globulin, iv gamma globulin and plasmapheresis are alternative therapies. 8. Is it safe to restart ICIs after treatment? The current recommendation is a definite discontinuation of ICI in case of grade 3 (severe) or life threatening (grade 4) immune related adverse events.May consider re-challenge in those with milder disease and complete cardiac recovery – individualized and multidisciplinary team approach. References ...

195. 1st Sanjay V Desai Lecture: Growth Mindset, Power of Yet, & Pursuit of Mastery with Dr. Keri Shafer and Dr. David Hirsh Apr 06, 2022

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The CardioNerds Academy Class of 2021 graduation ceremony kicked off the inaugural Sanjay V Desai Lecture: Growth Mindset, Power of Yet, & Pursuit of Mastery. Join us as Dr. Tommy Das (CardioNerds Academy Program Director), and Dr. Saman Nematollahi (CardioNerds Academy Director of Research) discuss Growth Mindset with Dr. Keri Shafer and Dr. David Hirsh. Terrific acting by Dr. Patrick Zakka, Dr. Teodora Donisan, Dr. Ahmed Ghoneem, and Dr. Jessie Holtzman. Dr. Sanjay V Desai serves as the Chief Academic Officer, The American Medical Association and is the former Program Director of the Osler Medical Residency at The Johns Hopkins Hospital. Dr. Keri Shafer is an adult congenital heart disease specialist at Boston Children’s Hospital, and an assistant professor of pediatrics within Harvard Medical School. She completed internal medicine residency at Beth Israel Deaconess Medical Center, before completing cardiology fellowship at UT Southwestern and Adult Congenital and Pulmonary Hypertension subspecialty training at Boston Children’s and BWH. Dr. David Hirsh is an associate professor of Medicine within Harvard Medical School, as well as the director of the HMS Academy fellowship in medical education and the associate dean of undergraduate medical education. Relevant disclosures: None CardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

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