Cardionerds: A Cardiology Podcast

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374. Case Report: Unraveling the Mystery – When Childhood Chest Pain Holds the Key to a Genetic Heart Condition – Wayne State University May 31, 2024

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This case report explores the intricacies of familial hypercholesterolemia (FH), delving into its genetic basis, atherosclerotic cascade, and early-onset cardiovascular complications. It examines established diagnostic criteria and emphasizes personalized management, including statins, novel therapies, and lifestyle modifications. CardioNerds cofounders (Drs. Amit Goyal and Danial Ambinder) join Dr. Irfan Shafi, Dr. Preeya Prakash, and Dr. Rebecca Theisen from the Wayne State University/DMC and Central Michigan University at Campus Martius in Downtown Detroit for some holiday ice-skating! They discuss an interesting pediatric case (see case synopsis below). Dr. Luis C Afonso provides the Expert CardioNerd Perspectives & Review segment for this episode. Audio editing by CardioNerds academy intern, Pace Wetstein. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. 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 Synopsis FH, a 9-year-old female with no previous medical history, recently moved back to the US from Iraq. She presented to establish care and discuss new-onset chest pain and dyspnea. A systolic ejection murmur was noted during her initial visit to the pediatrician, prompting cholesterol testing and a cardiology referral. Testing revealed, alarming cholesterol levels (Total Cholesterol: 802 mg/dL, LDL: 731 mg/dL, Triglycerides: 123 mg/dL) prompted concern for cardiac involvement. Due to persistent symptoms, FH was transferred to Children's Hospital of Michigan. Despite normal findings on EKG and chest x-ray, a 2/6 systolic murmur was noted. She was discharged with a cardiology clinic follow-up. However, two days later, FH experienced severe chest pain at rest, sweating, and difficulty breathing. She was transported to Children's Hospital again, and her troponin level measured 3000, and her total cholesterol was 695 mg/dL. An echocardiogram revealed valvar and supravalvar aortic stenosis, necessitating collaboration between Pediatric and Adult cardiology teams. CTA thorax revealed severe supravalvular stenosis, a hypoplastic right coronary artery, and significant coronary artery obstructions. Diagnostic cardiac catheterization confirmed severe aortic stenosis and coronary artery disease, leading to the decision for surgical intervention. FH underwent the Ross operation, left main coronary artery augmentation, and right coronary artery reimplantation. Intraoperatively, atherosclerotic plaques were observed in multiple cardiac structures. FH's recovery was uneventful, discharged on a regimen including Atorvastatin, Ezetimibe, evolocumab, and antiplatelet therapy. Persistent high LDL levels required regular plasmapheresis. Plans for evaluations in Genetics, Lipid Clinic, Endocrine, and Gastroenterology were made, potentially leading to a liver transplant assessment. Given the severity of her condition, a heart/liver transplant might be considered in the future. Conclusion: This case of FH highlights the complex presentation of severe aortic stenosis and coronary artery disease in a pediatric patient. Urgent diagnosis, interdisciplinary collaboration, and aggressive management were crucial. The case underscores the importance of comprehensive care for pediatric patients with rare cardiac conditions, emphasizing collaboration between specialties for optimal outcomes and long-term well-being. Case Media Pearls - Familial Hypercholesterolemia Mutations in LDLR, ApoB, or PCSK9 genes disrupt LDL-C clearance, leading to a cascade of events culminating in accelerated atherosclerosis and early-onset cardiovascular complications (e.g., CAD, aortic stenosis, PAD, stroke). Diagnosis of familial hypercholesterolemia relies on a combination of clinical features (xanthomas, corneal arcus, high LDL-C), family history, and genetic testing guided by established criteria like DCLN or NLA recommendations. Supravalvular aortic stenosis, while common in many congenital cases, should raise suspicion of homozygous familial hypercholesterolemia in the setting of extensively elevated LDL and unexpected coronary artery disease. A multidisciplinary approach, including involvement of pediatric and adult cardiology teams, lipid specialists and cardiothoracic surgeons, should be involved in the overall evaluation and management of these patients, both at initiation of diagnosis, and in an outpatient setting. In patients with FH, it is important to delineate between homozygous and heterozygous manifestations, as this can have extensive implications on treatment, management and the overall clinical prognosis and further disease sequelae that the patient may experience. References - Familial Hypercholesterolemia Shah, N. (2020). Familial hypercholesterolemia: Early diagnosis and treatment is key for cardiovascular prevention.Cleveland Clinic Journal of Medicine, 87(5), 109-120. https://pubmed.ncbi.nlm.nih.gov/23469913/ Turgeon, R. D., Barry, A. R., & Pearson, G. J. (2023). Familial hypercholesterolemia: Review of diagnosis,screening, and treatment. American Journal of Health-System Pharmacy, 80(11), 917-929.https://pubmed.ncbi.nlm.nih.gov/26796832/ Collins, R. T. (2018). Cardiovascular disease in Williams syndrome. Current Opinion in Pediatrics, 30(5), 609-615. https://www.ncbi.nlm.nih.gov/books/NBK544278/ Collins, R. T., Kaplan, P., Somes, G. W., & Rome, J. J. (2010). Long-term outcomes of patients with cardiovascular abnormalities and Williams syndrome. American Journal of Cardiology, 105(6), 874-878.https://pubmed.ncbi.nlm.nih.gov/30045083/ Honjo, R. S., Monteleone, V. F., Aiello, V. D., Wagenfuhr, J., Issa, V. S., Pomerantzeff, P. M. A., Furusawa, E. A.,Zanardo, E. A., Kulikowski, L. D., Bertola, D. R., & Kim, C. A. (2022). Cardiovascular findings in Williams-Beuren Syndrome: Experience of a single center with 127 cases. American Journal of Medical Genetics. Part A,188(3), 676-682. https://www.ncbi.nlm.nih.gov/books/NBK544278/ Pham, P. P., Moller, J. H., Hills, C., Larson, V., & Pyles, L. (2009). Cardiac catheterization and operative outcomes from a multicenter consortium for children with Williams syndrome. Pediatric Cardiology, 30(1), 9-14.https://pubmed.ncbi.nlm.nih.gov/19052807/ Olsen, M., Fahy, C. J., Costi, D. A., Kelly, A. J., & Burgoyne, L. L. (2014). Anaesthesia-related haemodynamic complications in Williams syndrome patients: A review of one institution's experience. Anaesthesia and Intensive Care, 42(6), 619-624. https://pubmed.ncbi.nlm.nih.gov/25233176/ Harada-Shiba, M., Arai, H., Ishigaki, Y., Ishibashi, S., Okamura, T., Ogura, M., Dobashi, K., Nohara, A., Bujo, H.,Miyauchi, K., Yamashita, S., & Yokote, K. (2018). Guidelines for diagnosis and treatment of familial hypercholesterolemia 2017. Journal of Atherosclerosis and Thrombosis, 25(8), 751-770.https://pubmed.ncbi.nlm.nih.gov/29877295/ Alnouri, F., & Santos, R. D. (2022). New trends and therapies for familial hypercholesterolemia. Journal of Clinical Medicine, 11(22), 6638. https://pubmed.ncbi.nlm.nih.gov/36431115/

373. Narratives in Cardiology: Becoming a “Big E” Medical Educator as a Cardiologist with Dr. James Arrighi May 30, 2024

Show notes

In this episode, Dr. Katie Fell (General Cardiology Fellow at University of Michigan and CardioNerds Academy Fellow) and Dr. Gurleen Kaur (incoming General Cardiology fellow at Brigham and Women’s Hospital and Director of CardioNerds Internship) discuss with Dr. James Arrighi (General Cardiologist and CEO of ACGME-International) about developing as a clinician educator and the concept of competency-based education. 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. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version - Becoming a “Big E” Medical Educator as a Cardiologist with Dr. James Arrighi https://youtu.be/xcrwnz6_9Qg Quoatables - Becoming a “Big E” Medical Educator as a Cardiologist with Dr. James Arrighi “You really have to have a passion or a love for what you do...that’s probably responsible for most of the success one has in life” (time 4:43) “Sub-subspecialty societies in Cardiology represent [a] great opportunity for junior faculty or even trainees to get involved, even before getting involved in ACC.” (time 5:30) “Competency-based medical education and time variable training are not synonymous.” (time 16:43) “As Cardiology evolves into more and more subspecialties...it begs the question... ‘Is Cardiology a primary specialty?’” (time 27:30) “We need to think about [a] more efficient ways for training.” (time 31:55) “As a clinician educator, there’s variety, there’s innovation!” (time 41:22) Notes - Becoming a “Big E” Medical Educator as a Cardiologist with Dr. James Arrighi How might one develop as a clinician educator on a national level? Junior faculty and trainees should consider taking advantage of education opportunities in various Cardiology sub-specialty societies (ex: American Society of Nuclear Cardiology, ASNC). This may include involvement in different committees. These opportunities are great ways to build connections and establish a reputation on a national level. This can help lead to other opportunities with larger national organizations (ex: ACC, AHA). Cardiology Training Oversight The Accreditation Council for Graduate Medical Education (ACGME) and American Board of Internal Medicine (ABIM) both have regulatory power over Cardiology training, providing the minimum clinical experience standards for Cardiology fellowship training programs.The ACGME oversees accreditation for Cardiology fellowships.The ABIM defines the requirements for eligibility for certification of individuals. Over time, the ACGME has transitioned to placing an emphasis on quality improvement, with a particular focus on continuous programmatic improvement. The American College of Cardiology (ACC) helps define more granular recommendations for Cardiology training programs and their curriculum.Periodically the ACC releases training guidelines for Cardiology fellowship programs, called Core Cardiovascular Training Statements, or COCATS. This document provides more contemporary, detailed, and specialty-specific recommendations for Cardiology training as compared to ACGME.While ACC has no regulatory authority over Cardiology training programs, COCATS documents provide a roadmap for program directors on how to structure training. The most recent version of the document, COCATS 4, incorporated in the concept of competency-based education (CBME). What is Competency-Based Education (CBME)? Medical education has evolved to focus more on outcome-based assessments of trainees structured around competency evaluations.In 2002, the ACGME defined competencies by which training programs should evaluate their trainees. As a result, training shifted from a time-based structure to one in which trainees must demonstrate specific competencies within a specific time frame.ACC further defined competencies for Cardiology training in the Core Cardiovascular Training Statement 4 (COCATS 4). This is the first COCATs document introducing aspects of CBME, including defining competencies, milestones, and tools to assess a Cardiology trainee’s performance.Each of these documents focuses on optimizing fellow time while in training, targeting education to the learner’s goals and their future career trajectory. Moving to a competency-based, time-variable training program in the U.S. would be challenging and would require significant restructuring of our current GME training system, including Medicare funding. What is ACGME-International (ACGME-I)? Group within the ACGME dedicated to improving health care internationally by assessing and advancing the quality of resident physicians’ education through accreditation.The organization is currently present in 12 countries at 23 sponsoring institutions (as of April 2024). ACGME-I provides postgraduate medical education programs with standardized frameworks on how to improve the quality of teaching, learning, research, and clinical practice for their trainees. References Weissman G, Auseon AJ, Arrighi JA, et al. Perceptions and Utilization of the U.S. Core Cardiovascular Training Statement. J Am Coll Cardiol. 2019;73(22):2896-2899. Halperin JL, Williams ES, Fuster V. COCATS 4 Introduction. J Am Coll Cardiol. 2015;65(17):1724-1733. Arrighi JA, Kilic S, Haines PG. Perspectives on Current Training Guidelines for Cardiac Imaging and Recommendations for the Future. Curr Cardiol Rep. 2018;20(6):43. Published 2018 Apr 23. ACGME Program Requirements for Graduate Medical Education in Cardiovascular Disease. Accessed February 2, 2024. Mendes LA, Weissman G, Berlacher K, et al. Competency-Based Alternative Training Pathway in Cardiovascular Disease and Clinical Cardiac Electrophysiology. J Am Coll Cardiol. 2022;79(25):2540-2542. Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

372. Case Report: Chronic Chagas Cardiomyopathy with Recurrent Ventricular Tachyarrhythmia – Georgetown University May 23, 2024

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CardioNerds (Dr. Jessie Holtzman, Chair for the CardioNerds Women’s Heart Disease Committee, and Dr. Naima Maqsood, Chair for the CardioNerds Electrophysiology Committee) join Dr. Ritika Gadodia, Dr. Namratha Meda, and Dr. Tsion Aberra from the Medstar Washington Hospital Center/Georgetown University Program for the National Cherry Blossom Festival. They discuss involving a patient with Chagas cardiomyopathy. Dr. Rachel Marcus provides the Expert CardioNerd Perspectives & Review segment for this episode. Episode audio was edited by Dr. Diane Masket. A 79-year-old male with a history of cardiomyopathy presented with recurrent ventricular tachycardia (VT) post-CRT-D placement. On arrival, the patient was in cardiogenic shock. Initial treatment with amiodarone and milrinone failed, necessitating the addition of mexiletine. Imaging was suggestive of a left ventricular ejection fraction of 20-25% with severe global hypokinesis. Prior coronary angiogram had shown nonobstructive coronary artery disease. Further non-ischemic cardiomyopathy evaluation was unrevealing. Given his El Salvadorian origins, Chagas serology results revealed Chronic Chagas Cardiomyopathy (CCM) confirmed by CDC testing. This case underscores the importance of suspecting CCM in patients with risk factors. An early diagnosis of CCM, can prevent catastrophic events (heart blocks, ventricular arrhythmias, thromboembolic events). In summary, this case takes the learner through the journey of a patient with non-ischemic cardiomyopathy and emphasizes the importance of approaching it with a wide range of differentials. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. 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 Pearls - Chronic Chagas Cardiomyopathy with Recurrent Ventricular Tachyarrhythmia Always consider Chagas cardiomyopathy when you have a patient from Latin America who presents with non-ischemic cardiomyopathy. Chagas cardiomyopathy is associated with an unfavorable prognosis and serves as an independent predictor of mortality. Chagas cardiomyopathy is arrhythmogenic and requires consideration for ICD and, when appropriate, catheter based ventricular tachycardia ablation. It is crucial to treat patients with nifurtimox and benznidazole when appropriate. Provide screening for first-degree family members or close relatives who may have lived in the same environment. Show Notes - Chronic Chagas Cardiomyopathy with Recurrent Ventricular Tachyarrhythmia What is the disease progression in Chagas disease5? Acute Stage:Initial infection occurs through contact with infected triatomine bug feces or contaminated blood products.Symptoms may be mild or absent but can include fever, fatigue, body aches, and swelling at the injection site (chagoma). Parasitemia is high during this stage. Intermediate/Indeterminate Stage:The infection becomes chronic if left untreated.Many individuals enter this stage with no noticeable symptoms.Parasitemia levels decrease, but the parasite remains in the body, mainly in muscle and cardiac tissue. This stage can last for years to decades. Chronic Stage:Some individuals will remain asymptomatic throughout their lives.Cardiac complications (chronic Chagas cardiomyopathy) can lead to arrhythmias, congestive heart failure, and sudden death. Digestive complications can result in enlarged esophagus (megaesophagus) and colon (megacolon), leading to difficulties in swallowing and digestion. When do we suspect, and who do we screen, for Chagas disease? The seroprevalence of CCM in the USA is as high as 19%16. Among patients with LVEF

371. Case Report: The Curious Case of Obstructive Cardiogenic Shock – Maine Medical Center May 14, 2024

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CardioNerds Dr. Josh Saef and Dr. Tommy Das join Dr. Omkar Betageri, Dr. Andrew Geissler, Dr. Philip Lacombe, and Dr. Cashel O’Brien from the Maine Medical Center in Portland, Maine to enjoy an afternoon by the famous Portland headlight. They discuss a case of a patient who presents with obstructive cardiogenic shock. Dr. Bram Geller and Dr. Jon Donnelly provide the Expert CardioNerd Perspectives & Review segment for this episode. Dr. Maxwell Afari, the Maine Medical Center cardiology fellowship program director highlights the fellowship program. Audio editing by CardioNerds Academy Intern, student doctor Tina Reddy. This is the case of a 42 year-old woman born with complicated Tetralogy of Fallot repair culminating in a 29mm Edwards Sapiens (ES) S3 valve placement within a pulmonary homograft for graft failure who was admitted to the cardiac ICU for progressive cardiogenic shock requiring vasopressors and inotropic support. Initial workup showed lactic acidosis, acute kidney injury, elevated NT-proBNP, and negative blood cultures. TTE showed at least moderate biventricular systolic dysfunction. She was placed on furosemide infusion, blood cultures were drawn and empiric antibiotics initiated. Right heart catheterization demonstrated elevated right sided filling pressures, blunted PA pressures with low PCWP, low cardiac index, and low pulmonary artery pulsatility index. Intracardiac echocardiography (ICE) showed a large mass within the ES valve apparatus causing restrictive valve motion with a low gradient across the pulmonic valve in the setting of poor RV function. Angiography revealed a large filling defect and balloon valvuloplasty was performed with immediate hemodynamic improvement. Blood cultures remained negative, she was gradually weaned off of inotropic and vasopressor support, and discharged. Despite empiric treatment for culture negative endocarditis and ongoing anticoagulation, she was readmitted for recurrent shock one month later at which time the pulmonic mass was revisualized on ICE. A valve-in-valve transcatheter pulmonary valve (29mm ES S3) was placed to compress what was likely pannus, with an excellent hemodynamic result and no visible mass on ICE. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. 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 Pearls - Obstructive Cardiogenic ShocK Tetralogy of Fallot is the most common cyanotic defect and can lead to long term complications after surgical repair including chronic pulmonary insufficiency, RV dysfunction, residual RVOT obstruction and branch pulmonary artery stenoses. Chronic RV failure may be more indicative of a structural defect and therefore require interventional or surgical management. Valve thrombosis, infective endocarditis and obstructive pannus formation should be considered in the differential of a patient with obstructive shock with a prosthetic valve. Bioprosthetic pulmonic valve obstruction may be effectively managed with balloon valvuloplasty in patients who present in acute extremis but TCPV will likely provide a more lasting result. While valvular gradients are typically assessed via echocardiography, invasive hemodynamics can serve as a critical adjunctive tool in its characterization. Show Notes - Obstructive Cardiogenic ShocK Notes were drafted by Drs. Omkar Betageri, Philip Lacombe, Cashel O’Brien, and Andrew Geissler. What are the common therapies and management for Tetralogy of Fallot? Tetralogy of Fallot is the most common cyanotic defect in children beyond the age of one year Anatomic Abnormalities: Anterior and Superior deviation of the conal septum creating a SubAo VSD and encroachment on the RVOT. The Ao follows the conal septum anteriorly to override the VSD and RVH is a consequence of an RV chamber that is at systemic pressure. The need for medical intervention is dependent on the degree of RVOT obstruction, pulmonary regurgitation, and/or peripheral pulmonary artery obstruction. Many patients are minimally cyanotic in newborn period and clinical follow-up with elective surgical correction between 3 months and 6 months of age is a preferred approach. Total surgical correction typically involves placing patients on cardiopulmonary bypass, relieving right sided obstruction (sometimes utilizing trans-annular patch), and connecting left ventricular blood flow with aortic, with VSD closure. Hypercyanotic “Tet” spells can occur in the neonatal period when there is an acute muscular spasm in the RVOT, fall in SVR or increase in PVR to facilitate right to left shunting at the VSD. It is managed medically with a stepwise approach placing the patient in knee-chest position, administer oxygen, IV fluids and a dose of narcotics, IV beta blocker, IV phenylephrine, ECMO Long term complications post-surgical repair include chronic pulmonary insufficiency, RV dysfunction, residual RVOT obstruction, peripheral PA obstruction, aortic root dilation, endocarditis, arrhythmias, and sudden cardiac death. How should we approach the management of chronic right ventricular failure? Briefly, RV failure can result in chamber dilatation, bowing of the interventricular septum to the LV, impairing LV stroke volume, and ultimately causing hemodynamic collapse. This is the frequently referenced “RV spiral” The primary step in management of RV cardiogenic shock should be to identify and reverse the primary etiology While patients in acute RV failure may respond well to therapies such as fluid resuscitation, inotropes and vasopressors, or inhaled nitric oxide, patients with chronic RV failure (such as in our case) are more likely to have structural defects driving their decompensation Chronic RV failure can result from etiologies related to preload (ASD, tricuspid and pulmonic insufficiency), afterload (pulmonic or pulmonary artery stenosis, pulmonary vascular disease, and left heart disease) or contractility (RV myopathy or ARVC).VSD is not volume loading to RV and Eisenmenger’s would be a pressure load b/c of increased PVR and actually volume unload the RV with R to L VSD shunting. In acute stabilization, it is reasonable to utilize methods used to manage acute RV failure, with the understanding that interventional/surgical management will ultimately be necessary for definitive management When should bioprosthetic valve obstruction be suspected and what is the differential for this? What is the initial workup? Obstruction should be suspected in any patient with a history of prosthetic valve placement who presents with a new murmur, new history of exercise intolerance, syncope/presyncope, or evidence of heart failure on exam. Differential diagnosis includes pannus ingrowth, thrombus, and vegetation. The anterior location of a surgically replaced RVOT/PV also makes it susceptible to compressive forces from the chest wall anteriorly and dilated Ao posteriorly, particularly in growing children. For bioprosthetic valves pannus is more common than acute thrombosis. Age of the valve, risk factors for infection, and anticoagulation status are clinical signs that may help differentiate. Diagnosis is typically made by transthoracic echocardiology (TTE): Increased gradients across the PV, RV hypertrophy, dilatation or dysfunction, increasing TR volume with elevated gradients from RV to RA. Cardiac CT or CMRI can also be helpful in characterizing the stenosis (discreet or long-segment, singular or stenoses in series). Invasive hemodynamic assessment in the catheterization laboratory can be especially helpful to more specifically characterize the degree and location of the obstruction as well as perform intervention (balloon, stent placement, TCPV) to relieve the obstruction. It is not uncommon that distal pulmonary artery stenting is required at the time of ballooning of the valve or valve-in-valve TCPVR. Lab testing sometimes performed includes INR, hemoglobin level, hemolysis labs, NT-BNP. If acute thrombosis of the bioprosthetic valve is diagnosed, a hypercoaguable work-up to include familial thrombophilia should be performed FDG PET may be an adjunctive tool to help evaluate for prosthetic valve endocarditis by detection of acute inflammation. What are the indications for management of valve obstruction? What are the primary management strategies? As previously discussed the differential diagnosis of bioprosthetic valve obstruction includes BPVT, pannus, and vegetation. Valve intervention is indicated for symptomatic severe stenosis and treatment strategy depends on the underlying cause. BPVT: If stable, can trial anticoagulation therapy. If unstable immediate therapy is required which requires surgery or fibrinolytics. Pannus: Severe stenosis caused by soft tissue overgrowth with degeneration and calcium requires stenting open the obstructive valve in the catheterization laboratory followed by a valve-in-valve TCPV placement. It is increasingly rare that an obstructed bioprosthetic PV cannot be managed in this fashion and surgical PVR is needed. Medical therapy is ineffective in treating the underlying cause although can treat consequences from heart failure. Vegetation: Endocarditis with vegetation causing severe stenosis is usually treated with surgical intervention. Decisions regarding surgical indications for endocarditis are complex and a trial of medical therapy is reasonable in less severe disease. For native pulmonic valve obstruction many patients are amenable to balloon valvuloplasty and recurrent stenosis is rare. Patients are usually left with some degree of pulmonic insufficiency....

370. CardioOncology: Advanced Heart Failure in CardioOncology with Dr. Richard Cheng May 13, 2024

Show notes

CardioNerds Co-Founder Dr. Daniel Ambinder, Episode Chair Dr. Dinu Balanescu, and FIT Lead Dr. Natalie Tapaskar discuss advanced heart failure in CardioOncology with expert Dr. Richard Cheng. Audio editing by CardioNerds Academy Intern, Dr. Akiva Rosenzveig. In this episode, we discuss the spectrum of advanced heart failure in patients with a history of cancer. We dissect cancer therapy-related cardiac dysfunction (CTRCD) cases and the imaging and biomarker tools available for risk stratification and disease monitoring. We delve into the data on the use of guideline-directed medical therapy (GDMT) and cardiac resynchronization therapy (CRT) in these patients. We discuss the risk of prior radiation and chemotherapy during cardiac surgery. Finally, we learn about the post-transplant risk of rejection, recurrent malignancy, and de-novo malignancies, as well as treatment strategies we can employ for these patients. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Advanced Heart Failure in CardioOncology Use the HFA-ICOS risk tool to understand the baseline risk of developing cancer therapy-related cardiac dysfunction (CTRCD). Key factors are type of cancer therapy, baseline CV risk factors, and age. A relative change in global longitudinal strain of more than 15% from baseline is a marker of early cardiac dysfunction and predicts the subsequent risk for systolic dysfunction in patients undergoing cardiotoxic chemotherapy. Statins may be useful in prevention of cardiovascular dysfunction in patients receiving anthracycline chemotherapy. There is limited data on the 4 pillars of GDMT in prevention of CTRCD, but should be started early once CRTCD is suspected or diagnosed! Mediastinal radiation causes adhesions and scarring which increase the risk of bleeding during cardiac surgery, lead to longer operative times, and can lead to RV failure and poor wound healing. Patients with a pre-transplant history of malignancy have a higher risk of mortality due to post-transplant malignancy. And patients with active cancer should not be considered for heart transplant. Post-transplant malignancy risk can be mitigated by utilizing an mTOR based, CNI free immunosuppression regimen. Show notes - Advanced Heart Failure in CardioOncology How do cardio-oncology and advanced heart failure intersect? There are 3 basic populations of patients to consider:Patients with advanced heart failure who develop cancer.Patients with pre-existing chemotherapy and radiation exposure for cancer treatment who later develop advanced heart failureHeart transplant recipients who, in the long term are at very high risk of developing cancer Cardio-oncologists must consider risk assessment and mitigation, long-term prognosis, and treatment strategies for each of these unique populations. How can we assess the risk of developing cardiovascular disease during cancer treatment (CTRCD)? There are many proposed risk tools. However, the majority are not well-validated. One of the most used tools is the HFA-ICOS risk tool.1You can select the planned cancer therapy for the patient (anthracyclines, HER-2, VEGF, RAF/MEK inhibitors, Kinase inhibitors, multiple myeloma therapies) and then calculate their risk of developing CV disease during cancer treatment based on baseline variables:1) previous history of CV disease,2) biomarkers – troponin and NT-proBNP3)age,4) CV risk factors -HTN, DM, CKD,5) previous cardio-toxic treatments,6) lifestyle risk factors- smoking, obesity The risk tool will then give you a ranking of very high, high, medium, or low risks. How should we use imaging to evaluate cardiac dysfunction in patients undergoing cancer treatments? Echo with global longitudinal strainA relative change in global longitudinal strain of more than 15% from baseline is a marker of early cardiac dysfunction and predicts the subsequent risk for systolic dysfunction.Data are mixed on the benefit of intervening on drops in GLS without a concomitant drop in LVEF. Current vendor software has improved the consistency in GLS measurements across vendors, which used to be quite problematic.Echo LVEFSome centers prefer to use 3D LVEF to track patients over time.For asymptomatic high-risk patients, we should obtain echocardiograms at 1, 3, and 5 years post-cancer therapies and then every 5 years thereafter.But surveillance should occur on a case-by-case basis. CPETCan be used to risk stratify patients with lung or colon cancer before starting cancer treatment.You can trend peak VO2 over time after cancer treatments. However, this is generally a data-sparse zone! Can we use serum biomarkers such as troponin or NT-proBNP in monitoring for the development of CTRCD? Elevations in BNP during cancer treatment are associated with subsequent cardiovascular disease.Elevations in troponin and myeloperoxidase in breast cancer patients receiving anthracyclines can predict the risk of cardiotoxicity. Novel biomarkers – data-free zoneCRP is a marker of inflammation and may be helpful in patients undergoing radiation therapy.Immunoglobulins- baseline elevated IgE levels have a lower risk for cardiotoxicity. Cell-free DNA – may be the future? What is the role of cardiovascular medications and devices in preventing and treating CTRCD? Prevention:Statins – The STOP-CA trial showed that use of atorvastatin 40 mg/day in patients with lymphoma receiving anthracycline chemotherapy reduced the incidence of cardiac systolic dysfunction compared to placebo.2SGLT2i – limited retrospective data in patients with diabetes and anthracycline chemotherapy. May have lower rates of cardiac events on SGLT2i.Currently there is not enough data to recommend routine use of SGLT2i, ARNI, and BB for cardioprotection before cancer therapies. Treatment: Treat these patients similarly to other heart failure patients. The four pillars of GDMT work! Early recognition is critical to confer better long-term outcomes. CRT-D: MADIT-CHIC3 showed that CRT therapy improved LVEF at 6 months in patients with chemotherapy-induced cardiomyopathy.Only consider ICD if life expectancy is >1 year.There is a risk of device reset for radiation directly over the device. ICDs are more sensitive to ionizing radiation, leading to inappropriate shocks. Can consider moving the device to a non-radiation field. What do we need to consider when patients with a history of cancer are being evaluated for heart transplant and left ventricular assist device (LVAD)? Heart transplantPatients with chemo-induced cardiomyopathy have no differences in post-transplant outcomes compared to patients with other causes of cardiomyopathy.Patients with a pre-transplant history of malignancy have a higher risk of mortality due to post-transplant malignancy, particularly in those with a history of hematologic malignancy.Patients with active cancer should not be considered for heart transplant.The duration and interval of waiting after active cancer before a heart transplant depends on the type and stage of cancer. LVADPatients with chemotherapy-induced cardiomyopathy have similar outcomes and rates of post-LVAD RV dysfunction as patients with other etiologies of cardiomyopathy. Limited data on performing LVAD in patients with active cancer. What risk does prior mediastinal radiation pose to cardiac surgery? Mediastinal radiationIncreases adhesions and scarring, increasing the risk of bleeding during cardiac surgery. Longer operative times may also increase the risk of RV failure. There can also be atrophy of sternal muscles, which can lead to poor wound healing What do the post-heart transplant rejection and malignancy profiles look like for patients with a history of chemotherapy-induced cardiomyopathy? Patients with prior chemotherapy have depressed immunosurveillance from their innate immune system and, thus, may have a lower risk of rejection. But there is limited data here. Patients with a history of pre-transplant malignancy are at increased risk of recurrence and PTLD. You can consider decreasing immunosuppression or switching to mTOR inhibitor-based regimen to reduce the risk. What must we know about de-novo malignancy post-heart transplant? Risk factors: history of prior malignancy, heavier immunosuppression, older recipient age, smoking history, radiation exposure, genetic variants.Treatment: reduce immunosuppression as much as possible and switch to an mTOR-based regimen. What about immune checkpoint inhibitors post-transplant? These work by upregulating T cell activity, which counteracts our transplant immunosuppression. High risk of rejection, but some successful case reports of use. References - Advanced Heart Failure in CardioOncology Lyon AR, Dent S, Stanway S, et al. Baseline cardiovascular risk assessment in cancer patients scheduled to receive cardiotoxic cancer therapies: a position statement and new risk assessment tools from the C ardio‐ O ncology S tudy G roup of the H eart F ailure A ssociation of the E uropean S ociety of C ardiology in collaboration with the I nternational C ardio‐ O ncology S ociety. Eur J Heart Fail. 2020;22(11):1945-1960. doi:10.1002/ejhf.1920 Neilan TG, Quinaglia T, Onoue T, et al. Atorvastatin for Anthracycline-Associated Cardiac Dysfunction: The STOP-CA Randomized Clinical Trial. JAMA. 2023;330(6):528. doi:10.1001/jama....

369. Case Report: Apical Obliteration with Biventricular Thrombus – West Virginia University May 07, 2024

Show notes

CardioNerds, Dr. Richard Ferraro and Dr. Dan ambinder join Dr. Li Pang, Dr. Emily Hendricks, and Dr. Bei Jiang from West Virginia University to discuss the following case that features apical obliteration with biventricular thrombus. Dr. Christopher Bianco provides the Expert CardioNerd Perspectives & Review (E-CPR) for this episode. Audio editing by CardioNerds Academy Intern, student doctor Tina Reddy. A 37-year-old Caucasian man with a history of tobacco smoking and hypertension who presented with chest pain and elevated troponin was admitted for non-ST elevation myocardial infarction (NSTEMI). Ischemic evaluation with an invasive coronary angiogram was negative. He was treated as NSTEMI and scheduled for outpatient cardiac MRI (CMR). The patient came back 2 months later with right arm weakness and confusion and was found to have an embolic stroke. Labs showed positive troponin with a flat trend and hypereosinophilia. Transthoracic echocardiogram (TTE) showed obliteration of LV and RV apex with thrombus and reduced LV systolic function. CMR was consistent with myocarditis with biventricular thrombus. The patient was started on corticosteroids and warfarin. Hypereosinophilia workup was positive for PDGFRA alpha rearrangement. He was diagnosed with primary hypereosinophila syndrome. Imatinib was initiated. The patient was followed up with the hematology clinic, achieved a complete hematologic response with normalized cell count, and remained free from any cardiovascular event at the 8-month follow-up. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. 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 Pearls - Apical Obliteration with Biventricular Thrombus Cardiac MRI is a valuable test for patients presenting with myocardial infarction with non-obstructive coronary arteries (MINOCA). Obliterated apex with apical thrombus on TTE with hypereosinophilia should raise high suspicion for eosinophilic myocarditis. Initiation of corticosteroids is the first-line treatment for eosinophilic myocarditis, which is associated with lower mortality in patients with myocarditis. For other potential complications, such as heart failure, intracardiac thrombus, arrhythmia, and pericardial effusion, the standard of care for each disorder is recommended. Hypereosinophilia can be seen in parasitic infections, vasculitis, asthma, allergy, hematological malignancies, and as a primary disorder. Show Notes - Apical Obliteration with Biventricular Thrombus What is the differential diagnosis for patients with elevated troponin and nonobstructive CAD? The occurrence of acute myocardial infarction (AMI) without significant CAD was reported 80 years ago. However, the term MINOCA (myocardial infarction with non-obstructive coronary arteries) has only been used recently to describe these patients. It involves ischemic and nonischemic etiologies. First, overlooked ischemic etiologies need to be ruled out by reconciling the angiogram images such as spontaneous coronary artery dissection (SCAD) and plaque disruption. Intracoronary imaging, such as intravascular ultrasound (IVUS) or optical coherence tomography (OCT), may be applied to evaluate for SCAD and subtypes of plaque disruption when indicated. The investigation continues with nonischemic causes such as stress cardiomyopathy, myocarditis, pulmonary embolism, demand ischemia from sepsis, anemia, chest trauma, heart failure exacerbation, arrhythmia, and stroke. The diagnosis of MINOCA is established when it fulfills the following criteria: First, it is AMI by the Fourth Universal Definition; Second, less than 50% of stenotic lesion on angiogram; Third, there is no alternate diagnosis. MINOCA etiologies include coronary artery spasms and microvascular dysfunction. It is recommended to perform CMR in all MINOCA patients without an obvious underlying cause. What are the common causes of LV thrombus? The incidence of LV thrombus has been reported between 4-39% after anterior MI. The temporal incidence has been decreasing. It is also commonly seen in dilated cardiomyopathy with an incidence of 2-36%. The pathophysiology of intracardiac thrombus formation obeys Virchow’s triad rule, which states that endocardial injury, hypercoagulability/inflammation, and stasis lead to thrombogenesis. Other etiologies of LV thrombus include eosinophilic myocarditis and LV noncompaction. What are the characteristic echocardiographic and CMR findings of eosinophilic myocarditis (EM)? During the acute necrotic stage, there is increased subendocardial echogenicity, wall thickening, impaired regional wall motion, and pericardial effusion; there is edema without fibrosis on CMR. During the thrombotic stage, intracardiac thrombus is often detected in the ventricles on TTE; on CMR, there is endomyocardial involvement and intracardiac thrombus. During the fibrotic stage, in addition to the cumulative findings from previous stages, restrictive physiology, valvular thickening, and restricted motion can occur on TTE; on CMR, endomyocardial fibrosis with LGE is present. What is the management for eosinophilic myocarditis (EM)? Two aspects must be considered in the treatment of eosinophilic myocarditis: the management of acute cardiac conditions and the treatment of underlying causes. Corticosteroids are the first-line treatment for EM. A meta-analysis of 179 cases showed that steroid use is associated with a lower mortality rate. No clinical trial data are available for the treatment of eosinophilic myocarditis. The dose and duration of corticosteroids in each individual case can be different. For intracardiac thrombus, vitamin K antagonists (VKAs) are the drugs of choice. Complete gradual resolution of intracardiac thrombus with VKA in eosinophilic myocarditis was reported at the 18-month follow-up. The INR target was 2-3. Emerging data showed the noninferiority of using DOAC for LV thrombus compared to warfarin as an alternative for stroke prevention. There is an increased risk of stroke in patients on VKA but with subtherapeutic INR levels. The guidelines recommend DOAC as a reasonable alternative to VKA to treat LV thrombus. For other potential complications such as heart failure, intracardiac thrombus, arrhythmia, and pericardial effusion, the standard of care for each complication is recommended. There is no large data to suggest a specific approach in eosinophilic myocarditis. It has been reported to achieve full recovery with GDMT in addition to treating the underlying cause in a case report of eosinophilic myocarditis with severely reduced LV systolic function. What is hypereosinophilic syndrome (HES)? HES is pleomorphic in clinical presentation and can be idiopathic or associated with a variety of underlying conditions, including allergic, rheumatologic, infectious, and neoplastic disorders. There are 4 groups. In primary HES, the hypereosinophilia is driven by a clonal process in stem cell or myeloid lineage. Patients usually present with a myeloid neoplasm and myeloid proliferative disorder. Besides eosinophilia, they may have other cytopenias, blasts, or dysplastic cells in peripheral blood. They can present with constitutional symptoms or hepatosplenomegaly. Some of these patients have disease-defining mutations or chromosome translocation. They require treatment for their underlying hematologic condition. Secondary HES usually have polyclonal eosinophilia secondary to some stimulus. The stimulus may be infections, rheumatology conditions, solid tumors, and lymphoid neoplasm. The underlying condition increases eosinophilic cytokines leading to an increase in eosinophil production. The third group is familial HES results from certain genetic factors. If no cause of HES can be identified, they fall into the category of idiopathic HES. Patients with HES secondary to myeloid and lymphoid disorders need to follow up with a hematology specialist. References - Apical Obliteration with Biventricular Thrombus Bondue A, Carpentier C, Roufosse F. Hypereosinophilic syndrome: considerations for the cardiologist. Heart 2022;108:164-171. Merlo M, Gagno G, Baritussio A et al. Clinical application of CMR in cardiomyopathies: evolving concepts and techniques : A position paper of myocardial and pericardial diseases and cardiac magnetic resonance working groups of Italian society of cardiology. Heart Fail Rev 2023;28:77-95. Murthy SB. Troponin Elevation After Ischemic Stroke and Future Cardiovascular Risk: Is the Heart in the Right Place? Journal of the American Heart Association 2021;10:e021474. Dhaliwal JSS, Ansari SA, Ghosh S, Chitkara A, Khizer U. Duet of Death: Biventricular Thrombus in a Methamphetamine User. Cureus 2023;15:e39917. Levine GN, McEvoy JW, Fang JC et al. Management of Patients at Risk for and With Left Ventricular Thrombus: A Scientific Statement From the American Heart Association. Circulation 2022;146:e205-e223. Parrillo JE. Heart Disease and the Eosinophil. New England Journal of Medicine 1990;323:1560-1561. Wright BL, Leiferman KM, Gleich GJ. Eosinophil Granule Protein Localization in Eosinophilic Endomyocardial Disease. New England Journal of Medicine 2011;365:187-188. Polte CL, Bobbio E, Bollano E et al. Cardiovascular Magnetic Resonance in Myocarditis. Diagnostics 2022;12:399. Ammirati E, Frigerio M, Adler ED et al. Management of Acute Myocarditis and Chronic Inflammatory Cardiomyopathy: An Expert Consensus Document. Circ Heart Fail 2020;13:e007405. Ito S, Isotani A, Yamaji K, Ando K. Follow-up magnetic resonance imaging of Löffler endocarditis: a case report....

368. Obesity: Procedural Management of Obesity with Dr. Steve Nissen May 05, 2024

Show notes

CardioNerds (Drs. Richard Ferraro, Gurleen Kaur, and Rupan Bose) discuss the growing epidemic of obesity and dive into the role of its procedural management with Dr. Steve Nissen, Chief Academic Officer at the Cleveland Clinic HVTI and past president of the American College of Cardiology. This is an exciting topic that reflects a major inflection point in cardiovascular care. In this episode, we discuss the importance of addressing obesity in cardiovascular care, as it is a major driver of cardiovascular disease and the progression of associated cardiovascular comorbidities. We look at the role of bariatric surgery and its ability to produce sustained weight loss. Finally, we look into the emerging role of new medical therapies such as GLP1 and GIP agonist medications. Notes were drafted by Dr. Rupan Bose and episode audio was edited by CardioNerds Intern Dr. Atefeh Ghorbanzadeh. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Novo Nordisk. See below for continuing medical education credit. Claim CME for this episode HERE. CardioNerds Prevention 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 - Procedural Management of Obesity with Dr. Steve Nissen Obesity is associated with adverse cardiovascular outcomes. Returning to a healthy weight can largely prevent the downstream consequences of obesity. Regarding lifestyle modifications, diet alone is insufficient in sustaining prolonged weight loss. It is associated with short-term weight loss, but it is generally necessary to supplement with exercise and activity to ensure sustained weight loss. Bariatric surgery should be considered for patients with BMI ≥40 kg/m2 or BMI ≥35 kg/m2 with obesity-related comorbid conditions who are motivated to lose weight and who have not responded to behavioral treatment with or without pharmacotherapy. New emerging medications, including GLP1 receptor agonists, GIP receptor agonists, and glucagon receptor agonists, are beginning to approach weight loss levels that were previously only seen with bariatric surgery. Further research in this dynamic area is ongoing. Show notes - Procedural Management of Obesity with Dr. Steve Nissen Notes drafted by Dr. Rupan Bose. What is the role of obesity in the burden of cardiovascular disease, and why is it so important for CardioNerds to address it? According to the AHA, approximately 2.8 to 3.5 billion people worldwide are either overweight or obese. It is estimated that by 2030, 30% of people in the US will have a BMI greater than 30. Adipose tissue is associated with cytokine release. Cytokines, in turn, can activate and increase levels of IL-1 beta, IL-6, and CRP, leading to an increased inflammatory state. This pro-inflammatory state then accelerates the rate of cardiovascular disease. Obesity is also associated with significant joint and orthopedic diseases, which further impact patients’ quality of life and morbidity. Additionally, obesity is associated with NASH cirrhosis. These adverse liver outcomes hold additional significant systemic implications and morbidity. How do you determine one’s goal weight and goal BMI? Is BMI a good standard for measuring obesity? BMI is a variable of both weight and height. However, it cannot differentiate those whose weight is from adipose tissue versus from muscle mass. Therefore, BMI measurements can sometimes be misleading. Waist circumference may be a better measurement standard for obesity and risk assessment. The “apple shape” body type, with more abdominal fat, is associated with higher inflammation and cardiovascular risk than the “pear-shaped” body type, which is where there is more fat deposition in the buttocks and thighs. A fat distribution that is more centralized corresponds with greater cardiovascular risk. “Normal” BMI and “normal” waist circumference can differ based on ethnicity. For example, a BMI of 22.6 in South Asians carries a similar risk to a BMI of 30 in White European patients. Therefore, providers must remain cognizant of these differences when making individual patient recommendations. Does childhood obesity correlate with obesity at later ages? At what age should we start screening for and addressing obesity? Childhood obesity, or obesity at a young age, often correlates with continued obesity later in life. But it is interesting that if one can return to a healthy body weight at some point in their life, one can largely prevent the downstream consequences of obesity The USPSTF recommends clinicians screen for obesity in children and adolescents age 6 and older and offer behavioral interventions to promote improvements in weight status (grade B recommendation) What procedures or surgeries are available to patients with obesity? Bariatric surgery is an excellent option with great outcomes if done for the right patient. The 2013 AHA/ACC/TOS guidelines for the management of overweight and obesity in adults recommend bariatric surgery for patients with BMI ≥40 kg/m2 or BMI ≥35 kg/m2 with obesity-related comorbid conditions who are motivated to lose weight and who have not responded to behavioral treatment with or without pharmacotherapy. Several studies have shown that patients with bariatric surgery had a huge reduction in myocardial infarction, stroke, kidney disease, and death. Bariatric surgery can help address other cardiovascular comorbidities. For example, the STAMPEDE trial (Schauer, R et al.) demonstrated that bariatric surgery plus intensive medical therapy was more effective than intensive medical therapy alone in decreasing or, in some cases, resolving hyperglycemia. Additionally, the magnitude of weight loss from bariatric surgery is often greater than the absolute magnitude of weight loss through medical therapy alone. Therefore, for patients with a very high BMI, bariatric surgery may be better suited to achieve the necessary weight loss. What emerging medications are available to patients with obesity? And what medications are just around the corner? GLP1 agonists, or dual GIP-GLP1 receptor agonists, drugs are associated with approximately 20% reduction in body weight. In the SELECT trial, semaglutide was associated with a 9.3% reduction in body weight (Please see GLP1 series for additional details!). In the SURMOUNT-1 trial, tirzepatide was associated with a 22% reduction in body weight. Future trials will look at triple agonists that combine GLP1, GIP, and glucagon agonist properties. One such drug is retatrutide, which previously demonstrated a 24% (and approximately 28.5% in females) reduction in body weight. These medications are approaching similar weight loss magnitudes to bariatric surgery (a Roux en Y procedure achieves approximately 25% weight loss on average), though additional studies are ongoing. What other strategies can one use to lower body weight and maintain that weight loss? Diet alone is not sustainable in reducing weight and keeping weight off. Unfortunately, the body subconsciously activates adaptive responses that down-regulate metabolism, which in turn burns fewer calories. Therefore, exercise and activity play a key role in continuing to burn calories, allowing for sustained weight loss. All patients should, therefore, be counseled on both diet and exercise strategies to address obesity and weight loss. Discussing weight and body image is often a sensitive subject and can carry a stigma for some patients. What are some recommendations on how we can address these topics in a safe and supportive manner? It is important to create a safe, supportive, and non-judgmental space when discussing weight with patients. We should also make an effort to understand the specific drivers of each individual patient’s weight gain. Some drivers include emotional stress, socio-economic factors, lifestyle barriers, etc. By understanding each specific driver, we can be more targeted in our approach and build more individualized plans with our patients. We can also recruit other clinical team members to assist the patient in their weight loss journey. Some such teammembers include dieticians, psychiatrists, social workers, etc. References - Procedural Management of Obesity with Dr. Steve Nissen Jastreboff, A. M., Aronne, L. J., Ahmad, N. N., Wharton, S., Connery, L., Alves, B., ... & Stefanski, A. (2022). Tirzepatide once weekly for the treatment of obesity. New England Journal of Medicine, 387(3), 205-216. https://www.nejm.org/doi/full/10.1056/NEJMoa2206038 Lincoff, A. M., Brown-Frandsen, K., Colhoun, H. M., Deanfield, J., Emerson, S. S., Esbjerg, S., ... & Ryan, D. H. (2023). Semaglutide and cardiovascular outcomes in obesity without diabetes. New England Journal of Medicine. https://www.nejm.org/doi/full/10.1056/NEJMoa2307563 Schauer, P. R., Bhatt, D. L., Kirwan, J. P., Wolski, K., Aminian, A., Brethauer, S. A., ... & Kashyap, S. R. (2017). Bariatric surgery versus intensive medical therapy for diabetes—5-year outcomes. New England Journal of Medicine, 376(7), 641-651. https://www.nejm.org/doi/full/10.1056/nejmoa1600869 Jensen, M. D., Ryan, D. H., Apovian, C. M., Ard, J. D., Comuzzie, A. G., Donato, K. A., ... & Yanovski, S. Z. (2014). 2013 AHA/ACC/TOS guideline for the management of overweight and obesity in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and The Obesity Society. Journal of the American college of cardiology, 63(25 Part B), 2985-3023. Powell-Wiley, T. M., Poirier, P., Burke, L. E., Després, J. P., Gordon-Larsen, P., Lavie, C. J., ......

367. GLP-1 Agonists: Clinical Implementation of GLP-1 Receptor Agonists with Dr. Neha Pagidapati May 03, 2024

Show notes

CardioNerds (Drs. Gurleen Kaur and Richard Ferraro) and episode FIT Lead Dr. Spencer Carter (Cardiology Fellow at UT Southwestern) discuss the clinical implementation of GLP-1 receptor agonists with Dr. Neha Pagidapati (Faculty at Duke University School of Medicine). In this episode of the CardioNerds Cardiovascular Prevention Series, we discuss the clinical implementation of glucagon-like peptide-1 (GLP-1) receptor agonists. We cover the clinical indications, metabolic and cardiovascular benefits, and potential limitations of these emerging and exciting therapies. Show notes were drafted by Dr. Spencer Carter. Audio editing was performed by CardioNerds Academy Intern, student Dr. Pacey Wetstein. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Novo Nordisk. See below for continuing medical education credit. Claim CME for this episode HERE. CardioNerds Prevention 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 - Clinical Implementation of GLP-1 Receptor Agonists GLP-1 agonists work through a variety of mechanisms to counteract metabolic disease. They increase insulin secretion, inhibit glucagon secretion, slow gastric motility, and increase satiety to limit excess energy intake. Patients with type II diabetes and an elevated risk for atherosclerotic cardiovascular disease should be considered for GLP-1 agonist therapy regardless of hemoglobin A1c. GLP-1 agonists offer significant ASCVD risk reduction even in the absence of diabetes. Newer data suggest a significant reduction in cardiovascular events with GLP-1 agonist therapy in patients who are overweight or obese and have a prior history of heart disease. GLP-1 agonists should generally be avoided in patients with a history of medullary thyroid cancer or MEN2. As these medications slow gastric emptying, relative contraindications include history of recurrent pancreatitis and gastroparesis. GLP-1 agonists should be initially prescribed at the lowest dose and slowly uptitrated to avoid gastrointestinal side effects. Show notes - Clinical Implementation of GLP-1 Receptor Agonists What were the groundbreaking findings of the STEP1 and SURMOUNT-1 trials and how these impact cardiovascular wellness? The STEP1 and SURMOUNT trials demonstrated sustained clinically relevant reduction in body weight with semaglutide and tripeptide, respectively, in patients with overweight and obesity. As obesity is an important risk factor for the development of cardiovascular disease, weight reduction meaningfully contributes to cardiovascular wellness. What were the findings of the LEADER trial and their implications for patients with type II diabetes and high cardiovascular risk? The LEADER trial demonstrated a significant reduction in the rate of cardiovascular death, nonfatal MI, or nonfatal stroke in patients with type II diabetes treated with liraglutide. GLP-1 receptor agonist therapy should be considered in all patients with type II diabetes and elevated ASCVD risk regardless of A1c or current hyperglycemic therapy. What are current indications for GLP1 agonists in the context of cardiometabolic disease. GLP-1 receptor agonists should be considered in patients with type II diabetes and high ASCVD risk OR patients without diabetes who are overweight/obese and have a history of cardiovascular disease. What are important side effects or contraindications to GLP1 agents when used for cardiovascular risk reduction and wellness? GLP-1 receptor agonists should be avoided in patients with a history of medullary thyroid cancer or MEN2. Relative contraindications include recurrent pancreatitis, gastroparesis, or ongoing unexplained gastrointestinal symptoms. What are practical concerns associated with GLP-1 use, and how can these be overcome? Affordability and availability remain the leading practical limitations for GLP-1 receptor agonist therapies. Many insurance companies will cover semaglutide and tirzepatide for patients with diabetes. Obtaining coverage may be difficult otherwise, but this is an evolving field as more clinical trial data emerge. Beware of unauthentic/alternate formulations of these medications, as they tend not to be FDA-regulated and can pose health risks. Some patients express concern about injectable therapies, but GLP-1 injectors are typically very well tolerated and easy to use. References - Clinical Implementation of GLP-1 Receptor Agonists Brown, E., Heerspink, H. J., Cuthbertson, D. J., & Wilding, J. P. (2021). SGLT2 inhibitors and GLP-1 receptor agonists: established and emerging indications. The Lancet, 398(10296), 262-276. https://www.sciencedirect.com/science/article/pii/S0140673621005365 Wilding, J. P., Batterham, R. L., Calanna, S., Davies, M., Van Gaal, L. F., Lingvay, I., ... & Kushner, R. F. (2021). Once-weekly semaglutide in adults with overweight or obesity. New England Journal of Medicine. https://www.nejm.org/doi/full/10.1056/NEJMoa2032183 Müller, T. D., Blüher, M., Tschöp, M. H., & DiMarchi, R. D. (2022). Anti-obesity drug discovery: advances and challenges. Nature Reviews Drug Discovery, 21(3), 201-223. https://www.nature.com/articles/s41573-021-00337-8 Jastreboff, A. M., Aronne, L. J., Ahmad, N. N., Wharton, S., Connery, L., Alves, B., ... & Stefanski, A. (2022). Tirzepatide once weekly for the treatment of obesity. New England Journal of Medicine, 387(3), 205-216. https://www.nejm.org/doi/full/10.1056/NEJMoa2206038 Lincoff, M, Brown-Frandsen K, Colhoun H, et al. Semaglutide and Cardiovascular Outcomes in Obesity without Diabetes. (2023). 389(24):2221-2232. https://www.nejm.org/doi/full/10.1056/NEJMoa2307563 Eberly, L, Yang L, Essien U, et al. (2021). Racial, ethnic, and socioeconomic inequities in glucagon-like-peptide-1 receptor agonist use among patients with diabetes in the US; 2(12):e214182. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8796881/

366. Digital Health: Integrating Digital Health into Practice with Dr. Alexis Beatty and Dr. Seth Martin Apr 25, 2024

Show notes

CardioNerds (Dr. Dan Ambinder), Dr. Nino Isakadze (EP Fellow at Johns Hopkins Hospital), and Dr. Karan Desai (Cardiology Faculty at Johns Hopkins Hospital) join Digital Health Experts, Dr. Alexis Beatty (Cardiologist and associate professor in the department of epidemiology and biostatistics at UCSF) and Dr. Seth Martin (Director of the Johns Hopkins Center for Mobile Technologies to Achieve Equity in Cardiovascular Health (mTECH), which is part of the American Heart Association (AHA) Strategically Focused Research Networks on Health Technology & Innovation) for another installment of the Digital Health Series. In this specific episode, we discuss pearls, pitfalls, and everything in between for emerging digital health innovators. This series is supported by an ACC Chapter Grant in collaboration with Corrie Health. Audio editing by CardioNerds Academy Intern, student doctor Shivani Reddy. In this series, supported by an ACC Chapter Grant and in collaboration with Corrie Health, we hope to provide all CardioNerds out there a primer on the role of digital heath in cardiovascular medicine. Use of versatile hardware and software devices is skyrocketing in everyday life. This provides unique platforms to support healthcare management outside the walls of the hospital for patients with or at risk for cardiovascular disease. In addition, evolution of artificial intelligence, machine learning, and telemedicine is augmenting clinical decision making at a new level fueling a revolution in cardiovascular disease care delivery. Digital health has the potential to bridge the gap in healthcare access, lower costs of healthcare and promote equitable delivery of evidence-based care to patients. This CardioNerds Digital Health series is made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Nino Isakadze and Dr. Karan Desai. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Digital Health Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

365: CardioOncology: Cardiotoxicity of Novel Immunotherapies with Dr. Tomas Neilan Apr 22, 2024

Show notes

Immunotherapy is a type of novel cancer therapy that leverages the body’s own immune system to target cancer cells. In this episode, we focused on the most common type of immunotherapy: immune checkpoint inhibitors or ICIs. ICIs are monoclonal antibodies targeting immune “checkpoints” or brakes to enhance T-cell recognition against tumors. ICI has become a pillar in cancer care, with over 100 approvals and 5,000 ongoing trials. ICIs can lead to non-specific activation of the immune system, causing off-target adverse events such as cardiotoxicities. ICI-related myocarditis, though less common, can be fatal in 30% of cases. Clinical manifestations vary but can include chest pain, dyspnea, palpitations, heart failure symptoms, and arrhythmias. Diagnosis involves echocardiography, cardiac MRI, and endomyocardial biopsy. Treatment includes high-dose corticosteroids with potential additional immunosuppressants. Baseline EKG and troponin are recommended before ICI initiation, but routine surveillance is not advised. Subclinical myocarditis is a challenge, with unclear management implications. So let’s dive in and learn about cardiotoxicity of novel immunotherapies with Drs. Giselle Suero (series co-chair), Evelyn Song (episode FIT lead), Daniel Ambinder (CardioNerds co-founder), and Tomas Neilan (faculty expert). Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Cardiotoxicity of Novel Immunotherapies Immune checkpoint inhibitors (ICI) play a crucial role in current oncology treatment by enhancing T-cell recognition against tumors. ICI-related cardiac immune-related adverse events (iRAEs) include myocarditis, heart failure, stress-cardiomyopathy, conduction abnormalities, venous thrombosis, pericardial disease, vasculitis, and atherosclerotic-related events. ICI myocarditis can be fatal; thus, prompt recognition and treatment is crucial. Management includes cessation of the ICI and treatment with corticosteroids and potentially other immunosuppressants. Close monitoring and collaboration with cardiology and oncology are crucial. Rechallenging patients with immunotherapies after developing an iRAE is controversial and requires careful consideration of risks and benefits, typically with the involvement of a multidisciplinary team. Show notes - Cardiotoxicity of Novel Immunotherapies What are immune checkpoint inhibitors (ICIs)? ICIs are monoclonal antibodies used to enhance the body’s immune response against cancer cells. Currently, there are four main classes of FDA-approved ICIs: monoclonal antibodies blocking cytotoxic T lymphocyte antigen-4 (CTLA-4), programed cell death protein-1 (PD-1), lymphocyte-activation gene 3 (LAG3), and programmed cell death ligand-1 (PD-L1). ICIs can lead to non-specific activation of the immune system, potentially causing off-target adverse events in various organs, including the heart, leading to myocarditis. The mechanisms of cardiac iRAEs are not fully understood, but they are believed to involve T-cell activation against cardiac antigens, which leads to inflammation and tissue damage. What are the cardiotoxicities related to ICI therapies? ICI-related cardiac immune-related adverse events (iRAEs) include myocarditis, heart failure, stress-cardiomyopathy, conduction abnormalities, venous thrombosis, pericardial disease, vasculitis, and atherosclerotic-related events. ICI-related myocarditis is considered rare compared to other systemic IRAEs. While the incidence rate of ICI-myocarditis is around 0.7-2.0%, it can be fatal in 30% of cases. Clinical manifestations vary but can include chest pain, dyspnea, palpitations, heart failure symptoms, and arrhythmias. Severe cases of ICI myocarditis can present as cardiogenic shock or complete heart block (a fulminant myocarditis picture). The timing of adverse events is typically within the first three months of starting immunotherapy, with the majority occurring early on; however, some cases may present after three months. Increased clinical suspicion is key for early recognition and prompt diagnosis and treatment. What is the general approach to the diagnosis of ICI-myocarditis? Diagnosis is based on clinical history and presentation, elevated troponin, and imaging findings. Echocardiography (with global longitudinal strain) and cardiac MRI (with T1 and T2 mapping as per the modified Lake Louise Criteria) are key diagnostic tools. If cardiac MRI is not diagnostic but suspicion remains high, an endomyocardial biopsy is the next diagnostic step. Baseline cardiac tests, such as ECG and troponin, are important before initiating ICIs in every patient to serve as a reference standard for comparison in case of troponin elevation during therapy. However, routine surveillance of asymptomatic patients on ICIs is not recommended. How do endomyocardial biopsy findings for ICI-myocarditis compare to other types of autoimmune-mediated conditions such as transplant rejection? ICI-myocarditis is pathologically almost identical to transplant rejection; therefore, a similar grading system used for transplant rejection is applied to ICI-myocarditis to determine the severity and provide guidance on the intensity of immunosuppression. What are the treatment strategies for ICI-myocarditis? In general, all patients with suspected ICI-myocarditis should have their immunotherapy held temporarily until the diagnosis is confirmed. Next, patients should be typically admitted to an inpatient unit with telemetry capabilities, given the risk of progression to complete heart block and cardiogenic shock. High-dose corticosteroids are the first-line pharmacological treatment, but the optimal dose varies between guidelines. An approach for severe life-threatening cases based on the NCCN and SITC guideline recommendations is a pulse of high-dose corticosteroids (consider 1000 mg methylprednisolone IV daily for 3–5 days until troponin normalizes) followed by a taper of 1–2 mg/kg methylprednisolone or oral prednisone for 4–6 weeks. For patients who do not respond to high-dose corticosteroids, additional immunosuppressive therapies can be considered, including intravenous immunoglobulin (IVIG), mycophenolate mofetil, anti-thymocyte globulin (ATG), alemtuzumab (monoclonal antibody to CD52), abatacept (CTLA-4 agonist), or plasmapheresis. This is an area where more data is needed to support guidelines for patient treatment. Currently, there are ongoing studies in this area, such as a phase 3 clinical of Abatacept for immune checkpoint inhibitor-associated myocarditis (ATRIUM, NCT053359280) High doses of corticosteroids used to treat ICI-associated myocarditis may adversely impact cancer outcomes. Further research is needed to understand the impact of cardiac toxicities and immunosuppressive treatments on cancer outcomes Can patients be re-treated after an episode of ICI myocarditis? Patients who develop ICI-associated adverse events, including myocarditis, may have a second chance and be rechallenged with ICIs after resolution of the adverse event, but this decision should be made carefully considering the risks and benefits. References - Cardiotoxicity of Novel Immunotherapies Zhang L, Reynolds KL, Lyon AR, Palaskas N, Neilan TG. The Evolving Immunotherapy Landscape and the Epidemiology, Diagnosis, and Management of Cardiotoxicity: JACC: CardioOncology Primer. JACC CardioOncology. 2021;3(1):35-47. doi:10.1016/J.JACCAO.2020.11.012 Drobni ZD, Alvi RM, Taron J, et al. Association Between Immune Checkpoint Inhibitors With Cardiovascular Events and Atherosclerotic Plaque. Circulation. 2020;142(24):2299-2311. doi:10.1161/CIRCULATIONAHA.120.049981 Stein-Merlob AF, Rothberg M V., Holman P, Yang EH. Immunotherapy-Associated Cardiotoxicity of Immune Checkpoint Inhibitors and Chimeric Antigen Receptor T Cell Therapy: Diagnostic and Management Challenges and Strategies. Curr Cardiol Rep. 2021;23(3):1-11. doi:10.1007/s11886-021-01440-3 Suero-Abreu GA, Zanni MV, Neilan TG. Atherosclerosis With Immune Checkpoint Inhibitor Therapy: Evidence, Diagnosis, and Management: JACC: CardioOncology State-of-the-Art Review. JACC CardioOncol. 2022 Dec 20;4(5):598-615. doi: 10.1016/j.jaccao.2022.11.011. PMID: 36636438; PMCID: PMC9830225.

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