Episodes
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CardioNerds (Dr. Dan Ambinder and guest host, Dr. Pooja Prasad) join Dr. Donny Mattia from Phoenix Children’s pediatric cardiology fellowship, Dr. Sri Nayak from the Mayo Clinic – Arizona adult cardiology fellowship, and Dr. Harrison VanDolah from the University of Arizona College of Medicine - Phoenix Med/Peds program for a sunrise hike of Piestewa Peak, followed by some coffee at Berdena’s in Old Town Scottsdale (before the bachelorette parties arrive), then finally a stroll through the Phoenix Desert Botanical Gardens to discuss a thought-provoking case series full of clinical cardiology pearls. Expert commentary is provided by Dr. Tabitha Moe. Episode audio was edited by Dan Ambinder.
They discuss the following case: Cardiology is consulted by the OB team for a 27-year-old female G1, now P1, who has just delivered a healthy baby boy at 34 weeks gestation after going into premature labor. She is experiencing shortness of breath and is found to have a significant past cardiac history, including atrial fibrillation and preexcitation, now with a pacemaker and intracardiac defibrillator. We review the differential diagnosis for peripartum cardiomyopathy (PPCM) and then combine findings from her infant son, who is seen by our pediatric cardiology colleagues and is found to have severe hypertrophic cardiomyopathy (HCM). Genetic testing for both ultimately reveals a LAMP2 mutation consistent with Danon Disease. The case discussion focuses on the differential diagnosis for PPCM, HCM, pearls on Danon Disease and other HCM “phenocopies,” and the importance of good history.
US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here.
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Case Media
Pearls
Peripartum cardiomyopathy is a diagnosis of exclusion – we must exclude other possible etiologies of heart failure!
Be on the lookout for features of non-sarcomeric HCM – as Dr. Michelle Kittleson said in Episode 166, “LVH plus” states. HCM with preexcitation, heart block, strong family history, or extracardiac symptoms such as peripheral neuropathy, myopathy, or cognitive impairment should be evaluated for infiltrative/inherited cardiomyopathies!
As an X-linked dominant disorder, Danon disease will present differently in males vs females, with males having much more severe and earlier onset disease with extracardiac features.
Making the diagnosis for genetic disorders such as Danon disease is important for getting the rest of family members tested as well as the opportunity for specialized treatments such as gene therapy
Up to 5% of Danon disease cases may be due to copy number variants, which may be missed in genetic testing that does not do targeted deletion/duplication analysis!).
Notes
What is the differential diagnosis for peripartum cardiomyopathy?
Peripartum cardiomyopathy is a diagnosis of exclusion – we must exclude other possible etiologies of heart failure!
First, ensure that you are not missing an acute life-threatening etiology of acute decompensated heart failure – pulmonary embolism, amniotic fluid embolism, ACS, and SCAD should all be ruled out.
Second, a careful history can identify underlying heart disease or risk factors for the development of heart failure, such as substance use, high-risk behaviors that put one at risk for HIV infection, and family history that suggests an inheritable cardiomyopathy.
Lastly, a careful review of echocardiographic imaging may also identify underlying etiologies that warrant a change in management.
Diagnosis of peripartum cardiomyopathy is important to consider as within 7 days of onset, patients may be eligible for treatment with bromocriptine – consider referring ... -
CardioNerds (Dr. Dan Ambinder and Dr. Yoav Karpenshif – Chair of the CardioNerds Critical Care Cardiology Council) join Dr. Munim Khan, Dr. Shravani Gangidi, and Dr. Rachel Goodman from Tufts Medical Center’s general cardiology fellowship program for hot pot in China Town in Boston. They discuss a case involving a patient who presented with stress cardiomyopathy leading to cardiogenic shock. Expert commentary is provided by Dr. Michael Faulx from the Cleveland Clinic. Notes were drafted by Dr. Rachel Goodman. Audio editing by Dr. Diane Masket.
A young woman presents with de novo heart-failure cardiogenic shock requiring temporary mechanical circulatory support who is found to have basal variant takotsubo cardiomyopathy. We review the definition and natural history of takotsubo cardiomyopathy, discuss initial evaluation and echocardiographic findings, and review theories regarding pathophysiology of the clinical syndrome. We also highlight complications of takotsubo cardiomyopathy, with a focus on left ventricular outflow obstruction, cardiogenic shock, and arrythmias.
US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here.
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Pearls
Takotsubo cardiomyopathy is defined as a reversible systolic dysfunction with wall motion abnormalities that do not follow a coronary vascular distribution.
Takotsubo cardiomyopathy is a diagnosis of exclusion; patients often undergo coronary angiography to rule out epicardial coronary artery disease given an overlap in presentation and symptoms with acute myocardial infarction.
There are multiple echocardiographic variants of takotsubo. Apical ballooning is the classic finding, but mid-ventricular, basal, and biventricular variants exist as well.
Patients with takotsubo cardiomyopathy generally recover, but there are important complications to be aware of. These include arrhythmia, left ventricular outflow tract (LVOT) obstruction related to a hyperdynamic base in the context of apical ballooning, and cardiogenic shock.
Patients with Impella devices are at risk of clot formation and stroke. Assessing the motor current can be a clue to what is happening at the level of the motor or screw.
Notes
What is Takotsubo Syndrome (TTS)?
TTS is a syndrome characterized by acute heart failure without epicardial CAD with regional wall motion abnormalities seen on echocardiography that do not correspond to a coronary artery territory (see below).1
TTS classically develops following an acute stressor—this can be an emotional or physical stressor.1
An important feature of TTS is that the systolic dysfunction is reversible. The time frame of reversibility is variable, though generally hours to weeks.2
Epidemiologically, TTS has a predilection for post-menopausal women, however anyone can develop this syndrome.1
TTS is a diagnosis of exclusion. Coronary artery disease (acute coronary syndrome, spontaneous coronary artery dissection, coronary embolus, etc) should be excluded when considering TTS. Myocarditis is on the differential diagnosis.
What are the echocardiographic findings of takotsubo cardiomyopathy?
The classic echocardiographic findings of TTS is “apical ballooning,” which is a way of descripting basal hyperkinesis with mid- and apical hypokinesis, akinesis, or dyskinesis.3
There are multiple variants of TTS. The four most common are listed below:3(1) Apical ballooning (classic TTS)(2) Mid-ventricular variant(3) Basal variant
(4) Focal variant
Less common variants include the biventricular variant and the isolated right ventricular variant.3
Do patients with TTS generally have EKG changes or biomarker elevation?
Patients often have elevated troponin, -
Episodes manquant?
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In this episode, CardioNerds Dr. Gurleen Kaur and Dr. Akiva Rosenzveig are joined by Cardio-Rheumatology experts, Dr. Brittany Weber and Dr. Michael Garshick to discuss treating inflammation, delving into the pathophysiology behind the inflammatory hypothesis of atherosclerotic cardiovascular disease and the evolving data on anti-inflammatory therapies for reducing ASCVD risk, with insights on real-world implementation.
Show notes were drafted by. Dr. Akiva Rosenzveig.
This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Agepha Pharma.
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Pearls - Treating Inflammation
Our understanding of the pathophysiology of atherosclerosis has undergone a few iterations from the incrustation hypothesis to the lipid hypothesis to the response-to-injury hypothesis and culminating with our current understanding of the inflammation hypothesis.
Both the adaptive and innate immune systems play instrumental roles in the pathogenesis of atherosclerosis.
After adequately controlling classic modifiable risk factors such as blood pressure, dyslipidemia, glucose intolerance, and obesity, systemic inflammation as assessed by CRP can be ascertained as CRP is associated with ~1.8-fold increased risk of cardiovascular events
Although the most common side effect of colchicine is gastrointestinal intolerance, colchicine can induce lactose intolerance, so a lactose free diet may help ameliorate colchicine-induced GI symptoms.
Anti-inflammatory therapeutics have shown promise in reducing cardiovascular risk but much more is to be learned with ongoing and future basic, translational, and clinical research.
Show notes - Treating Inflammation
What are the origins of the inflammatory hypothesis?
The first hypothesis as to the pathogenesis of atherosclerosis was the incrustation hypothesis by Carl Von Rokitansky in 1852. He suggested that atherosclerosis begins in the intima with thrombus deposition.In 1856, Rudolf Virchow suggested the lipid hypothesis whereby high levels of cholesterol in the blood lead to atherosclerosis. He observed inflammatory changes in the arterial walls associated with atherosclerotic plaque growth, called endo-arteritis chronica deformans.In 1977, Russell Ross suggested the response-to-injury hypothesis, that atherosclerosis develops from injury to the arterial wall.In the 1990’s the role of inflammation in ASCVD became more recognized. Both the adaptive and innate immune system are critical in atherosclerosis. Lipids and inflammation are synergistic in that lipid exposure is required but they translocate through damaged endothelium which occurs by way of inflammatory cytokines, namely within the NLRP3 inflammasome (IL-1, IL-6 etc.).Smooth muscle cells are also involved. They migrate to the endothelial region and secrete collagen to create the fibrous cap. They can also transform into macrophage-like cells to take up lipids and become foam cells.
T, B, and K cells are also part of this milieu. In fact, neutrophils, macrophages and monocytes make up only a small portion of the cells involved in the atherosclerotic process.
What are ways to individually optimize one’s ASCVD risk?Ensure the patient is on appropriate antiplatelet therapy, lipid lowering therapy, blood pressure is well controlled, and the Hemoglobin A1c is well controlled. Smoking cessation is pivotal.If the patient has an elevated Lipoprotein (a), pursue more aggressive lipid lowering therapy. Targeted therapies may become available in the future.
Assess the patient’s systemic inflammatory risk as measured by C-Reactive Protein (CRP)
What is the evidence for utilizing CRP in risk stra... -
The following question refers to Sections 7.3.3 and 7.3.6 of the 2022 ACC/AHA/HFSA Guideline for the Management of Heart Failure.The question is asked by Palisades Medical Center medicine resident & CardioNerds Academy Fellow Dr. Maryam Barkhordarian, answered first by UTSW AHFT Cardiologist & CardioNerds FIT Ambassador Dr. Natalie Tapaskar, and then by expert faculty Dr. Robert Mentz.Dr. Mentz is associate professor of medicine and section chief for Heart Failure at Duke University, a clinical researcher at the Duke Clinical Research Institute, and editor-in-chief of the Journal of Cardiac Failure. Dr. Mentz has been a mentor for the CardioNerds Clinical Trials Network as lead principal investigator for PARAGLIDE-HF and is a series mentor for this very Decipher the Guidelines Series. For these reasons and many more, he was awarded the Master CardioNerd Award during ACC22.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
American Heart Association’s Scientific Sessions 2024As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership!
Question #39
Ms. Kay Lotsa is a 48-year-old woman with a history of CKD stage 2 (baseline creatinine ~1.2 mg/dL) & type 2 diabetes mellitus. She has recently noticed progressively reduced exercise tolerance, leg swelling, and trouble lying flat. This prompted a hospital admission with a new diagnosis of decompensated heart failure. A transthoracic echocardiogram reveals LVEF of 35%. Ms. Lotsa is diuresed to euvolemia, and she is started on carvedilol 25mg BID, sacubitril/valsartan 49-51mg BID, and empagliflozin 10mg daily, which she tolerates well. Her eGFR is at her baseline of 55 mL/min/1.73 m2 and serum potassium concentration is 3.9 mEq/L. Your team is anticipating she will be discharged home in the next one to two days and wants to start spironolactone. Which of the following is most important regarding her treatment with mineralocorticoid antagonists?ASpironolactone is contraindicated based on her level of renal impairment and should not be startedBSerum potassium levels and kidney function should be assessed within 1-2 weeks of starting spironolactoneCEplerenone confers a higher risk of gynecomastia than does spironolactoneDThe patient will likely not benefit from initiation of spironolactone if her cardiomyopathy is ischemic in origin
Answer #39
ExplanationThe correct answer is B – after starting a mineralocorticoid receptor antagonist (MRA), it is important to closely monitor renal function and serum potassium levels.MRA (also known as aldosterone antagonists or anti-mineralocorticoids) show consistent improvements in all-cause mortality, HF hospitalizations, and SCD across a wide range of patients with HFrEF. -
The following question refers to Sections 7.4 and 7.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by the Director of the CardioNerds Internship Dr. Akiva Rosenzveig, answered first by Vanderbilt AHFT cardiology fellow Dr. Jenna Skowronski, and then by expert faculty Dr. Randall Starling.Dr. Starling is Professor of Medicine and an advanced heart failure and transplant cardiologist at the Cleveland Clinic where he was formerly the Section Head of Heart Failure, Vice Chairman of Cardiovascular Medicine, and member of the Cleveland Clinic Board of Governors. Dr. Starling is also Past President of the Heart Failure Society of America in 2018-2019. Dr. Staring was among the earliest CardioNerds faculty guests and has since been a valuable source of mentorship and inspiration. Dr. Starling’s sponsorship and support was instrumental in the origins of the CardioNerds Clinical Trials Program.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
American Heart Association’s Scientific Sessions 2024As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership!
Question #38
Mrs. M is a 65-year-old woman with non-ischemic dilated cardiomyopathy (LVEF 40%) and moderate to severe mitral regurgitation (MR) presenting for outpatient follow-up. Despite improvement overall, she continues to experience dyspnea on exertion with two flights of stairs and occasional PND. She reports adherence with her medication regimen of sacubitril-valsartan 97-103mg twice daily, metoprolol succinate 200mg daily, spironolactone 25mg daily, empagliflozin 10mg daily, and furosemide 80mg daily. A transthoracic echocardiogram today shows an LVEF of 35%, an LVESD of 60 mm, severe MR with a regurgitant fraction of 60%, and an estimated right ventricular systolic pressure of 40 mmHg. Her EKG shows normal sinus rhythm at 65 bpm and a QRS complex width of 100 ms. What is the most appropriate recommendation for management of her heart failure?AContinue maximally tolerated GDMT; no other changesBRefer for cardiac resynchronization therapy (CRT)CRefer for transcatheter mitral valve intervention
Answer #38
ExplanationChoice C is correct. The 2020 ACC/AHA Guidelines for the management of patients with valvular heart disease outline specific recommendations.In patients with chronic severe secondary MR related to LV systolic dysfunction (LVEF <50%) who have persistent symptoms (NYHA class II, III, or IV) while on optimal GDMT for HF (Stage D), M-TEER is reasonable in patients with appropriate anatomy as defined on TEE and with LVEF between 20% and 50%, LVESD ≤70 mm, and pulmonary artery systolic pressure ≤70 mmHg (Class 2a, LOE B-R).Conversely, -
In this episode, Dr. Paul Ridker, a pioneer in the field of cardiovascular inflammation, joins the CardioNerds (Dr. Gurleen Kaur, Dr. Richard Ferraro, and Dr. Nidhi Patel) to discuss the evolving landscape of inflammation as a key factor in cardiovascular risk reduction. The discussion dives into the importance of biomarkers like high-sensitivity C-reactive protein (hs-CRP) in guiding treatment strategies, the insights gleaned from landmark trials like the JUPITER and CANTOS studies, and the future of targeted anti-inflammatory therapies in cardiology.
Show notes were drafted by Dr. Nidhi Patel. Audio editing by CardioNerds academy intern, Grace Qiu.
This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Lexicon Pharmaceuticals.
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Pearls - Targeting Inflammation for Cardiovascular Risk
"If you don’t measure it, you can’t treat it”: Incorporate hs-CRP into routine practice for patients at risk of cardiovascular events, as it provides crucial information for risk stratification and management.
Recognize the dual benefits of statins in lowering both LDL and inflammation, particularly in patients with elevated hs-CRP.
Encourage patients to adopt heart-healthy habits, as lifestyle changes remain foundational in reducing both cholesterol and inflammatory risk.
Reminder that most autoimmune or inflammatory diseases, from psoriasis to Addison’s disease to lupus to scleroderma to inflammatory bowel disease, have been shown to have elevated cardiovascular risk
Ongoing randomized trials including ZEUS, HERMES, and ARTEMIS will inform whether novel targeting of IL-6 can safely lower cardiovascular event rates or slow renal progression
Show notes - Targeting Inflammation for Cardiovascular Risk
Why is it important to measure both LDL and hs-CRP, and what factors increase hs-CRP?
Inflammation and hyperlipidemia are synergistic in promoting atherosclerosis. They interact to exacerbate plaque formation and instability, increasing the risk of cardiovascular events.
Just like we measure blood pressure and LDL to know what to treat, we should measure hs-CRP to guide targeted therapy.
Clinical Example: in Ms. Flame's case, despite achieving target LDL levels with statins, her elevated hs-CRP indicates ongoing inflammation and residual cardiovascular risk that should be assessed.
Residual inflammatory risk should be assessed in both primary and secondary prevention.
Increased BMI1, smoking2, a sedentary lifestyle3, and genetics4 (such as a higher risk of metabolic disease in South Asians) all raise hs-CRP levels.
SGLTi5 and GLP-1 agonists6 have also been shown to decrease hs-CRP levels.
What data do we have to support measuring hs-CRP?
Women’s Health Study7: an early study showing that hs-CRP predicted risk at least as well as LDL cholesterol and that models incorporating hs-CRP in addition to lipids were significantly better at predicting risk than models based on lipids alone.
JUPITER Trial8 (Primary Prevention): Among patients with normal LDL but elevated hs-CRP there was a 44% reduction in major cardiovascular events (>50% in MI and stroke) and a 20% reduction in all-cause mortality in patients treated with statins. These results led to changes in guidelines in recognizing the need to measure and treat inflammation.
CANTOS Trial9 (Secondary Prevention): Randomized >10K patients with previous MI and hs-CRP ≥ 2mg/L and found that canakinumab reduced hs-CRP level from baseline in a dose-dependent manner, without reduction in the LDL, ApoB, TG, or blood pressure.
What are the guidelines and supportive data on using Colchicine? -
The following question refers to Section 7.4 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by the Director of the CardioNerds Internship Dr. Akiva Rosenzveig, answered first by Vanderbilt AHFT cardiology fellow Dr. Jenna Skowronski, and then by expert faculty Dr. Clyde Yancy.Dr. Yancy is Professor of Medicine and Medical Social Sciences, Chief of Cardiology, and Vice Dean for Diversity and Inclusion at Northwestern University, and a member of the ACC/AHA Joint Committee on Clinical Practice Guidelines.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
American Heart Association’s Scientific Sessions 2024As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership!
Question #37
Mr. S is an 80-year-old man with a history of hypertension, type II diabetes mellitus, and hypothyroidism who had an anterior myocardial infarction (MI) treated with a drug-eluting stent to the left anterior descending artery (LAD) 45 days ago. His course was complicated by a new LVEF reduction to 30%, and left bundle branch block (LBBB) with QRS duration of 152 ms in normal sinus rhythm. He reports he is feeling well and is able to enjoy gardening without symptoms, though he experiences dyspnea while walking to his bedroom on the second floor of his house. Repeat TTE shows persistent LVEF of 30% despite initiation of goal-directed medical therapy (GDMT). What is the best next step in his management?AMonitor for LVEF improvement for a total of 60 days prior to further interventionBImplantation of a dual-chamber ICDCImplantation of a CRT-DDContinue current management as device implantation is contraindicated given his advanced age
Answer #37
Explanation Choice C is correct. Implantation of a CRT-D is the best next step. In patients with nonischemic DCM or ischemic heart disease at least 40 days post-MI with LVEF ≤35% and NYHA class II or III symptoms on chronic GDMT, who have reasonable expectation of meaningful survival for >1 year,ICD therapy is recommended for primary prevention of SCD to reduce total mortality (Class 1, LOE A). A transvenous ICD provides high economic value in this setting, particularly when a patient’s risk of death from ventricular arrhythmia is deemed high and the risk of nonarrhythmic death is deemed low. In addition, for patients who have LVEF ≤35%, sinus rhythm, left bundle branch block (LBBB) with a QRS duration ≥150 ms, and NYHA class II, III, orambulatory IV symptoms on GDMT, cardiac resynchronization therapy (CRT) is indicated to reduce total mortality, reduce hospitalizations, and improve symptoms and QOL. Cardiac resynchronization provides high economic value in this setting. Mr. -
In this episode, Dr. Gurleen Kaur (Cardiology FIT at Brigham and Women’s Hospital and APD of the CardioNerds Academy) and Dr. Diane Masket (Medicine Resident at the University of Chicago Northshore and CardioNerds Academy Intern) discuss with Dr. Minnow Walsh (Medical Director of the Heart Failure and Cardiovascular programs at Ascension St. Vincent Heart Center in Indianapolis) about her personal and professional journey in Cardiology. They discuss Dr. Walsh’s authorship of the recent ACC statement on career flexibility in Cardiology, her involvement with the ACC at both the local and national levels, and her passion for making cardiology a more inclusive and welcoming field for all.Notes were drafted by Dr. Diane Masket and episode audio was engineered by student Dr. Grace Qiu.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 RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!Video version - Career Flexibility in Cardiologyhttps://youtu.be/ygNH6fcQ5ekQuoatables - Career Flexibility in Cardiology“You have to learn to live with ambivalence. You can’t do everything. You can’t do everything all at one time”“One of the most important things the College is behind and pushing, is that competency-based evaluation is what should be used in fellowship rather than this sort of cookie cutter approach where you have to do these many months of echo and this much of cath lab. So, I think flexibility moving from volume to competency is one push.”“Fellowship is daunting, and internal medicine residency is too, but I think culture is how we feel every day. And I think the more we increase flexibility the more that culture is going to shift.Notes - Career Flexibility in CardiologyProcess of developing ACC Health Policy StatementsThese documents address issues that require ACC influence and usually involve a variety of institutions, governing bodies, and other stakeholders. ACC comes to an agreement on how they will approach this topic and shares it broadly.Most of the existing ACC health policy statements are disease-based instead of profession-based. The ACC Career Flexibility statement grew out of the diversity, equity, and inclusion task force, which is a standing committee.A variety of authors are included in health policy statements to reflect the perspectives of many different interest groups.All policy statements, including the one about career flexibility, are available online on JACC.org 1Major Components of the ACC Career Flexibility Health Policy StatementThere are 18 principles that highlight the most important aspects regarding career flexibility in cardiology.2Flexibility allows for deceleration (decrease in work hours, responsibilities, etc.) and acceleration based on the needs of the physician. For example, during childbearing and rearing time periods, there could be a deceleration, which could accelerate when parenthood responsibilities have decreased.It does not only need to be based around parenting; physicians who are not parents also desire flexibility and enjoy spending time on activities other than their careers. These needs will be unique for each person.
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The following question refers to Sections 2.1
and 4.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by CardioNerds Academy Intern Dr. Adriana Mares, answered first by CardioNerds FIT Trialist Dr. Christabel Nyange, and then by expert faculty Dr. Shelley Zieroth.
Dr. Zieroth is an advanced heart failure and transplant cardiologist, Head of the Medical Heart Failure Program, the Winnipeg Regional Health Authority Cardiac Sciences Program, and an Associate Professor in the Section of Cardiology at the University of Manitoba. Dr. Zieroth is a past president of the Canadian Heart Failure Society. She has been a PI Mentor for the CardioNerds Clinical Trials Program.
The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
American Heart Association’s Scientific Sessions 2024As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership!
Question #36
A 50-year-old woman presents to establish care. Her medical history includes COPD, prediabetes, and hypertension. She is being treated with chlorthalidone, amlodipine, lisinopril, and a tiotropium inhaler. She denies chest pain, dyspnea on exertion, or lower extremity edema. On physical exam, blood pressure is 154/88 mmHg, heart rate is 90 beats/min, and respiration rate is 22 breaths/min with an oxygen saturation of 94% breathing ambient room air. BMI is 36 kg/m2. Jugular venous pulsations are difficult to assess due to her body habitus. Breath sounds are distant, with occasional end-expiratory wheezing. Heart sounds are distant, and extra sounds or murmurs are not detected. Extremities are warm and without peripheral edema. B-type natriuretic peptide level is 28 pg/mL (28 ng/L). A chest radiograph shows increased radiolucency of the lungs, flattened diaphragms, and a narrow heart shadow consistent with COPD. An electrocardiogram shows evidence of left ventricular hypertrophy. The echocardiogram showed normal LV and RV function with no significant valvular abnormalities. In which stage of HF would this patient be classified?AStage A: At Risk for HFBStage B: Pre-HFCStage C: Symptomatic HFDStage D: Advanced HF
Answer #36
Explanation The correct answer is A – Stage A or at risk for HF. This asymptomatic patient with no evidence of structural heart disease or positive cardiac biomarkers for stretch or injury would be classified as Stage A or “at risk” for HF. The ACC/AHA stages of HF emphasize the development and progression of disease with specific therapeutic interventions at each stage. Advanced stages and disease progression are associated with reduced survival. The stages were revised in this edition of guidelines to emphasize new terminologies of “at risk” for Stage A and “pre... -
CardioNerds (Dr. Dan Ambinder and Dr. Rick Ferraro) join Dr. Mansi Oberoi and Dr. Mohan Gudiwada from the University of Nebraska Medical Center discuss a case of constrictive pericarditis. Expert commentary is provided by Dr. Adam Burdorf, who serves as the Program Director for the Cardiovascular Medicine Fellowship at the University of Nebraska Medical Center.
The case discussed involves a 76-year-old woman with a history of monoclonal gammopathy of undetermined significance, chronic obstructive pulmonary disease, type 2 diabetes mellitus, and squamous cell carcinoma was admitted to the hospital for worsening shortness of breath, swelling in lower extremities, hyponatremia, and urinary tract infection. CT chest to evaluate for pulmonary embolism showed incidental pericardial calcifications; the heart failure team was consulted for the management of her decompensated heart failure. Echo images were nondiagnostic. Subsequent invasive hemodynamic monitoring showed elevated right and left-sided filling pressures, diastolic equalization of LV and RV pressures, and positive RV square root sign with ventricular interdependence. Cardiac MRI showed septal flattening on deep inspiration and septal bounce, suggestive of interventricular dependence. After a heart team discussion and with shared-decision making the patient opted for medical management owing to her comorbidities and frailty.
Enjoy this 2024 JACC State-of-the-Art Review to learn more about pericardial diseases and best practices for pericardiectomy (Al-Kazac et al., JACC 2024)
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Case Media - Constrictive Pericarditis
Echo: Left Ventricular ejection fraction = 55-60%. Unclear septal motion in the setting of atrial fibrillation
MRI: Diastolic septal flattening with deep inspiration as well as a septal bounce suggestive of interventricular dependence and constrictive physiology
References
Garcia, M. Constrictive Pericarditis Versus Restrictive Cardiomyopathy. Journal of the American College of Cardiology, vol. 67, no. 17, 2016, pp. 2061–2076.
Pathophysiology and Diagnosis of Constrictive Pericarditis. American College of Cardiology, 2017.
Geske, J., Anavekar, N., Nishimura, R., et al. Differentiation of Constriction and Restriction: Complex Cardiovascular Hemodynamics. Journal of the American College of Cardiology, vol. 68, no. 21, 2016, pp. 2329–2347.
Constrictive Pericarditis. ScienceDirect.
Constrictive Pericarditis. Journal of the American College of Cardiology, vol. 83, no. 12, 2024, pp. 1500-1512. -
Dr. Amit Goyal, along with episode chair Dr. Dinu Balanescu (Mayo Clinic, Rochester), and FIT leads Dr. Sonu Abraham (University of Kentucky) and Dr. Natasha Vedage (MGH), dive into the fascinating topic of channelopathies with Dr. Michael Ackerman, a genetic cardiologist and professor of medicine, pediatrics, and pharmacology at Mayo Clinic, Rochester, Minnesota. Using a case-based approach, they review the nuances of diagnosis and treatment of channelopathies, including Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT), and long QT syndrome. Dr. Sonu Abraham drafted show notes. Audio engineering for this episode was expertly handled by CardioNerds intern, Christiana Dangas.
The CardioNerds Beyond the Boards Series was inspired by the Mayo Clinic Cardiovascular Board Review Course and designed in collaboration with the course directors Dr. Amy Pollak, Dr. Jeffrey Geske, and Dr. Michael Cullen.
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Pearls and Quotes - Channelopathies
One cannot equate the presence of type 1 Brugada ECG pattern to the diagnosis of Brugada syndrome. Clinical history, family history, and/or genetic testing results are required to make a definitive diagnosis.
The loss-of-function variants in the SCN5A gene, which encodes for the α-subunit of the NaV1.5 sodium channel, is the only Brugada susceptibility gene with sufficient evidence supporting pathogenicity.
Exertional syncope is an “alarm” symptom that demands a comprehensive evaluation with 4 diagnostic tests: ECG, echocardiography, exercise treadmill test, and Holter monitor. Think of catecholaminergic polymorphic ventricular tachycardia (CPVT) in a patient with exertional syncope and normal EKG!
ICD therapy is never prescribed as monotherapy in patients with CPVT. Medical therapy with a combination of nadolol plus flecainide is the current standard of care.
Long QT syndrome is one of the few clinical scenarios where genetic testing clearly guides management, particularly with respect to variability in beta-blocker responsiveness.
Notes - Channelopathies
1. What are the diagnostic criteria for Brugada syndrome (BrS)?
Three repolarization patterns are associated with Brugada syndrome in the right precordial leads (V1-V2):
Type 1: Prominent coved ST-segment elevation displaying J-point amplitude or ST-segment elevation ≥2 mm, followed by a negative T wave.
Type 2/3: Saddleback ST-segment configuration with variable levels of ST-segment elevation.
It is important to note that only a type 1 pattern is diagnostic for Brugada syndrome, whereas patients with type 2/3 patterns may benefit from further testing.
The Shanghai score acknowledges that relying solely on induced type 1 ECG changes has limitations. Therefore, one cannot equate the presence of a type 1 Brugada ECG pattern alone to the diagnosis of Brugada syndrome. The score suggests incorporating additional information—such as clinical history, family history, and/or genetic testing results—to achieve a definitive diagnosis.
2. What is the significance of genetic testing in Brugada syndrome?
There are 23 alleged Brugada syndrome susceptibility genes published with varying levels of evidence. However, only one gene mutation, the loss-of-function variants in the SCN5A gene encoding for the α-subunit of the NaV1.5 sodium channel, is considered to have sufficient evidence.
The overall yield of BrS genetic testing is 20%. The presence of PR prolongation (>200 ms) along with type I EKG pattern increases the yield to 40%. On the contrary, in the presence of a normal PR interval, the likelihood of SCN5A positivity drops to <10%.
3. How would you risk-stratify a patient with Brugada syndrome? -
The CardioNerds Academy is excited to present the 3rd Annual Sanjay V. Desai Lecture in Medical Education, featuring a deep dive into the evolving role of Artificial Intelligence in Medical Education. Join us as Dr. Kathryn Berlacher, Dr. Melissa McNeil, and Dr. Alfred Shoukry explore the transformative potential of AI in training future healthcare professionals and enhancing educational methodologies. Their insightful discussion sheds light on the integration of cutting-edge technologies to improve medical learning and patient care. The conversation is faciliated by Dr. Tommy Das, Program Director of the CardioNerds Academy, and CardioNerds Academy Chiefs: Dr. Callie Clark, Dr. Rachel Goodman, Dr. Ronaldo Correa Fabiano, and Dr. Claire Cambron, who bring their expertise and enthusiasm to this engaging discussion on the future of medical education. Special thanks to Pace Wetstein, CardioNerds academy intern, for his exceptional audio editing in this episode.
Dr. Kathryn Berlacher is a graduate of The Ohio State University College of Medicine and completed her internal medicine residency, chief residency, and cardiology fellowship at UPMC, where she has been on faculty since 2012. She earned a master's degree in medical education from the University of Pittsburgh and has served as the Program Director of the Cardiovascular Fellowship Program since 2015. In 2021, she was appointed Associate Chief of Education for the UPMC Heart and Vascular Institute. Additionally, Dr. Berlacher is the director of the McGee Women's Heart Program and chief of medicine at McGee Women's Hospital. Nationally, she serves as the chair for the American College of Cardiology’s Annual Scientific Sessions for 2025 and 2026, regularly speaking on women's cardiology, medical education, diversity, inclusion, and health equity.Dr. Alfred Shoukry graduated from Northwestern University with dual degrees in Neurobiology and Biomedical Engineering. He completed medical school and internal medicine residency at UPMC, where he also earned a certificate in medical education. Dr. Shoukry serves as core faculty at the University of Pittsburgh School of Medicine and cares for patients at the VA in Pittsburgh. As the course director for Population Health, he teaches on topics such as patient safety, quality improvement, and bioinformatics. He is an expert on the impact of large language models in medical education, presenting locally and nationally on the subject.Dr. Melissa McNeil received her undergraduate degree from Princeton University, her MD from the University of Pittsburgh, and a Master of Public Health from the same institution. She is a professor emeritus of medicine at the University of Pittsburgh and recently joined the faculty at Brown University as a professor of medicine. Dr. McNeil serves as an academic hospitalist and senior consultant to the Women's Health Division at Brown. Her expertise lies in developing training programs to foster leaders in women's health education and research. She has been recognized nationally for her contributions, including being named the Society of General Internal Medicine Distinguished Professor of Women's Health in 2014 and receiving their Career Achievement in Medical Education award in 2016.
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.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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CardioNerds Drs. Jason Feinman, Gurleen Kaur, and Rick Ferraro discuss the implementation of SGLT inhibitors in clinical practice with Dr. Alison Bailey. Notes were drafted by Dr. Jason Feinman.
In this episode, we discuss the implementation of SGLTi in clinical practice scenarios, including for individuals with heart failure regardless of ejection fraction, those with chronic kidney disease, and those with diabetes mellitus. The group also discusses important side effects to monitor for, as well as how to counsel patients when prescribing these medications.
This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Lexicon Pharmaceuticals.
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Pearls - Clinical Implementation of SGLT Inhibitors
For patients with heart failure with reduced ejection fraction, SGLT inhibitors reduce the composite outcome of cardiovascular death or heart failure hospitalization by 25%.
SGLT inhibitors can be safely started in patients with an eGFR as low as 20. There are ongoing trials investigating the safety of these medications in individuals with eGFR lower than 20 or those who are receiving dialysis.
An eGFR decrease of 3-5 ml/min on average is expected after starting an SGLTi, but this will stabilize over time and provides protective effects of renal dysfunction in the long run.
Early data that suggested an association between SGLTi and bacterial UTI development hasn’t panned out in the long run, but there is an association between SGLTi and the development of either genital mycotic infections or yeast infections. Perineal hygiene is important to prevent the development of either.
A patient-centered, shared decision-making approach should guide the choice of agents for individuals with type 2 diabetes mellitus. In certain patients, it may be reasonable to choose an SGLTi as the first-line agent.
Show notes - Clinical Implementation of SGLT Inhibitors
What is the data supporting the use of SGLTi in HFpEF?
The EMPEROR-Preserved and DELIVER trials investigated the impact of empagliflozin and dapagliflozin, respectively, on cardiovascular outcomes in patients with mildly reduced or preserved ejection fraction.
The SOLOIST-WHF trial investigated a combined SGLT1/2 inhibitor, sotagliflozin, in patients with recently worsening heart failure, irrespective of ejection.SGLTi have been demonstrated to reduce the risk of cardiovascular death or worsening heart failure, including heart failure hospitalization, in these individuals.
A meta-analysis of the EMPEROR-Preserved and DELIVER trials demonstrated a hazard ratio of 0.80 for cardiovascular death or first hospitalization for heart failure for empagliflozin or dapagliflozin over placebo in the setting of HFpEF.
What is the data supporting the use of SGLTi in HFrEF?
In addition to the SOLOIST-WHF trial that was previously discussed, the EMPEROR-HF and DAPA-HF investigated the impact of SGLTi medications in patients with HFrEF.
In patients with HFrEF, SGLTi medications have been demonstrated to reduce the risk of either cardiovascular death or heart failure hospitalization.
Dapagliflozin and empagliflozin had a pooled risk reduction of all-cause death of 13%, a pooled risk reduction of cardiovascular death of 14%, and a 26% reduction in the combination of CV death or first hospitalization for heart failure.
What is the expected impact of SGLTi on renal function?
Dapagliflozin, empagliflozin, sotagliflozin, ertugliflozin, and canagliflozin have all been studied for their impact on renal dysfunction in individuals both with and without diabetes.
In the CANVAS trial, -
CardioNerds (Amit Goyal) join Dr. Merna Hussien, Dr. Akhil Kallur, Dr. Abhinav Saxena, and Dr. Brody Deb from the MedStar Georgetown - Washington Hospital Center in DC for a stroll around Rock Creek Park as they discuss an unusual case of cobalt cardiomyopathy. Expert commentary is provided by Dr. Nana Afari Armah. Episode audio was edited by CardioNerds Intern Christiana Dangas.
The case is of a middle-aged woman with a past medical history of hypertension, hyperlipidemia, and bilateral hip replacements, who presented with subacute progressive exertional dyspnea, orthopnea, and constitutional symptoms and was found to have SCAI Stage C cardiogenic shock. Transthoracic echocardiogram showed severely reduced left ventricular ejection fraction (LVEF, 20-25%) and a moderate pericardial effusion. Cardiac catheterization revealed biventricular failure with elevated filling pressures. A cardiac MRI showed diffuse late gadolinium enhancement (LGE) in the left ventricle. Endomyocardial biopsy showed nonspecific chronic inflammation. However, the evidence of mitochondrial heavy metal toxicity and elevated cobalt levels made the diagnosis of cobalt cardiomyopathy. The patient underwent revision of hip joint implants to ceramic implants and started chelation therapy. However, due to persistent stage D heart failure despite normalization of cobalt levels, she underwent orthotropic heart transplantation.
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Case MEdia - Cobalt Cardiomyopathy
Pearls - Cobalt Cardiomyopathy
A good history goes a long way in diagnosing non-ischemic cardiomyopathy (NICM).
Common problems can have uncommon presentations requiring a high degree of suspicion for diagnosis.
Imaging features can overlap between causes of NICM. History helps in targeting further histological workup and uncovering the root cause.
Multidisciplinary effort is essential in making a rare diagnosis.
Taken from1 - Singh M, Krishnan M, Ghazzal A, Halushka M, Tozzi JE, Bunning RD, Rodrigo ME, Najjar SS, Molina EJ, Sheikh FH. From Hip to Heart: A Comprehensive Evaluation of an Infiltrative Cardiomyopathy. CJC Open. 2021 Nov 1;3(11):1392–5.
Notes - Cobalt Cardiomyopathy
How common is cobalt cardiomyopathy? When should it be suspected?
Cobalt cardiomyopathy is incredibly rare, with only a handful of reported cases. 2 It is also known as beer drinkers’ cardiomyopathy, as cobalt was added to beer for fortification in Quebec 3, where it was first reported. Cobalt cardiomyopathy is characterized by its rapidly progressive nature, the presence of low voltages on EKG, and diffuse infiltration. Patients also complained of a previous history of anorexia and weight loss and were found to have polycythemia and thyroid abnormalities on labs. This syndrome was very similar to wet beriberi except for the absence of a therapeutic response to thiamine.
Taken from - 2
Later, this was noted in patients with total metal hip arthroplasty 4–6, especially in patients with metal-on-metal hip arthroplasty, which led to corrosion and leakage of cobalt into the bloodstream. The syndrome in these patients was similar to those in beer drinkers from Quebec.
This figure, taken from 2, shows the reports of Cobalt cardiomyopathy after cobalt alloy prostheses. [HX1]
What is the pathophysiology of cobalt cardiomyopathy?
Cobalt has a variety of effects on the heart, both microscopically and biochemically.Cobalt may have multiple calcium-mediated cardiac effects and may also interfere with the Krebs cycle and ATP generation by mitochondria. Histology may show modest changes with no inflammatory response o... -
The following question refers to Section 2.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by University of Colorado internal medicine resident Dr. Hirsh Elhence, answered first by University of Chicago advanced heart failure cardiologist and Co-Chair for the CardioNerds Critical Care Cardiology Series Dr. Mark Belkin, and then by expert faculty Dr. Mark Drazner.Dr. Drazner is an advanced heart failure and transplant cardiologist, Professor of Medicine, and Clinical Chief of Cardiology at UT Southwestern. He is the President of the Heart Failure Society of America.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
Question #35
A 50-year-old woman with a history of congestive heart failure, hypertension, type 2 diabetes mellitus, and obstructive sleep apnea presents to the outpatient clinic to follow up on her heart failure management. One year prior, echocardiogram showed an ejection fraction of 30% with an elevated BNP, for which she was started on appropriate GDMT. Repeat echocardiogram today showed an EF of 50%. Which of the following best describes her heart failure status?
A
HFrEF (HF with reduced EF)
B
HFimpEF (HF with improved EF)
C
HFmrEF (HF with mildly reduced EF)
D
HFpEF (HF with preserved EF)
Answer #35
Explanation
The correct answer is B – HFimpEF, or heart failure with improved ejection fraction, best describes her current heart failure status.
Left ventricular ejection fraction is an important factor in classifying heart failure given differences in prognosis, response to treatment, and use in clinical trial enrollment criteria.
The classification of heart failure by EF (adopted from the Universal Definition of HF):
– HFrEF (HF with reduced EF): LVEF ≤40%
– HFimpEF (HF with improved EF): previous LVEF ≤40%, a ≥10% increase from baseline LVEF, and a second measurement of LVEF >40%.
– HFmrEF (HF with mildly reduced EF): LVEF 41%–49%, andevidence of spontaneous or provokable increased LV filling pressures (e.g., elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement)
– HFpEF (HF with preserved EF): LVEF ≥50%, and evidence of spontaneous or provokable increased LV filling pressures (e.g., elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement)
Patients with HFmrEF are usually in a dynamic state of improving from HFrEF or deteriorating towards HFrEF. Therefore, patients with HFmrEF may benefit from follow-up evaluation of systolic function and etiology of sub-normal EF.
Improvements in EF are associated with better outcomes but do not indicate full myocardial recovery or normalization of LV function. Indeed, structural and functional abnormalities such as LV dilation and systolic or diastolic dysfunction often persist. Moreover, EF may remain dynamic with fluctuations in either direction depending on factors such as GDMT adherence and re-exposure to cardiotoxic agents. As such, the term heart failure with “improved EF” was deliberately chosen over “recovered EF” and “preserved EF”. Importantly, in patients with HFimpEF while on GDMT, the EF may decrease after withdrawal of GDMT.
Main Takeaway -
CardioNerds Cardio-Rheumatology Series Co-Chairs Dr. Rick Ferraro, Dr. Gurleen Kaur, and and Dr. Bree Hansen discuss how to decipher cardiovascular risk in patients with rheumatological conditions with cardio-rheumatology experts Dr. Brittany Weber and Dr. Michael Garshick.
In this episode, Drs. Weber and Garshick take us through the role of inflammation in patients with rheumatologic conditions and cardiovascular disease. They discuss the increased prevalence of traditional cardiac risk factors in this population and how these standard cardiac risk factors do not account for the full extent of cardiovascular risk. Dr. Bree Hansen drafted show notes. Audio editing by CardioNerds intern Christiana Dangas.
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Pearls - Cardio-Rheumatology - Deciphering Cardiovascular Risk in Patients with Rheumatological Conditions
Cardiovascular disease prevalence: cardiovascular disease is common in patients with autoimmune rheumatologic disease; therefore, we must take every opportunity to screen patients early.
Limitations of Traditional Scores: conventional risk calculators often underestimate cardiovascular risk for autoimmune disease patients, necessitating additional methods to assess risk accurately.
Integration of Disease-Specific Biomarkers: using biomarkers specific to autoimmune diseases, such as lupus, enhances risk assessment and helps in tailoring treatment strategies.
Value of Imaging and Risk Enhancers: incorporating imaging (like CAC scoring and carotid ultrasound) and evaluating additional risk factors (such as lipoprotein(a) and high-sensitivity CRP) provides a more comprehensive view of cardiovascular risk and guides more effective management.
Show notes - Cardio-Rheumatology - Deciphering Cardiovascular Risk in Patients with Rheumatological Conditions
Show notes (Drafted by Dr. Bree Hansen):
How does inflammation contribute to atherosclerosis, specifically in autoimmune rheumatologic diseases like psoriasis?
Lipids need to enter the intimal space of blood vessels, which can be facilitated by endothelial damage caused by chronic cytokine stimulation, such as TNF or IL-6. Once in the intima, lipids are recognized as foreign, leading to the recruitment of monocytes that transform into macrophages to clear these lipids. However, this process often exacerbates the problem, leading to persistent inflammation and atherosclerotic plaque formation.
Specifically, in psoriasis, the endothelial damage is particularly pronounced due to cytokines like TNF, IL-17, and interferons. The inflammasome pathway, which is highly active in psoriasis, also contributes to endothelial damage. Additionally, hyperactivated platelets in psoriasis can further damage the endothelium and contribute to atherosclerosis.
Overall, atherosclerosis results from a combination of traditional risk factors and systemic inflammation, leading to the development of cardiovascular disease.
Which traditional cardiovascular risk factors are increased in patients with rheumatologic conditions?
Patients with autoimmune diseases may be up to > three times more likely to develop cardiovascular disease, similar to the risk of type 2 diabetes; therefore, it is important to screen patients with autoimmune rheumatologic disorders for cardiovascular disease
Most common cardiovascular risk factors, such as smoking, diabetes, hypertension, and dyslipidemia, are also increased in patients with autoimmune rheumatologic disorders. Smoking, specifically, is highly prevalent in psoriasis and exhibits a dose-response relationship with psoriasis severity.
Hyperlipidemia is another common risk factor present in patients with autoimmune rheumatologic disease; however, -
CardioNerds Dan Ambinder and Dr. Devesh Rai join cardiology fellows and National Lipid Association lipid scholars Dr. Jelani Grant from Johns Hopkins University and Dr. Alexander Razavi from Emory University. They discuss a case involving a patient with familial hypercholesterolemia. Dr. Archna Bajaj from University of Pennsylvania provides expert commentary. Drs. Jelani Grant and Alexander Razavi drafted notes. CardioNerds Intern Pacey Wetstein engineered episode audio.
This episode is part of a case reports series developed in collaboration with the National Lipid Association and their Lipid Scholarship Program, with mentorship from Dr. Daniel Soffer and Dr. Eugenia Gianos.
A classic finding in patients with familial hypercholesterolemia is the presence of markedly elevated levels of total and low-density lipoprotein cholesterol (LDL-C) with an LDL-C concentration of 190 mg/dL or greater. However, severe hypercholesterolemia is not inevitably present, and many patients who carry this diagnosis may have lower LDL-C levels. This case history describes a young woman whose mother and brother met clinical and genetic criteria for heterozygous familial hypercholesterolemia but who had only a mild elevation in LDL-C, falling to 130 mg/dL after dietary intervention. Despite this finding, genetic testing revealed the presence of the same genetic variants as were noted in her mother and brother. In addition, a second genetic variant predisposing them to cholesterol gallstone formation was identified in all three family members. If genetic testing had not been performed, the diagnosis may have been missed or delayed, resulting in an increased risk for vascular complications associated with familial hypercholesterolemia. This case supports the value of genetic testing of family members of those with familial hypercholesterolemia, even when LDL-C levels are not severely elevated.
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Pearls - Exposing an Unusual Presentation of Familial Hypercholesterolemia – National Lipid Association
Familial hypercholesterolemia (FH) is among the most common autosomal co-dominant genetic conditions (approximately 1:200 to 1:300 for HeFH, 1:160,000 to 1:300,000 for HoFH).
Genetic testing has a role for all first-degree relatives when a family history of FH is strongly suggestive, regardless of LDL-C level.
Heterogeneity in ASCVD risk among individuals with FH is derived from background polygenic risk, clinical risk factors (e.g., timing of lipid-lowering initiation and adjacent risk factors), as well as subclinical atherosclerosis burden.
In clinical or genetically confirmed FH, an LDL-C goal of 55 mg/dL is recommended.
Beyond statins, FDA-approved non-statin therapies for FH include ezetimibe, PCSK9 mAb, bempedoic acid, inclisiran, evolocumab (only HoFH), lomitapide (only HoFH), and LDL apheresis.
Notes - Exposing an Unusual Presentation of Familial Hypercholesterolemia – National Lipid Association
What are the diagnostic criteria for FH?
Dutch Lipid Clinic Network1
Variables: family history, clinical history, physical exam, LDL-C level, DNA (LDLR, APOB, PCSK9)
Simon-Broome1
Variables: total or LDL-C, physical exam, DNA (LDLR, APOB, PCSK9), family history
Emphasis on clinical history and physical exam reduces sensitivity
U.S. Make Early Diagnosis Prevent Early Death (MEDPED) 1
Only one of the three where no genetic testing is required, may work well in cascade screening
Variables: age, total cholesterol, family relative (and degree) with FH
Definite, probable, possible, unlikely
Emphasis on clinical history and physical exam reduces sensitivity -
CardioNerds Cofounder Dr. Amit Goyal, Chair of the CardioNerds Heart Failure Committee Dr. Jenna Skowronski, and Episode FIT Lead Dr. Shazli Khan discuss iron deficiency and its impact on heart failure with Dr. Robert Mentz, Chief of Heart Failure at Duke University and principal investigator of the HEART-FID trial. In this case-based discussion, they cover the diagnostic criteria of iron deficiency in heart failure, epidemiology, and strengths and limitations of different iron formulations. They also review clinical trials examining the impact of iron deficiency on quality of life, heart failure hospitalizations, and mortality. Importantly, they stress the relevance of iron metabolism in heart failure, irrespective of the presence of anemia. They also discuss the approach to addressing outpatient management of iron in heart failure and future directions of research needed in this domain.
Notes were drafted by Dr. Shazli Khan, and Dr. Daniel Ambinder engineered episode audio.
Click here for CME.
This episode was created in collaboration with the Cardiometabolic Health Congress and is supported by an educational grant from American Regent. Please follow the link in the show notes for free CME. All CardioNerds education is planned, produced, and reviewed by CardioNerds.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls - Iron Deficiency in Heart Failure
Think about iron deficiency in ALL patients with heart failure and send appropriate diagnostic labs, even if there is no evidence of anemia!
Iron deficiency in heart failure has a specific and distinguished definition, defined as a ferritin level of <100 ng/mL, or a ferritin level between 100-300 ng/mL with a transferrin saturation of <20%.
Data thus far suggests that treatment of iron deficiency in heart failure results in improved quality of life, as well as a probable reduction in heart failure hospitalizations, and that administration of intravenous iron has a favorable safety profile.
Not all formulations of iron are created equal – intravenous iron formulations have been shown to be effective in this population, but oral iron therapy has not.
Management of iron deficiency in the outpatient setting is an evolving area of research, but patients should typically receive surveillance labs and additional treatment with IV iron if indicated.
Show notes - Iron Deficiency in Heart Failure
How is iron deficiency in heart failure defined, and how prevalent is iron deficiency in this patient population?
Iron deficiency is common in patients with heart failure, with an estimated prevalence of 50-60%.Iron deficiency in heart failure is associated with worse outcomes, including increased hospitalization and mortality and poorer functional status and quality of life.Iron deficiency in heart failure is defined as a ferritin level of <100 ng/mL or a ferritin level of 100-300 ng/mL plus a transferrin saturation of <20%.
There is an evolving school of thought that suggests transferrin saturation alone may be the best indicator of iron deficiency in heart failure, but more data are needed.
Importantly, iron deficiency in heart failure can be seen in patients with both reduced and preserved ejection fraction. Which patients should be screened for iron deficiency?
There is a class I indication to send iron studies in all patients with heart failure as a part of the initial diagnostic work-up for the underlying etiology of the cardiomyopathy, as well as to assess for the presence of iron deficiency.The presence of anemia is not required to check iron studies, as many patients with iron deficiency in heart failure may not have conc... -
CardioNerds Cardio-Rheumatology Series Co-Chairs Dr. Rick Ferraro, Dr. Gurleen Kaur, and Episode Lead Dr. Ronaldo Correa discuss “The Role of Inflammation in Cardiovascular Disease” with Dr. Antonio Abbate.
Join the CardioNerds as they kick off the Cardio-Rheumatology series with Dr. Antonio Abbate. In this episode, Dr. Abbate, a leading expert in cardio-immunology, discusses the role of inflammation in cardiovascular disease. We explore the molecular mechanisms linking inflammation to atherosclerosis, the impact of chronic low-grade systemic inflammation on heart disease, and potential therapeutic targets. Dr. Abbate shares insights on how genes and lifestyle factors contribute to inflammation, the use of inflammatory markers in clinical practice, and emerging anti-inflammatory therapies in atherosclerotic cardiovascular disease. Tune in for an enlightening conversation on the intersection of inflammation and cardiovascular health.
Dr. Ronaldo Correa drafted the notes. Episode audio was engineered by Dr. Amit Goyal.
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Pearls - Cardio-Rheumatology: The Role of Inflammation in Cardiovascular Disease
Inflammation is key in the pathogenesis and progression of atherosclerosis. Estimating systemic inflammation is part of a comprehensive preventive assessment (primary/secondary).
Patients with autoimmune inflammatory diseases are at a higher risk for cardiovascular events.
C-reactive protein (CRP) can estimate systemic inflammation and help assess residual inflammatory risk in patients with traditional intermediate/low cardiovascular disease, guiding management consideration with lipid-lowering therapy, aspirin, and colchicine.
The pharmacological management of atherosclerosis is evolving beyond primarily lipid-lowering therapies to focus on targeting the underlying residual inflammatory process. Colchicine (inflammasome blocker as an anti-mitotic drug) is approved for use in chronic stable CVD in selected cases, and interleukin pathway blockers, especially IL-1 and IL-6, are under clinical trial investigation.
First things first! Prioritize treating and optimizing traditional risk factors and comorbidities and emphasize lifestyle modifications to reduce cardiovascular disease (control diabetes and hypertension, reduce or cease smoking/alcohol, lose weight, and engage in regular physical activity). They all impact inflammation directly or indirectly
Show notes - Cardio-Rheumatology: The Role of Inflammation in Cardiovascular Disease
Notes: Notes drafted by Dr. Ronaldo Correa.
What is the link between inflammation and cardiovascular atherosclerosis?
Inflammation is involved both in the pathogenesis and progression of atherosclerosis.Histopathological coronary atherosclerosis studies have demonstrated the presence of inflammatory mediators as well as a central role of factors of innate immunity such as macrophages and T cells which can interact with vascular smooth muscle cells in the progression of atherosclerotic plaque.Patients with autoimmune inflammatory conditions have earlier and higher cardiovascular event rates (accelerated atherosclerosis due to residual inflammatory risk).
Elevated inflammatory markers (for example, high CRP) predict cardiovascular events.
How should inflammation be considered in the context of residual cardiovascular risk?
Inflammation may be the inciting factor in atherosclerosis, or it may amplify the process driven primarily by other risk factors. Therefore, treating the comorbidities and traditional CVD contributors is key to reducing the vicious inflammatory cycle.Assessing residual risk using inflammatory markers can assist in management. C-reactive protein (CRP) can estimate systemic inflammation and help assess re... -
CardioNerds (Drs. Teodora Donisan, Jenna Skowronski, and Johnny Hourmozdi) discuss Cardiomyopathies with Dr. Steve Ommen. Through a case-based discussion, we review the diagnostic evaluation of suspected restrictive cardiomyopathy, and Dr. Ommen shares his expertise in the nuances of caring for patients with hypertrophic cardiomyopathy, from counseling to pharmacologic, device, and septal reduction therapies. We cover the foundations of diagnosis and management that will be helpful to CardioNerds preparing to encounter hypertrophic cardiomyopathy on the boards or on the wards.
Dr. Johnny Hourmozdi drafted notes. The audio was engineered by Dr. Atefeh Ghorbanzadeh.
The CardioNerds Beyond the Boards Series was inspired by the Mayo Clinic Cardiovascular Board Review Course and designed in collaboration with the course directors Dr. Amy Pollak, Dr. Jeffrey Geske, and Dr. Michael Cullen.
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Pearls and Quotes - Cardiomyopathies
The presence of an S4 and a rapid y-descent in the jugular venous pulsation on exam should clue you to the presence of a restrictive filling pattern. Restrictive filling doesn’t necessarily mean restrictive cardiomyopathy and is more commonly due to dilated or ischemic cardiomyopathy.
The five main topics of counseling that every hypertrophic cardiomyopathy (HCM) patient should understand: (1) Prognosis, (2) Family Screening, (3) Risk of Sudden Death, (4) Treatments, and (5) Physical Activity.
Remember 1/3: In clinical trials of cardiac myosin inhibitors for HCM (mavacamten), about a third of patients had a tremendous improvement in symptoms, another third had some improvement, and the final third had no improvement or had to discontinue the drug due to negative inotropy.
When counseling patients about septal reduction therapy, consider the patient’s age. For younger patients, surgical myectomy at an experienced center offers a higher success rate and greater durability with lower rates of pacemaker placement when compared to alcohol septal ablation.
Historically, the conclusion that it was higher risk to be an athlete with HCM was unfortunately generalized to mean that it was high risk to exercise for patients with HCM. “And we turned a generation of HCM patients into HCM cardiometabolic syndrome patients, which is actually a worse combination.”
Notes - Cardiomyopathies
What is the initial approach to evaluating a patient with new or suspected cardiomyopathy, including hypertrophic cardiomyopathy (HCM)?
A history and physical exam, including a thorough past medical and family history, is always the first step and helps determine the patient’s risk for potential underlying etiologies, including genetic cardiomyopathies, hypertrophic cardiomyopathy, or those related to treatments of previous cancer.
In terms of ECG findings, pay attention to QRS voltage (high or low) and the presence of any arrhythmias.
TTE should be obtained in all patients and is often sufficient to diagnose many underlying cardiomyopathies, including HCM.
Cardiac MRI (CMR) is helpful as an adjunct when TTE alone is inconclusive or imaging quality is poor. CMR can help provide a better idea of chamber sizes and wall thickness, and late gadolinium contrast enhancement (LGE) can also be helpful if present in a specific pattern, though often HCM patients may have non-specific patterns of LGE.
Invasive hemodynamics assessment is reserved for patients with discordance between non-invasive testing and the clinical impression. It can also be useful to guide the management of heart failure, especially in advanced disease.
How do you treat patients with hypertrophic obstructive cardiomyopathy (HOCM)?
In patients with HCM and LVOT obstruction (defined a... - Montre plus
