Cardionerds: A Cardiology Podcast

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.

“To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here.

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What is Takotsubo Syndrome (TTS)?

What are the echocardiographic findings of takotsubo cardiomyopathy?

Do patients with TTS generally have EKG changes or biomarker elevation?

What are complications of takotsubo cardiomyopathy?

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 Lexicon Pharmaceuticals.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here.

CardioNerds Prevention Page
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CardioNerds Journal Club
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Check out CardioNerds SWAG!
Become a CardioNerds Patron!

Nidorf SM, Eikelboom JW, Budgeon CA, Thompson PL. Low-dose colchicine for secondary prevention of cardiovascular disease. J Am Coll Cardiol. 2013;61(4):404-410. doi:10.1016/j.jacc.2012.10.027

Nidorf SM, Fiolet ATL, Mosterd A, et al. Colchicine in Patients with Chronic Coronary Disease. N Engl J Med. 2020;383(19):1838-1847. doi:10.1056/NEJMoa2021372

Tardif JC, Kouz S, Waters DD, et al. Efficacy and Safety of Low-Dose Colchicine after Myocardial Infarction. N Engl J Med. 2019;381(26):2497-2505. doi:10.1056/NEJMoa1912388

Hennessy T, Soh L, Bowman M, et al. The Low Dose Colchicine after Myocardial Infarction (LoDoCo-MI) study: A pilot randomized placebo controlled trial of colchicine following acute myocardial infarction. Am Heart J. 2019;215:62-69. doi:10.1016/j.ahj.2019.06.003

Tong DC, Quinn S, Nasis A, et al. Colchicine in Patients With Acute Coronary Syndrome: The Australian COPS Randomized Clinical Trial. Circulation. 2020;142(20):1890-1900. doi:10.1161/CIRCULATIONAHA.120.050771

Ridker PM, Everett BM, Thuren T, et al. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease. N Engl J Med. 2017;377(12):1119-1131. doi:10.1056/NEJMoa1707914

Ridker PM, Everett BM, Pradhan A, et al. Low-Dose Methotrexate for the Prevention of Atherosclerotic Events. N Engl J Med. 2019;380(8):752-762. doi:10.1056/NEJMoa1809798

Potere N, Bonaventura A, Abbate A. Novel Therapeutics and Upcoming Clinical Trials Targeting Inflammation in Cardiovascular Diseases. Arterioscler Thromb Vasc Biol. Published online October 10, 2024. doi:10.1161/ATVBAHA.124.319980

Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men [published correction appears in N Engl J Med 1997 Jul 31;337(5):356]. N Engl J Med. 1997;336(14):973-979. doi:10.1056/NEJM199704033361401

Ridker PM, Danielson E, Fonseca FA, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008;359(21):2195-2207. doi:10.1056/NEJMoa0807646

Ridker PM, Bhatt DL, Pradhan AD, et al. Inflammation and cholesterol as predictors of cardiovascular events among patients receiving statin therapy: a collaborative analysis of three randomised trials. Lancet. 2023;401(10384):1293-1301. doi:10.1016/S0140-6736(23)00215-5

Fernandez DM, Rahman AH, Fernandez NF, et al. Single-cell immune landscape of human atherosclerotic plaques. Nat Med. 2019;25(10):1576-1588. doi:10.1038/s41591-019-0590-4

Moran CA, Collins LF, Beydoun N, et al. Cardiovascular Implications of Immune Disorders in Women. Circ Res. 2022;130(4):593-610. doi:10.1161/CIRCRESAHA.121.319877

Kushner I. C-reactive protein – My perspective on its first half century, 1930-1982. Front Immunol. 2023;14:1150103. Published 2023 Mar 2. doi:10.3389/fimmu.2023.1150103

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.

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?

A

Spironolactone is contraindicated based on her level of renal impairment and should not be started

B

Serum potassium levels and kidney function should be assessed within 1-2 weeks of starting spironolactone

C

Eplerenone confers a higher risk of gynecomastia than does spironolactone

D

The patient will likely not benefit from initiation of spironolactone if her cardiomyopathy is ischemic in origin

Explanation

The 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 RALES trial of spironolactone vs. placebo in highly symptomatic HFrEF (LVEF ≤ 35%, NYHA III-IV), trial of eplerenone vs placebo post-MI in patients with LVEF ≤ 40%, and EMPHASIS-HF trial of eplerenone vs placebo in less symptomatic HFrEF (LVEF ≤ 35%, NYHA II) altogether suggest MRAs confer improvements in all-cause mortality, HF hospitalizations, and sudden cardiac death in patients with HFrEF. Importantly, these benefits have been demonstrated across a wide range of HFrEF severity and etiologies, including ischemic cardiomyopathy (Option D).

Therefore, in patients with HFrEF and NYHA class II to IV symptoms, an MRA (spironolactone or eplerenone) is recommended to reduce morbidity and mortality, if eGFR is >30 mL/min/1.73 m2 and serum potassium is <5.0 mEq/L. Careful monitoring of potassium, renal function, and diuretic dosing should be performed at initiation and closely monitored thereafter to minimize risk of hyperkalemia and renal insufficiency (Class 1, LOE A). MRA therapy in this context provides high economic value.

Adverse Effects of MRAs

Both spironolactone and eplerenone are excreted by the kidney and due to their inhibition of aldosterone signaling, reduce potassium excretion in the urine. For these reasons, the initiation of MRAs is contraindicated in patients with eGFR of ≤30 mL/min/1.73m2 or serum potassium levels of ≥5.0 mEq/L. After starting or intensifying MRA therapy, serum potassium levels and renal function should be rechecked at approximately 1 week, at 4 weeks, and every 6 months thereafter, provided clinical stability. Hyperkalemia can increase the risk of ventricular arrhythmias and death. Unfortunately, this often results in de-escalation or discontinuation of RAASi and a subsequent loss of long-term cardiorenal benefits of maximally tolerated GDMT.

The utility of prescribing potassium binders (e.g., patiromer, sodium zirconium cyclosilicate) to improve outcomes by facilitating continuation of  Patiromer and sodium zirconium cyclosilicate remove potassium by exchanging cations leading to increased fecal excretion and thereby lowering serum potassium levels. These have been FDA approved for treatment of hyperkalemia for patients receiving RAASi.

Therefore, the use of potassium binders (patiromer, sodium zirconium cyclosilicate) to improve outcomes by facilitating the continuation of RAASi therapy in patients with HF who experience hyperkalemia (serum potassium level ≥5.5 mEq/L) received a Class 2b recommendation (LOE B-R), but overall utility remains uncertain.

In the DIAMOND trial, patients with HFrEF and hyperkalemia were randomized to patiromer vs. control. In the run-in phase, all patients were started on patiromer, and subsequently, RAASi therapy was initiated/optimized. After this, patients were randomized to continue vs stop patiromer. Hard clinical primary endpoints of time to CV death or first CV hospitalization were changed to mean change in serum potassium due to challenges with recruitment related to the COVID-19 pandemic. There was a significant reduction in the mean change of potassium (0.03 mEq/L in the patiromer group vs. 0.13 mEq/L in the control). Additionally, 85% of the patiromer arm was able to be optimized on RAASi.

Aside from hyperkalemia, troublesome side effects of MRAs include gynecomastia and vaginal bleeding. Eplerenone results in lower rates of these side effects than spironolactone given greater specificity for the aldosterone receptor (Option C).

Main Takeaway

Mineralocorticoid receptor antagonists, like spironolactone and eplerenone, reduce all-cause mortality, HF hospitalizations, and sudden cardiac death in a wide range of patients with HFrEF. Monitoring renal function and potassium levels while on MRA therapy is imperative.

Guideline Loc.

Section 7.3.3
Section 7.3.6

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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.

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?

A

Continue maximally tolerated GDMT; no other changes

B

Refer for cardiac resynchronization therapy (CRT)

C

Refer for transcatheter mitral valve intervention

Explanation

Choice 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, mitral valve surgery may have a role in the following contexts:

Choice A is incorrect. GDMT has been shown to improve MR and LV dimensions in patients with HFrEF and secondary MR, and it is a Class 1 recommendation (LOE B-R) to optimize GDMT before any intervention for secondary MR related to LV dysfunction. This includes both medical GDMT and cardiac resynchronization therapy (CRT) where appropriate. Our patient is still having symptoms despite being on the maximally tolerated doses of medical GDMT. This highlights the importance of a multidisciplinary approach to the management of valvular heart disease in patients with HF in accordance with clinical practice guidelines to prevent worsening of HF and adverse clinical outcomes (Class 1, LOE B-R). A cardiologist with expertise in the management of HF is integral in the shared decision-making for valve intervention and should guide optimization of GDMT to ensure that medical options for HF and secondary MR have been effectively applied for an appropriate time-period and exhausted before considering intervention.

Choice B is incorrect. While CRT has been shown to improve MR, LV dimensions, and outcomes in patients with HFrEF and secondary MR in appropriately selected patients, our patient would not be a candidate given that her QRS duration was < 120ms (Class 3: no benefit, LOE B-R).

Main Takeaway

In patients with severe secondary MR and reduced ejection fraction with persistent symptoms despite GDMT, 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. Conversely, surgery may be appropriate for some patients. HF ad VHD should be managed in a multidisciplinary fashion. 

Guideline Loc.

Sections 7.4-7.5

Figure 10

Also: Section 7.3 from “Otto, C. M., Nishimura, R. A., Bonow, R. O., Carabello, B. A., rwin, J. P., Gentile, F., Jneid, H., Krieger, ric v., Mack, M., McLeod, C., O’Gara, P. T., Rigolin, V. H., Sundt, T. M., Thompson, A., & Toly, C. (2021). 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. In Circulation (Vol. 143, Issue 5, pp. E72–E227). Lippincott Williams and Wilkins. https://doi.org/10.1161/CIR.0000000000000923”

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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.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here.

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Why is it important to measure both LDL and hs-CRP, and what factors increase hs-CRP?

What data do we have to support measuring hs-CRP? 

What are the guidelines and supportive data on using Colchicine? 

What are examples of ongoing trials that will shape the future of our anti-inflammatory toolbox?

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.

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?

A

Monitor for LVEF improvement for a total of 60 days prior to further intervention

B

Implantation of a dual-chamber ICD

C

Implantation of a CRT-D

D

Continue current management as device implantation is contraindicated given his advanced age

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, or

ambulatory 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. S therefore meets criteria for both ICD and CRT.

Choice A is incorrect. All patients should be on maximally tolerated doses of GDMT prior to consideration of device implantation to allow for assessment of LVEF recovery. Patients who have experienced myocardial infarction should be reassessed 40 days after the event and after achieving maximally tolerated doses of GDMT. 

Choice B in incorrect. For patients in sinus rhythm with a LBBB morphology and QRS duration >150 ms with an LVEF ≤35%, there were significant improvements in 6-minute walk test performance, quality of life, NYHA classification, and LVEF after implantation of CRT. Mortality and hospitalizations were also found to be decreased in patients with CRT-P & CRT-D. Overall, CRT has been shown to have high economic value in these patients.

It should be noted that CRT has the most benefit in patients with a wide QRS (>150 ms), LBBB morphology, and LVEF ≤35%, though trials have shown a modest benefit in special populations. CRT has a Class 2a recommendation (LOE B-NR) in patients with LVEF ≤35%, sinus rhythm, and NYHA Class II, III, or ambulatory IV symptoms on GDMT, with either:

a)    Non-LBBB pattern with a QRS duration ≥150 ms

b)    LBBB with a QRS duration of 120 to 149 ms

Choice D is incorrect. If LVEF remains ≤35% in a patient with a life expectancy >1 year, trials have shown that ICD placement for primary prevention reduces sudden cardiac death and also has a high economic value. There is no indication that this patient has a life expectancy < 1 year.

Main Takeaway

In patients 40 days post-MI on GDMT with an LVEF that remains ≤35%, ICD therapy for primary prevention is appropriate and cost effective.  For those additional with a LBBB and QRS >150 ms, CRT-D is also appropriate and cost effective.

Guideline Loc.

Section 7.4

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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.

This episode is supported by the 5th Annual Going Back to the Heart of Cardiology (A MedscapeLIVE Conference). Join co-chairs Dr. Robert Harrington and Dr. Fatima Rodriguez January 24-26, 2025 at the Fontainebleau Hotel in Miami Beach, Florida.

The agenda will explore the latest advancements in cardiology including cardiovascular prevention, atherosclerosis and thrombosis, cardiovascular dysfunction, arrhythmias, and valvular heart disease. Network, attend engaging presentations by renowned cardiologists, visit the exhibit and poster hall, participate in an exclusive immersive experience, and earn up to 13 CME/CE credits.

Register today with code CARDIONERDS for 30% OFF your registration. Click here for more information.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza.

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Process of developing ACC Health Policy Statements

Major Components of the ACC Career Flexibility Health Policy Statement

The following question refers to Sections 2.1

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.

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?

A

Stage A: At Risk for HF

B

Stage B: Pre-HF

C

Stage C: Symptomatic HF

D

Stage D: Advanced HF

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-HF” for Stage B.

At Stage A, emphasis is placed on the prevention of structural heart disease by aggressive risk factor modification. Healthy lifestyle habits, including regular physical activity, maintaining a normal weight, healthy dietary habits, and avoiding smoking, help reduce the future risk of HF.

For patients with established hypertension, coronary disease, or diabetes, optimal control of risk factors is crucial.

For hypertension, the SPRINT trial and subsequent meta-analysis of 35 BP-lowering trials have demonstrated a substantial reduction in incident HF and mortality with aggressive BP control.

For diabetes, SGLT2 inhibitors have demonstrated reductions in HF hospitalizations regardless of baseline HF status.

Screening patients “at risk” for HF for disease progression may be beneficial. The STOP-HF study randomized patients with risk factors but without established LV systolic dysfunction or symptomatic HF to screening with BNP testing or usual care. Screening with BNP followed by an echocardiogram and referral to a cardiovascular specialist for those with levels ≥50 pg/mL led to a reduction in the composite endpoint of incident asymptomatic LV dysfunction with or without newly diagnosed HF. Accordingly, BNP or NT–proBNP–based screening followed by team-based care, including a cardiovascular specialist, has a Class 2a (LOE B-R) recommendation in patients at risk of developing HF to prevent the development of LV dysfunction or new-onset HF.

Our patients should be counseled on healthy lifestyles, smoking cessation, and weight loss. Her anti-hypertensive regimen should be intensified for blood pressure optimization. Her ASCVD risk should be calculated, and counseling regarding statin use should be provided accordingly. If she develops overt diabetes, she should be started on an SGLT-2 inhibitor. Given her BNP level, she does not currently warrant further evaluation with an echocardiogram or referral to a specialist.

Main Takeaway

Patients with Stage A HF are those who are at risk for HF but are without symptoms, structural heart disease, or cardiac biomarkers of stretch or injury. At this stage, the emphasis should be on identifying and modifying risk factors.

Guideline Loc.

Sections 2.1 and 4.2

Decipher the Guidelines: 2022 Heart Failure Guidelines Page
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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)

“To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here.

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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 

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.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here.

CardioNerds Beyond the Boards Series
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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):

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?

Serious arrhythmic events (SAE), including resuscitated cardiac arrest and sudden cardiac death, rarely represent the initial symptoms of Brugada syndrome. Thus, risk stratification is important.

Factors that increase risk include:

4. What are the treatment options for Brugada syndrome?

5. What are the four diagnostic tests to be done in a patient who presents with an episode of exertional syncope?

Exertional syncope is a high-risk presentation that demands a comprehensive evaluation! This includes:

Do not stop at an EKG and echo alone!

Think of catecholaminergic polymorphic ventricular tachycardia (CPVT) in a patient with exertional syncope and a normal EKG!

6. What are the features on the exercise treadmill test that increase the suspicion for CPVT?

Bidirectional VT is considered a hallmark of CPVT, with digoxin toxicity being the only real imitator. This finding is specific in the absence of digoxin but not sensitive.

During exercise testing in CPVT, as the patient’s heart rate rises with increasing workload, PVCs begin to appear, progressing to bigeminy, couplets, and, in some instances, bidirectional couplets. The ectopy typically vanishes within 30 seconds of the recovery phase. This pattern increases suspicion of CPVT and warrants a detailed family history and genetic testing.

7. What are the genetic underpinnings of CPVT?

Mutations in the ryanodine receptor (RyR2 gene) render calcium release channels leaky, leading to diastolic calcium overload. This ultimately triggers arrhythmias in CPVT.

8. What are therapeutic interventions for a patient with CPVT?

Medical therapy is the mainstay of treatment in CPVT. Drugs include non-selective beta-blockers like nadolol or propranolol. Standard of care currently includes a combination of nadolol plus flecainide. An ICD is indicated only in the case of an aborted cardiac arrest. ICD therapy is never prescribed as monotherapy in these patients.

9. How do we correctly measure the QTc?

The QT interval is measured from the beginning of the QRS complex to the end of the T wave. The end of the T wave is determined using the maximum slope intercept method, in which a tangent line is drawn through the maximum down slope of the T wave. The point at which this tangent line crosses the isoelectric line is the end of the T wave. The U wave is excluded.

10. What are the three primary mutations implicated in Long QT syndrome?