Rounds Archives - Cardionerds

It’s another session of CardioNerds Rounds! In these rounds, Dr. Jenna Skowronski (Chief FIT at University of Pittsburgh) and Dr. Natalie Stokes (Formerly FIT at University of Pittsburgh and now General Cardiology Faculty at University of Pittsburgh) join transformational leader, educator and researcher, Dr. Mary Norine Walsh (Director of Heart Failure and Transplantation at Ascension St. Vincent Heart Center and Program Director of AHFT at St. Vincent) to discuss cardio-obstetrics and heart failure cases. Amongst her many accomplishments, Dr. Walsh is past president of the American College of Cardiology, Deputy Editor of JACC Case Reports, and a preeminent voice and thought leader in women’s cardiovascular health. Audio editing by CardioNerds academy intern, Pace Wetstein.

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

This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. 

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Case 1 Synopsis:

A woman in her earlier 30s, G1P1, with a history significant for peripartum cardiomyopathy presents to clinic for pre-conception counseling.  Her prior pregnancy was in her late 20s with an uneventful pre-natal course and a spontaneous vaginal delivery at 37w2d.  Two weeks after delivery, she experienced symptoms of heart failure and was found to have a new diagnosis of HFrEF. At that time TTE showed LVEF 30-35%, LVIDd 5.1cm (top normal size), diffuse hypokinesis. At that time, she was diuresed and discharged on metoprolol succinate 25mg po daily and furosemide 20mg po daily.  She had one follow up visit 6 months postpartum and the furosemide was discontinued.  Today in your office, she has NYHA Class I symptoms with no signs of symptoms of congestion. She walks daily and does vigorous exercise 1-2 times per week, while remaining on metoprolol.  Repeat TTE with LVEF 45-50% and similar LV size. She would like to have another child and was referred to you for counseling.

Case 1 Rounding Pearls:

Case 2 Synopsis:

A woman in her early 30s, G4P2022, with a history significant for polysubstance use disorder is transferred to your hospital POD #0 from an emergent C-section at 37w in cardiogenic shock.  She presented to the local hospital with cough, dyspnea, and abdominal pain and urine toxicology was positive for methamphetamines.  During evaluation she went into an SVT that was treated with metoprolol and was complicated by fetal decelerations. TTE showed LVEF 15%, LV dilation, and RV dysfunction. Given the fetal decelerations she had an emergent C-Section. We discussed her management as she progressed into SCAI Stage E Cardiogenic Shock.

Case 2 Rounding Pearls:

It’s another session of CardioNerds Rounds! In these rounds, Dr. Karan Desai (Formerly FIT at University of Maryland Medical Center and currently faculty at Johns Hopkins School of Medicine) joins Dr. Dan Burkhoff (Director of Heart Failure, Hemodynamics and MCS Research at the Cardiovascular Research Foundation) to discuss mechanical circulatory support options through the lens of pressure-volume loops! Dr. Burkhoff is the author of Harvi, an interactive simulation-based application for teaching and researching many aspects of ventricular hemodynamics. Don’t miss this wonderfully nerdy episode with a world-renowned expert in hemodynamics and MCS! Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah.

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

This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. 

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Case Synopsis:

Case Synopsis
We focused on one case during these rounds. A man in his mid-50s presented to his local community hospital with 3 days of chest pain, nausea, and vomiting. He appeared ill in the emergency room with HR in the 150s, BP 90/70s and ECG demonstrating inferior ST elevations. He was taken emergently to the catheterization lab and received overlapping stents to his right coronary artery. Over the next 24 hours, he developed a new harsh systolic murmur heard throughout his precordium and progressed to cardiogenic shock. Echocardiogram demonstrated a large basal inferoseptum ventricular septal rupture. From this point, we discussed the hemodynamics of VSR and MCS options.

Case Takeaways

Enjoy this ACC.org Expert Analysis by Goyal and Menon to learn more about post-myocardial infarction ventricular septal rupture.

It’s another session of CardioNerds Rounds! In these rounds, Dr. Loie Farina (Advanced Heart Failure and Transplant Fellow at Northwestern University) joins Dr. Jane Wilcox (Chief of the Section of Heart Failure Treatment and Recovery at Northwestern University) to discuss the nuances of HFpEF diagnosis and management. Dr. Wilcox is also the Associate Director of the T1 Center for Cardiovascular Therapeutics in the Bluhm Cardiovascular Institute and Director of the Myocardial Recovery Clinic at Northwestern University. Dr. Wilcox is a prolific researcher, clinician, and thought leader in Heart Failure and we are honored to have her on CardioNerds Rounds! Notes were drafted by Dr. Karan Desai. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig.

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

This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. 

Speaker disclosures: None

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Case #1 Synopsis:

A woman in her 80s with a history of HFpEF presented with worsening dyspnea on exertion over the course of a year but significantly worsening over the past two months. Her other history includes prior breast cancer with chemotherapy and radiation therapy, permanent atrial fibrillation with AV node ablation and CRT-P, and CKD Stage III. She presented for an outpatient RHC with exercise to further characterize her HFpEF. Her echo showed normal LV size, no LVH, LVEF of 50%, decreased RV systolic function, severe left atrial enlargement, significantly elevated E/e’ and mild MR. Right heart catheterization showed moderately elevated bi-ventricular filling pressures at rest but with passive leg raise and Stage 1 exercise the wedge pressure rose significantly. We were asked to comment on management.

Case #1 Takeaways

Case #2 Synopsis:

A woman in her 70s with history of hypertension, obesity, and COPD presented to the office for an evaluation of dyspnea. She had noted two years of dyspnea with moderate exercise and had developed lower extremity swelling. She had an echocardiogram that showed normal LV size and function, no LVH, global longitudinal strain at -21% (normal), grade 1 diastolic dysfunction and mild left atrial enlargement. Amongst the initial questions we were asked was how would we approach the diagnostic evaluation of her dyspnea?

Case #2 Takeaways

It’s another session of CardioNerds Rounds! In these rounds, Dr. Priya Kothapalli (Interventional FIT at University of Texas at Auston, Dell Medical School) joins Dr. Deepak Bhatt (Dr. Valentin Fuster Professor of Medicine and Director of Mount Sinai Heart) to discuss the nuances of antithrombotic therapy. As one of the most prolific cardiovascular researchers, clinicians, and educators, CardioNerds is honored to have Dr. Bhatt on Rounds, especially given that Dr. Bhatt has led numerous breakthroughs in antithrombotic therapy. Come round with us today by listening to the episodes of #CardsRounds! Audio editing by CardioNerds Academy Intern, Dr. Christian Faaborg-Andersen.

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

This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. 

Speaker disclosures: None

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Case #1 Synopsis:

A woman in her early 70s with a history of hypertension, hyperlipidemia, and paroxysmal atrial fibrillation presented with sudden-onset chest pressure and diaphoresis while at rest and was found to have an acute thrombotic 99% mid-LAD occlusion. The patient received OCT-guided PCI with a single drug-eluting stent. We discussed what the appropriate antithrombotic strategy would be for a patient with recent acute coronary syndrome and atrial fibrillation.

Case #1Takeaways

1. According to the recent 2021 revascularization guidelines, in patients with atrial fibrillation undergoing PCI and taking oral anticoagulant therapy, it is recommended to discontinue aspirin after 1 to 4 weeks while maintaining P2Y12 inhibitors in addition to a non-vitamin K oral anticoagulant or warfarin.
2. There are two recent trials – AUGUSTUS and the ENTRUST-AF PCI trial – that evaluated regimens of apixaban and edoxaban, respectively, that support earlier findings reporting lower bleeding rates in patients maintained on oral anticoagulant plus a P2Y12 inhibitor compared to triple therapy.
3. Of note, none of these trials were specifically powered for ischemic endpoints, but when pooling data from these trials, rates of death, MI and stent thrombosis with dual therapy were similar to those seen in patients on triple therapy.
4. Additionally, all of these patients enrolled in these trials were briefly treated with triple therapy after PCI before the aspirin was discontinued. In the 2021 guidelines, it is noted that analyses of stent thrombosis suggest that 80% of events occur within 30 days of PCI. Thus, it is reasonable to consider extending triply therapy to 1 month after PCI in high risk patients to reduce risk of stent thromboses.
5. In AUGUSTUS, 90% of patients received clopidogrel as their P2Y12 inhibitor

Case #2 Synopsis:

A man in his mid-50s with a history of peripheral vascular disease with prior SFA stent for chronic limb ischemia, hyperlipidemia, tobacco use, diabetes, and chronic kidney disease presented with a two day history of “reflux” that was worse with exertion and that improved with rest and associated with diaphoresis. He was diagnosed with an NSTEMI. His LHC revealed 99% mid-RCA thrombotic occlusion with moderate disease in the LAD. He underwent thrombectomy and PCI with a single drug-eluting stent to the RCA. We discussed his short-term and long-term antithrombotic therapy

Case #2 Takeaways

1. There were several things discussed regarding the management of this patient’s “poly-vascular disease.” One of the aspects was what to do with his antithrombotic therapy after one year and specifically how the COMPASS trial may apply to this patient.
2. In the COMPASS trial, more than 27,000 patients with stable CAD or peripheral arterial disease (PAD) were randomly assigned to rivaroxaban plus aspirin, rivaroxaban alone, or aspirin alone with a mean follow-up of about 23 months. Of note, the dose of rivaroxaban in the combination arm was 2.5 mg orally twice per day. The patients on combination therapy compared to aspirin alone had a 23% relative risk reduction in CV mortality (1.7 vs. 2.2%; HR 0.78 [95% CI 0.64-0.96]) and nearly 50% reduction in ischemic stroke. As expected, there was high rates of major bleeding in the combination arm (3.1 vs. 1.9%; HR 1.7 [95% CI 1.4-2.05]).
3. As with most decisions in medicine, each clinician would need to balance reducing ischemic events with bleeding risk for each individual patient. However, the COMPASS trial provides further evidence that low-dose oral anticoagulant with rivaroxaban in addition to aspirin can be effective in reducing ischemic events and CV mortality in patients with established atherosclerotic disease.

Case #3 Synopsis

A man in his early 60s with a history of hypertension and active tobacco use presented to a local hospital with anteroseptal STEMI c/b cardiac arrest with ventricular tachycardia. After multiple defibrillation attempts and CPR, the patient was able to achieve return of spontaneous circulation with intact mental status. The patient was pre-loaded with aspirin, ticagrelor, cangrelor and heparin and brought to the catheterization lab. There was diffuse moderate to severe stenoses in the RCA and a hazy distal LM lesion, but the culprit was a complete occlusion of the proximal LAD to which the patient received a single DES and another to the mid LAD. The patient was then brought to a tertiary care center where consideration was given for elective CABG given the residual disease. We discussed timing of CABG and when/if to pursue it, as well as antithrombotic management in this circumstance

Case #3 Takeaways

1. Amongst the things we discussed was the role of cangrelor pre-left heart catheterization. Cangrelor is a potent, short-acting, and reversible intravenous P2Y12 inhibitor with rapid onset of platelet inhibition. And within 1 hour of discontinuation, platelet function can be restored.
2. In the small CANTIC trial, patients undergoing primary PCI pre-treated with crushed 180-mg loading dose of ticagrelor were randomized to cangrelor versus placebo. Within five minutes, cangrelor led to significant P2y12 inhibition which persisted throughout the drug infusion. Of note, there were no drug interactions with ticagrelor given concomitantly with cangrelor at the start of PCI. Thus, in this trial, cangrelor proved to be an effective strategy in bridging latent platelet inhibition that can be seen with oral drugs.
3. This trial was not powered for clinical outcomes, but serves as evidence that cangrelor can be considered for pre-treatment to bridge the gap in platelet inhibitor effects in select patients in whom oral absorption may be compromised or slowed.

1. Eikelboom JW, Connolly SJ, Bosch J et al. Rivaroxaban with or without Aspirin in Stable Cardiovascular Disease. N Engl J Med. 2017 Oct 5;377(14):1319-1330.
2. Franchi F, Rollini F, Rivas A et al. Platelet Inhibition With Cangrelor and Crushed Ticagrelor in Patients With ST-Segment-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention. Circulation. 2019 Apr 2;139(14):1661-1670.
3. Lopes RD, Heizer G, Aronson R, et al. Antithrombotic therapy after acute coronary syndrome or PCI in atrial fibrillation. N Engl J Med. 2019; 380:1509–1524.
4. Writing Committee Members, Lawton JS, Tamis-Holland JE et al. 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization: Executive Summary: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2022 Jan 18;79(2):197-215

It’s another session of CardioNerds Rounds! In these rounds, Dr. Natalie Stokes (Formerly FIT at University of Pittsburgh and now General Cardiology Faculty at University of Pittsburgh) and Dr. Karan Desai (formerly FIT at University of Maryland and now General Cardiology faculty at Johns Hopkins) join Dr. Rick Nishimura (Professor of Medicine at Mayo Clinic) to discuss the nuances of managing mitral regurgitation through real cases. Dr. Nishimura has been an author or Chair of the ACC/AHA valve guidelines going back 20 years and has been recognized internationally as one of the world’s best educators, so you don’t want to miss the #NishFactor on these #CardsRounds! Audio editing by CardioNerds academy intern, Pace Wetstein.

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

This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. 

Speaker disclosures: None

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Case #1 Synopsis:

A man in his 70s with a history of non-ischemic cardiomyopathy (last known LVEF 15-20%) and atrial fibrillation, presented with decompensated heart failure in the setting of moderate to severe mitral regurgitation. He was diuresed, transitioned to GDMT, and referred to cardiac rehabilitation. Over the next 6 months, he continued to have debilitating dyspnea (NHYA Class IIIa) and his outpatient physicians were limited on titrating GDMT further due to hypotension. A TEE was done which demonstrated EF 15%, severe MR by color and quantitation (EROA of 0.5 cm2; Regurgitant Volume of 65 mL), systolic flow reversal in the pulmonary vein and severe tricuspid regurgitation. We were asked how we would approach this case

Case #1Takeaways

1. In attempting to keep the evaluation of chronic mitral regurgitation relatively simple, we should ask ourselves three primary questions: (1) What is causing the MR; (2) How much MR is there; and (3) What is the hemodynamic consequence of the MR.
2. To the first question of what is the etiology of the MR – a simple framework is to think of the etiology as an issue of the valve (primary) or an issue of the ventricle/atria (secondary). There is further classification that can be made based on the Carpentier Classification which speaks to the valve leaflet movement and position (normal leaflet motion, excessive leaflet motion [e.g., prolapse], or restricted in systole and/or diastole [e.g., rheumatic heart disease]).
3. During rounds, Dr. Nishimura provided some historical context in that the original valve guidelines had recommendations for intervention on primary mitral regurgitation and not secondary – given that it is considered a disease of the ventricle. Trials like the COAPT trial have greatly shifted our practice in treating secondary mitral regurgitation. Though, we have to be familiar with which patients with secondary MR would truly derive benefit from mitral valve intervention
4. In regards to the COAPT trial, patients with moderate to severe (3+) or severe (4+) mitral regurgitation who remained symptomatic despite maximally tolerated guideline-directed medical therapy (GDMT) were included. Dr. Nishimura makes the point that about one-third of patients intended to be enrolled in the trial were not included because they improved so much on GDMT. And thus, when evaluating patients for consideration of mitral valve intervention in secondary MR – and specifically transcatheter edge to edge repair (TEER) – every effort to optimize GDMT should be made first before intervening. Other important inclusion and exclusion criteria included that patients had LVEF between 20-50%, LV end-systolic diameter less than or equal to 70 mm, and absence of severe pulmonary hypertension (defined as pulmonary artery systolic pressure > 70 mmHg despite vasodilator therapy) or moderate to severe right ventricular failure.
5. Dr. Nishimura asks our audience if the patient is truly on optimal GDMT and/or optimized? There are basic tools that clue us into optimization including chest x-ray (e.g., is there still pulmonary vascular congestion) and physical examination (e.g., what is the venous pressure).
6. Dr. Nishimura makes an interesting point in correlating our examination with the echocardiographic findings. In patients with largely secondary MR, where the leaflets have poor coaptation and we have a weak ventricle we may not expect to hear a very loud murmur on examination (e.g., there isn’t enough pump to generate the murmur). However, if we hear a significant murmur (e.g., like our patient described in the case with a loud, 3/6, blowing murmur) with presumed secondary MR, our antennae should be up for a possible primary component.

Case #2 Synopsis:

A man in his early 60s with a history of prior LAD PCI in the setting of an NSTEMI and diabetes presented to your hospital in SCAI Stage C to D Cardiogenic Shock with the background of worsening orthopnea and edema several weeks prior. You are told the patient had a recent echo with LVEF 15%, mild LV dilation, reduced RV function and moderate to severe functional MR. When you meet the patient, he is confused, nauseous and with poor perfusion (e.g., cool extremities and Lactate of 7 mmol/L). The patient is taken for left and right heart catheterization with RHC showing significant elevated filling pressures, large V-waves, and low cardiac index. An IABP is placed and LHC is performed where an acute appearing lesion in the proximal LAD and Mid-RCA are treated with PCI. Over the next week the IABP is weaned and removed and low doses of GDMT started. But once the IABP is removed, nausea returns and lactate starts rising again. Hemodynamics and TEE images are obtained with the IABP at 1:1 and on standby and show significant worsening of the hemodynamics and MR with IABP on standby, with the MR in the severe category, and we are asked to comment on what to do next.

Case #2 Takeaways

1. Dr. Nishimura suggests we approach this complex case with a simple question: how much of his shock/congestion is a result of his pump (the LV) versus how much is a result of his valve? Dr. Nishimura notes there is a subset of patients who have dynamic mitral regurgitation, which is primarily related to changes in the structure of the annulus/apparatus that happen with changes in preload/afterload/contractility. These patients can go from mild to severe depending on the loading conditions, as they are exquisitely sensitive to these conditions
2. Dr. Nishimura notes the continuous wave doppler of the mitral regurgitation can give us a rich amount of detail. The MR continuous wave doppler signal reflects the instantaneous doppler between the left ventricle and left atrium. If we pay attention to the signal during isovolumic contraction – if there is a rapid rise in the signal, that suggests that we are generating LV systolic pressure rather quickly and contractility may be preserved (e.g., this refers to dP/dT which has several caveats but qualitatively can be informative us).
3. These patients with dynamic MR who we cannot control the loading conditions, it may be better to treat the MR itself.

References

1. Stone GW, Lindenfeld J, Abraham WT, Kar S, Lim DS, Mishell JM, Whisenant B, Grayburn PA, Rinaldi M, Kapadia SR, Rajagopal V, Sarembock IJ, Brieke A, Marx SO, Cohen DJ, Weissman NJ, Mack MJ; COAPT Investigators. Transcatheter Mitral-Valve Repair in Patients with Heart Failure. N Engl J Med. 2018 Dec 13;379(24):2307-2318.
2. Writing Committee Members, Otto CM, Nishimura RA, Bonow RO, Carabello BA, Erwin JP 3rd, Gentile F, Jneid H, Krieger EV, Mack M, McLeod C, O’Gara PT, Rigolin VH, Sundt TM 3rd, Thompson A, Toly C. 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. J Am Coll Cardiol. 2021 Feb 2;77(4):e25-e197.

It’s another session of CardioNerds Rounds! In these rounds, Dr. Stephanie Fuentes (EP FIT at Houston Methodist) joins Dr. Hugh Calkins (Professor of Medicine and Director of the Electrophysiology Laboratory and Arrhythmia Service at Johns Hopkins Hospital) to discuss the nuances of atrial fibrillation (AF) management through challenging cases. As an author of several guideline and expert consensus statements in the management of AF and renowned clinician, educator, and researcher, Dr. Calkins gives us many pearls on the management of AF, so don’t miss these #CardsRounds! 

This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. 

Speaker disclosures: None

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Case #1 Synopsis:

A woman in her mid-60s presents with symptomatic paroxysmal atrial fibrillation (AF). An echocardiogram has demonstrated that she has a structurally normal heart. Her primary care doctor had started Metoprolol 50 mg twice a day but she has remained symptomatic. In office, an EKG confirms AF, but she converts to sinus while there. She is seeking advice to prevent further episodes and in general wants to avoid additional medications

Case #2 Takeaways

1. We discussed several potential options for treatment. Amongst the first things we discussed was amiodarone. In a patient of this nature without structural heart disease and under the age of 70, Dr. Calkins discussed that he would probably consider amiodarone as a 2nd line option. While amiodarone may be effective in maintaining sinus rhythm in comparison to other antiarrhythmic medications like sotalol, flecainide, and propafenone, it does have significant toxicity.
2. If antiarrhythmic drugs (AAD) were to be considered, we also discussed the options of dofetilide versus sotalol. Dofetilide typically requires inpatient initiation due to the risk of QT
    prolongation and Torsades. Since women tend to have longer corrected QT (QTc) intervals, high dose dofetilide may be more proarrhythmogenic in women. Though, Dr. Calkins noted that many patients don’t tolerate sotalol due to fatigue and generally dofetilide is well tolerated.
3. When it comes to the “pill in the pocket” approach, Dr. Calkins noted that its utility is more so in patients with persistent AF that is known to not stop on its own. For instance, an individual who has AF a few times a year that is persistent may benefit from flecainide or propafenone (“in the pocket”) instead of being brought in for an electrical cardioversion. In this scenario, the first time one of these agents is used, the patient ought to be closely monitored. For our patient, her episodes were too frequent and self-terminating for a “pill in the pocket” approach to be effective.
4. Current guideline recommendations for catheter ablation include a Class IA recommendation for patients with paroxysmal AF refractory to AADs, and a Class IIA recommendation as first-line therapy for patients with paroxysmal AF.
5. In the 2020 ESC Atrial Fibrillation Guidelines, catheter ablation is given a Class IA recommendation to improve symptoms of AF recurrences in patients who have failed or are intolerant of one Class I or III AADs. For patients who have failed or have been intolerant of beta blocker alone for rhythm control, catheter ablation is given a Class IIA recommendation. As first-line therapy in paroxysmal AF, catheter ablation is given a Class IIA recommendation as well.
6. Of note, three recent trials have demonstrated catheter ablation as first line therapy is reasonable and newer guidelines will reflect this. Specifically, EARLY-AF compared ablation (cryoablation) vs AAD (mainly with flecainide/propafenone) as a first line therapy. The cryoablation arm showed significantly less recurrence of AF at one year
   • The guidelines clearly state that aligning the treatment plan with the patient’s goals and risk tolerance are paramount. Catheter ablation does have potential complications such as pericardial effusion or access-related issues, though these are rare. Furthermore, as time has passed, catheter ablation success rates have improved.
   • Up and coming techniques such as electroporation may be game-changing with regards to success rate and safety. Waiting times for a procedure may be an issue, so one could consider an AAD, such as flecainide, as a standing dose awaiting the procedure.
7. Regarding predictors of success for catheter ablation, Dr. Calkins noted that the key factor was type of AF. With paroxysmal AF there is roughly 70-80% success rate with the 1st procedure, 50-70% with persistent AF, and 30-50% with longstanding persistent AF. Other predictors of success include BMI (higher BMI associated with a lower success rate and a higher rate of complications), left atrial size (with a linear dimension of ≥ 5.5 cm indicating less likelihood of success), age, and obstructive sleep apnea.
8. One of the questions that was raised was screening for structural heart disease before starting flecainide/propafenone. Typically, an EKG and TTE are done, and if they are not suggestive of structural heart disease, Dr. Calkins noted it would be reasonable to use these agents. With increasing age, there’s increased risk of subclinical CAD, though it is not in the guidelines to perform functional testing or anatomic imaging prior to starting these agents.
9. Finally, Dr. Calkins noted as an aside that in patients with sick sinus syndrome, management in the past has involved placing a permanent pacemaker (PPM) followed by AAD agents. However, catheter ablation may be a better option because it treats AF and improves the sinus rate because of its effect on the autonomic system, eliminating pauses that would have otherwise warranted a pacemaker. After ablation, the resting HR can improve 10-30 bpm and this can be a marker of successful catheter ablation.

Case #2 Synopsis:

A man in his mid-60s with a history of surgically placed bioprosthetic AVR, CAD with prior CABG, newly diagnosed ischemic cardiomyopathy with LVEF 20-25% with imaging revealing reversible ischemia in multiple coronary territories, presented to the clinic with dyspnea in the setting of persistent AF now 6 weeks after multi-vessel PCI. Other relevant information is that he appears congested in clinic and his EKG demonstrates a left bundle branck block (LBBB) with QRS at 172 ms. He seeks your opinion for management options.

Case #2 Takeaways

1. Dr. Calkins discussed that the only safe AAD in this circumstance would be Amiodarone, and that the risk of developing complete heart block (CHB) in a patient with LBBB placed on amiodarone is not high enough to preclude its use. One strategy would be to give this patient an amiodarone load followed by direct current cardioversion (DCCV). Following DCCV, if the patient maintains sinus rhythm, one could consider continuing with amiodarone at a lower dose or pursuing catheter ablation as a next strategy.
2. Dr. Calkins emphasized understanding the temporal relationship between AF and HF in patients with reduced ejection fraction. In patients with new-onset AF and reduced EF, aggressive rhythm control with catheter ablation would be warranted because there is a higher likelihood of improving the cardiomyopathy.
3. Another option to consider in patients with HFrEF and permanent atrial fibrillation that remain symptomatic or who have had hospitalizations with HF is AV node ablation with cardiac resynchronization therapy, though for a patient like this other viable treatment options remain to be tested. Regarding an ICD, the patient may recover their EF post-revascularization and implementation of guideline-directed therapy. Thus, with ischemic cardiomyopathy post revascularization, the decision to place an ICD should wait 90 days. Furthermore, the EF may improve with control of the AF.

Case #3 Synopsis:

A woman in her mid-80s with hypertension and recent COVID-19 pneumonia is admitted to the hospital with hypoxia, reduced LVEF and found to have AF with rapid ventricular response. The patient’s underlying conditions were treated and attempts at ventricular rate control were attempted but limited by blood pressure. A DCCV with amiodarone loading was also attempted but failed to maintain sinus rhythm. 

Case #3 Takeaways

1. Some feasible options in this circumstance include further loading with amiodarone and reconsidering another DCCV versus an AV node ablation with permanent pacemaker implantation if medical therapies are limited or failing.
2. Digoxin use for rate control alone in critically ill patients is typically discouraged. This is because we now know that its mechanism of action involves raising vagal tone and acutely ill patients typically have low vagal tone so it may not be helpful. However, in patients with rapid AF and HF, it is reasonable to use it. When used in combination with amiodarone, one may reduce the dose of digoxin in half given its drug-drug interaction

It’s another session of CardioNerds Rounds! In these rounds, Co-Chair, Dr. Karan Desai (previous FIT at the University of Maryland Medical Center, and now faculty at Johns Hopkins) joins Dr. Ryan Tedford (Professor of Medicine and Chief of Heart Failure and Medical Directory of Cardiac Transplantation at the Medical University of South Carolina in Charleston, SC) to discuss the nuances of managing pulmonary hypertension in the setting of left-sided heart disease. Dr. Tedford is an internationally-recognized clinical researcher, educator, clinician and mentor, with research focuses that include the hemodynamic assessment of the right ventricle and its interaction with the pulmonary circulation and left heart.

This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. 

Speaker disclosures: None

Cases discussed and Show Notes • References • Production Team

CardioNerds Rounds Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll

CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!

Case #1 Synopsis:

A woman in her late 30s presented to the hospital with 4 weeks of worsening dyspnea. Her history includes dilated non-ischemic cardiomyopathy diagnosed in the setting of a VT arrest around 10 years prior. Over the past 10 years she has been on guideline-directed medical therapy with symptoms that had been relatively controlled (characterized as NYHA Class II), but without objective improvement in her LV dimensions or ejection fraction (LVEF 15-20% by TTE and CMR and LVIDd at 6.8 cm). Over the past few months she had been noting decreased exercise tolerance, worsening orthopnea, and episodes of symptomatic hypotension at home. When she arrived to the hospital, she presented with BP 95/70 mmHg, increased respiratory effort, congestion and an overall profile consistent with SCAI Stage C-HF shock. In the case, we go through the hemodynamics at various points during her hospitalization and discuss options for management including medical therapy and mechanical support. The patient was eventually bridged to transplant with an Impella 5.5.

Initial Hemodynamics

Right Atrium (RA) Pressure Tracing:

Right Ventricle (RV) Pressure Tracing:

Pulmonary Artery (PA) Pressure Tracing:

Pulmonary Capillary Wedge Pressure (PCWP) Tracing:

Case 1 Rounding Pearls

1. One of the first points that Dr. Tedford made was thinking about our classic frameworks of characterizing acute decompensated heart failure, specifically the “Stevenson” classification developed by Dr. Lynne Stevenson that phenotypes patients along two axes: congestion (wet or dry) and perfusion (warm or cold). Dr. Tedford cautioned that young patients may not fit into these classic boxes well, and that a normal lactate should not re-assure the clinician that perfusion is normal.
2. In reviewing the waveforms, Dr. Tedford took a moment to note that besides just recording the absolute values of the pressures transduced in each chamber or vessel, it is critical to understand the morphology of the tracings themselves. For instance, with the RA pressure tracing above, there is no respiratory variation in the mean pressure. This is essentially a “resting Kussmaul’s sign,” which is typically indicative of significant RV dysfunction. Thus, even though our echocardiogram in this case did not necessarily show a significantly dilated RV with mildly reduced longitudinal function (TAPSE), hemodynamically the patient is demonstrating significant RV compromise.
3. If we compare the RA pressure tracing to the PCWP, we see that there is respiratory variation in the PCWP tracing. We typically think of pronounced respiratory variation in the RA or PCWP tracing in the setting of obesity or lung disease, but loading conditions can also lead to significant respiratory variation.
4. As was noted during the case discussion, irreversible pulmonary hypertension is considered an absolute contraindication to heart transplantation though there is variation on the absolute threshold above which transplantation is contraindicated. Generally, a pulmonary vascular resistance (PVR) of 3 Woods Units is considered a contraindication to isolated cardiac transplantation. Testing for reversibility of an elevated PVR with a vasodilator like nitroprusside is common in this patient population.
5. In a study by Dr. Steven Hsu and colleagues, Pulmonary Artery Pulsatility Index (PAPi) was shown to be the hemodynamic factor that best correlated with intrinsic RV myocyte dysfunction in patients with advanced heart failure (using a cutoff of PAPi of 1.85). Dr. Tedford made note to remember that PAPi is highly influenced by RA pressure (the denominator in the ratio).

Case #2 Synopsis:

A woman in her late 40s presented to clinic for another opinion regarding her PH management. In regards to her history, in the 1990s she underwent a mechanical mitral valve replacement (MVR) for mixed mitral valve disease in the setting of rheumatic fever as well as a single vessel CABG (SVG to the RCA). In the early 2000s, she had developed severe and symptomatic tricuspid regurgitation (TR) and underwent redo sternotomy for TV repair (TVr). She had generally done well until the past year when she started developing dyspnea on light exertion, abdominal fullness, lower extremity edema and over the course of a year she had four hospitalizations for heart failure. Over her hospitalizations, she was also diagnosed with hemolytic anemia. Diagnostic work-up revealed pre and post-capillary PH. Dr. Tedford reviews the subsequent hemodynamic evaluation and provides insight on managing PH post valvular intervention. She was ultimately diagnosed with mitral paravalvular regurgitation treated with transcatheter PVL closure.

Initial Hemodynamics

RA Pressure Tracing

RV Pressure Tracing

PA Pressure Tracing

PCW Pressure Tracing

Left Ventricular (LV) Pressure Tracing

PCW and LV Simultaneous Pressure Tracing

Case 2 Rounding Pearls:

1. The patient had been placed on sildenafil for persistent PH post-valve intervention. Dr. Tedford briefly mentioned the SIOVAC trial which was designed to evaluate treatment with sildenafil (40 mg TID) compared with placebo amongst patients with persistent PH (mean PA pressure ≥ 30 mmHg) 1 year after valvular replacement or repair (majority of whom were patients that had mitral valve intervention). In this study, sildenafil was associated with worse functional status, specifically heart failure or dyspnea compared to placebo (34% vs. 20%, p = 0.04).
2. Dr. Tedford briefly touched upon the prognostic value of the diastolic pulmonary gradient (DPG, calculated as diastolic PA pressure subtracted by PCWP) in patients being considered for cardiac transplantation. We commonly use PVR and transpulmonary gradient (TPG) to characterize the degree of pre-capillary PH and suitability for transplantation. However, these markers are not ideal surrogates for pulmonary vascular remodeling and differentiating between fixed remodeling versus reversible changes. For instance, the TPG can be elevated not only as a result of pulmonary vascular remodeling but elevated LA pressures passively transmitted back to the pulmonary vasculature leading to elevations in the diastolic PA pressure.
3. The DPG was thought to potentially define higher risk left heart failure patients with clinically significant pre-capillary PH. However, in Dr. Tedford’s 2014 analysis, the DPG did not delineate higher risk among patients with elevated TPG and PVR undergoing cardiac transplantation. There could be several explanations including that the cutoff for abnormal DPG is low (≥7) and thus small errors in measurement could have significant influence on what is characterized as abnormal. Furthermore, the diastolic PA pressure measurement is particularly prone to ringing artifact.

1. Aslam MI, Jani V, Lin BL, et al. Pulmonary artery pulsatility index predicts right ventricular myofilament dysfunction in advanced human heart failure. Eur J Heart Fail. 2021 Feb;23(2):339-341. doi: 10.1002/ejhf.2084. Epub 2021 Jan 5. PMID: 33347674; PMCID: PMC8574988.
2. Bermejo J, Yotti R, García-Orta R, et al., on behalf of the Sildenafil for Improving Outcomes after VAlvular Correction (SIOVAC) investigators. Sildenafil for improving outcomes in patients with corrected valvular heart disease and persistent pulmonary hypertension: a multicenter, double-blind, randomized clinical trial.
3. Mehra MR, Canter CE, Hannan MM, et al; International Society for Heart Lung Transplantation (ISHLT) Infectious Diseases, Pediatric and Heart Failure and Transplantation Councils. The 2016 International Society for Heart Lung Transplantation listing criteria for heart transplantation: A 10-year update. J Heart Lung Transplant. 2016 Jan;35(1):1-23. doi: 10.1016/j.healun.2015.10.023. PMID: 26776864.
4. Tedford RJ, Beaty CA, Mathai SC et al. Prognostic value of the pre-transplant diastolic pulmonary artery pressure-to-pulmonary capillary wedge pressure gradient in cardiac transplant recipients with pulmonary hypertension. J Heart Lung Transplant. 2014 Mar;33(3):289-97. doi: 10.1016/j.healun.2013.11.008. Epub 2013 Nov 28. Erratum in: J Heart Lung Transplant. 2019 Feb;38(2):233. PMID: 24462554; PMCID: PMC3955214.
5. Thibodeau JT, Drazner MH. “The Role of the Clinical Examination in Patients With Heart Failure.” JACC Heart Failure (2018): 543-551.

It’s another session of CardioNerds Rounds! In these rounds, Co-Chairs, Dr. Karan Desai and Dr. Natalie Stokes and Dr. Tiffany Dong (FIT at Cleveland Clinic) joins Dr. Randall Starling (Professor of Medicine and Director of Heart Transplant and Mechanical Circulatory Support at Cleveland Clinic) to discuss the nuances of guideline directed medical therapy (GDMT) through real cases. As a past president of the Heart Failure Society of America (HFSA) and author on several guidelines, Dr. Starling gives us man pearls on GDMT. Come round with us today by listening to the episodes and joining future sessions of #CardsRounds!

This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. 

Speaker disclosures: None

Cases discussed and Show Notes • References • Production Team

CardioNerds Rounds Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll

CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!

Case #1 Synopsis:

A man in his 60s with known genetic MYPBC3 cardiomyopathy and heart failure with a reduced ejection fraction of 30% presents with worsening dyspnea on exertion over the past 6 months. His past medical history also included atrial fibrillation with prior ablation and sick sinus syndrome with pacemaker implantation. Medications are listed below. He underwent an elective right heart catheterization prior to defibrillator upgrade for primary prevention. At the time of right heart catheterization, his blood pressure was 153/99 with a heart rate of 60. His RHC demonstrated a RA pressure of 15mmHg, RV 52/16, PA 59/32 (mean 41), and PCWP 28 with Fick CO/CI of 2.8 L/min and index of 1.2 L/min/m2. His SVR  was 1900 dynes/s/cm-5. He was admitted to the cardiac ICU and started on nitroprusside that was transitioned to a regimen of Sacubitril-Valsartan and Eplerenone. His final RHC numbers were RA 7, PA 46/18/29, PCWP 16 and Fick CO/CI 6.1/2.6. His discharge medications are shown below.

Takeaways from Case #1

1. Unless there are contraindications (cardiogenic shock or AV block), continue a patient’s home beta blocker to maintain the neurohormonal blockade benefits. A low cardiac index should be interpreted in the full context of the patient, including their symptoms, other markers of perfusion (e.g., urine output, mentation, serum lactate), and mean arterial pressure before holding or stopping beta blockade. Carvedilol, metoprolol succinate and bisoprolol are all evidence-based options for beta blockers in heart failure with reduced ejection fraction.
2. If there is concern of lowering blood pressure too much with Sacubitril/Valsartan, one method is to trial low dose of valsartan first and then transition to Sac/Val. Note, in the PARADIGM-HF trial, the initial exclusion criteria for starting Sac/Val included no symptomatic hypotension and SBP ≥ 100. At subsequent up-titration visits, the blood pressure criteria was decreased to SBP ≥ 95.
3. In multiple studies, protocol-driven titration of GDMT has shown to improve clinical outcomes, yet titration remains poor. The following image from Greene et al. in JACC shows that in contemporary US outpatient practices that GDMT titration is poor with few patients reaching target dosing.

Case #2 Synopsis:

A 43 year-old male with a past medical history of familial dilated cardiomyopathy requiring HVAD placement two years prior now comes in with low flow alarms. He is feeling well otherwise with chronic dyspnea on exertion. A CT chest and abdomen with contrast for showed outflow graft occlusion. Given a TTE showed LV recovery that correlated with invasive hemodynamics, his LVAD was decommissioned. He was tried on a low dose Sacubitril/Valsartan but was unable to tolerate it due to hypotension. He was discharged on carvedilol 3.125mg BID and lisinopril 5mg daily. Over the next 10 months in clinic, his GDMT was titrated to carvedilol 25mg BID, spironolactone 25mg daily and Sacubitril/Valsartan 49-51mg BID.

 Takeaways Case #2

1. In patients with ventricular assist devices, the differential for low flow alarms includes hypovolemia, arrhythmias, RV failure, cardiac tamponade and inflow cannula obstruction. A careful history, exam (with particular attention to the JVD), and bedside echocardiogram can help differentiate the cause.
2. EF recovery occurs in about 5% of patients in large LVAD registries. Favorable prognostic factors for EF recovery include female sex and nonischemic cardiomyopathy of short duration.
3. In the TRED-HF trial, patients were randomly assigned to phased withdrawal or continuation of GDMT over 6 months. The primary endpoint was relapse defined as a reduction in LVEF of more than 10% and to less than 50%, an increase in LVEDV by more than 10% and to higher than the normal range, a two-fold rise in NT-pro-BNP and to more than 400 ng/L or clinical evidence of heart failure. While a small trial (51 patients were enrolled), over the first 6 months, 44% of patients assigned to treatment withdrawal met the primary endpoint of relapse compared with none assigned to continue treatment (estimated of event rate 45.7% [95% CI 28.5-67.2]; p=0.0001).
4. We still do not have great predictors of relapse, and thus for most patients with HFrecEF, GDMT should continue indefinitely.

1. Halliday BP, Wassall R, Lota AS, et al. Withdrawal of pharmacological treatment for heart failure in patients with recovered dilated cardiomyopathy (TRED-HF): an open-label, pilot, randomised trial. Lancet. 2019 Jan 5;393(10166):61-73. doi: 10.1016/S0140-6736(18)32484-X. Epub 2018 Nov 11. PMID: 30429050; PMCID: PMC6319251.
2. Greene SJ, Fonarow GC, DeVore AD, et al. Titration of Medical Therapy for Heart Failure With Reduced Ejection Fraction. J Am Coll Cardiol. 2019 May 21;73(19):2365-2383. doi: 10.1016/j.jacc.2019.02.015. Epub 2019 Mar 4. PMID: 30844480; PMCID: PMC7197490.
3. McMurray JJ, Packer M, Desai AS, et al. Angiotensin-neprilysin inhibition versus enalapril in heart failure. N Engl J Med. 2014 Sep 11;371(11):993-1004. doi: 10.1056/NEJMoa1409077. Epub 2014 Aug 30. PMID: 25176015.

CardioNerds Rounds Co-Chairs, Dr. Karan Desai and Dr. Natalie Stokes and CardioNerds Academy Fellow, Dr. Najah Khan, join Dr. Martha Gulati – President-Elect of the American Society for Preventive Cardiology (ASPC) and prior Chief of Cardiology and Professor of Medicine at the University of Arizona – to discuss challenging cases in cardiac prevention. As an author on numerous papers regarding cardiac prevention and women’s health, Dr. Gulati provides many prevention pearls to help guide patient care. Come round with us today by listening to the episodes now and joining future sessions of #CardsRounds!

This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. 

Speaker disclosures: None

Cases discussed and Show Notes • References • Production Team

CardioNerds Rounds Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll

CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!

Case #1 Synopsis:

A 55-year-old South Asian woman presents to prevention clinic for an evaluation of an elevated LDL-C. Her prior history includes hyperlipidemia, hypertension, obesity, and pre-eclampsia. She was told she had “high cholesterol” a few years prior and would need medication. She started exercising regularly and cut out sweets from her diet. Before clinic, labs showed: Total Cholesterol (mg/dL) of 320, HDL 45, Triglycerides 175, and (directly measured) LCL-C 180. Her Lipoprotein(a) is 90 mg/dL (ULN being ~ 30 mg/dL). Her HbA1C is 5.2% and her 10-year ASCVD Risk (by the Pooled Cohorts Equation) is 5.4%. Her recent CAC score was 110. She prefers not to be on medication and seeks a second opinion.

Takeaways from Case #1

1. As Dr. Gulati notes, in the 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease, South Asian ethnicity is considered a “risk enhancing factor.” The pooled cohort equations (PCE) may underestimate risk in South Asians. Furthermore, risk varies within different South Asian populations, with the risk for cardiovascular events seemingly higher in those individuals of Bangladeshi versus Pakistani or Indian origin. There are multiple hypotheses for why this may be the case including cultural aspects, such as diet, physical activity, and tobacco use. A better understanding of these factors could inform targeted preventive measures.
2. In the same 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease mentioned above, history of an adverse pregnancy outcome (APO) increases later ASCVD risk (e.g., preeclampsia) and is also included as a “risk-enhancing factor.” Studies have shown that preeclampsia is an independent risk factor for developing early onset coronary artery calcification.
3. Recent data has shown that the risk for developing preeclampsia is not the same across race and ethnicity, with Black women more likely to develop preeclampsia. Black women also had the highest rates of peripartum cardiomyopathy, heart failure, and acute renal failure. After adjustment for socioeconomic factors and co-morbidities, preeclampsia was associated with increased risk of CVD events in all women, the risk was highest among Asian and Pacific Islander women. Listen to Episode #174. Black Maternal Health with Dr. Rachel Bond to learn more about race-based disparities in cardio-obstetric care and outcomes.
4. Our patient thus has multiple risk-enhancing factors to help in shared decision making and personalize her decision for statin use. Another risk-enhancing factor for her is an elevated Lp(a), which is considered elevated when ≥ 50 mg/dL or ≥ 125 nmol/L.
5. One other aspect that Dr. Gulati briefly covered was how CAC score may inform Aspirin use for primary prevention. There continues to be debate over when to prescribe aspirin when there is demonstrable calcium on imaging. In the MESA study, for individuals with CAC ≥ 100, the NNT (for 5 years to prevent an ASCVD event) was a 140 and NNH was 518.

Case #2 Synopsis:

A 58-year-old woman presents to establish care at a general cardiology clinic for shortness of breath. Her history includes hypertension, cutaneous lupus, and ongoing tobacco use. A year ago, she started having nausea, more common with stress or on exertion. She saw her PCP who obtained an EKG and GI evaluation. Endoscopy was unrevealing and EKG showed non-specific ST-T changes inferiorly. She was treated for GERD and then 6 months prior she developed dyspnea on exertion while exercising on her stationary bike after 10 minutes; she previously could go 30 minutes. She suffered a left knee meniscal tear shortly thereafter. She sees a cardiologist and obtains a cardiac PET-Stress which showed a small area of reversible ischemia in the basal to mid inferior wall and borderline reduced coronary flow reserve. Her symptoms continued and she was referred for LHC which showed non-obstructive CAD. No intracoronary physiologic testing was done. She is started on aspirin but still having symptoms. She seeks your opinion on how to prevent cardiovascular events.

 Takeaways Case #2

1. In the VIRGO study, investigators interviewed 2009 women and 976 men aged 18 to 55 years hospitalized for acute myocardial infarction (AMI) at 103 United States hospitals. Approximately 29.5% of women and 22.1% of men sought medical care for similar chest pain symptoms before their hospitalization; however, 53% of women reported that their provider did not think these symptoms were heart-related in comparison with 37% of men (p < 0.001).
2. As Dr. Gulati noted, angiographically obstructive CAD is just the tip of the iceberg when it comes to ischemic heart disease. There are several important phenotypes including diffuse non-obstructive CAD and coronary microvascular dysfunction. Dr. Gulati shared the following image to demonstrate how ischemic heart disease is a unifying term for different syndromes.

Academy Fellow, Dr. Najah Khan, has created the following infographic that provides a distinction between INOCA (ischemia and no obstructive coronary artery disease) and MINOCA (myocardial infarction with non-obstructive coronary arteries).

Case #3 Synopsis:

A 50-year-old man presents to cardiology clinic after a STEMI. His history includes hypertension, diabetes, obesity, and prior tobacco use. Four months ago, the patient suffered an inferior STEMI complicated by VF arrest treated with PCI to the proximal RCA. There was significant residual CAD and tentative plan for staged CABG. The patient was discharged on Aspirin, Prasugrel, Metoprolol Succinate, Lisinopril, Metformin and Atorvastatin. However, he started having muscle aches and so he stopped his Atorvastatin. He sees his PCP and before clinic gets a Lipid Panel (mg/dL) with Total Ch at 230, TG 237, HDL at 36 and LDL-C at 140. The patient starts ezetimibe and then comes to see you a month later to discuss best secondary prevention measures.

Case #3 Takeaways:

1. There are multiple opportunities for secondary prevention following acute coronary syndrome, with many patients undertreated. This includes but not limited to LDL-lowering medications, smoking cessation, cardiac rehabilitation, blood pressure control, diabetes management, weight loss, and targeting non-LDL particles when appropriate.
2. Dr. Gulati points out that we need to make sure we categorize a patient’s risk appropriately, including patients at “very high risk” of ASCVD. This requires multiple ASCVD events (recent ACS, history of MI, history of ischemic stroke, symptomatic PAD) or an ASCVD event with multiple high-risk conditions (e.g., Age ≥ 65, heterozygous familial hypercholesterolemia, history of prior CABG or PCI outside of major ASCVD events, diabetes, hypertension, CKD, current tobacco use, persistently elevated LDL-C despite max statin therapy and ezetimibe, and/or history of congestive heart failure).
3. Patients at very high risk of ASCVD should be on a high intensity statin or maximally tolerated statin (Class I). If PCSK9 inhibitors are considered, it is Class I to add ezetimibe to maximal statin therapy before initiating PCSK9i. If a patient is deemed to be on the maximal LDL-C lowering therapy that s/he is able to tolerate but LDL-C remains ≥ 70 mg/dL or non-HDL-C ≥ 100 mg/dL, adding PCSK9i is reasonable (Class IIa).
4. A take home message from Dr. Gulati is that after more than a quarter century of treating LDL-C, generally the lower we can drive LDL-C levels the better for patient outcomes.

1. Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019 Sep 10;140(11):e596-e646. doi: 10.1161/CIR.0000000000000678. Epub 2019 Mar 17. Erratum in: Circulation. 2019 Sep 10;140(11):e649-e650. Erratum in: Circulation. 2020 Jan 28;141(4):e60. Erratum in: Circulation. 2020 Apr 21;141(16):e774. PMID: 30879355; PMCID: PMC7734661.
2. Benschop L, Brouwers L, Zoet GA, et al. Early Onset of Coronary Artery Calcification in Women With Previous Preeclampsia. Circ Cardiovasc Imaging. 2020 Nov;13(11):e010340. doi: 10.1161/CIRCIMAGING.119.010340. Epub 2020 Nov 16. PMID: 33190533.
3. Cainzos-Achirica M, Miedema MD, McEvoy JW, et al. Coronary Artery Calcium for Personalized Allocation of Aspirin in Primary Prevention of Cardiovascular Disease in 2019: The MESA Study (Multi-Ethnic Study of Atherosclerosis). Circulation. 2020 May 12;141(19):1541-1553. doi: 10.1161/CIRCULATIONAHA.119.045010. Epub 2020 Apr 1. PMID: 32233663; PMCID: PMC7217722.
4. Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2019 Jun 25;73(24):3168-3209. doi: 10.1016/j.jacc.2018.11.002. Epub 2018 Nov 10. Erratum in: J Am Coll Cardiol. 2019 Jun 25;73(24):3234-3237. PMID: 30423391.
5. Lichtman JH, Leifheit EC, Safdar B, et al. Sex Differences in the Presentation and Perception of Symptoms Among Young Patients With Myocardial Infarction: Evidence from the VIRGO Study (Variation in Recovery: Role of Gender on Outcomes of Young AMI Patients). Circulation. 2018 Feb 20;137(8):781-790. doi: 10.1161/CIRCULATIONAHA.117.031650. PMID: 29459463; PMCID: PMC5822747.
6. Minhas AS, Ogunwole SM, Vaught AJ, et al. Racial Disparities in Cardiovascular Complications With Pregnancy-Induced Hypertension in the United States. Hypertension. 2021 Aug;78(2):480-488. doi: 10.1161/HYPERTENSIONAHA.121.17104. Epub 2021 Jun 8. PMID: 34098730; PMCID: PMC8266726.
7. Volgman AS, Palaniappan LS, Aggarwal NT et al. Atherosclerotic Cardiovascular Disease in South Asians in the United States: Epidemiology, Risk Factors, and Treatments: A Scientific Statement From the American Heart Association. Circulation. 2018 Jul 3;138(1):e1-e34. doi: 10.1161/CIR.0000000000000580. Epub 2018 May 24. Erratum in: Circulation. 2018 Jul 31;138(5):e76. PMID: 29794080.

CardioNerds Rounds Co-Chair, Dr. Karan Desai, joins Dr. Michelle Kittleson (Director of Postgraduate Education in Heart Failure and Transplantation, Director of Heart Failure Research, and Professor of Medicine at the Smidt Heart Institute at Cedars-Sinai) to discuss challenging cases of hypertrophic cardiomyopathy. As a guideline author on the 2020 ACC/AHA Hypertrophic Cardiomyopathy Guidelines, Dr. Kittleson shows us how the latest evidence informs our management of HCM patients, while sharing many #Kittlesonrules and pearls on clinical care. Come round with us today by listening to the episodes now and joining future sessions of #CardsRounds!

This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. 

Speaker disclosures: None

Cases discussed and Show Notes • References • Production Team

CardioNerds Rounds Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll

CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!

Case #1 Synopsis:

Two non-white brothers in their early 20s come to clinic to establish care. They have no cardiopulmonary symptoms, normal EKGs and normal echos, but there was a possible family history of HCM. Their mother had LV hypertrophy and underwent septal myectomy, but she could not afford genetic testing and was no longer in the patients’ lives. The path report suggested “myocyte hypertrophy without disarray or bundles of myocytes.” How would you advise these patients regarding screening and surveillance? Listen to #CardsRounds for the full details!

 Quotes from Case #1:

“Let’s take a walk down memory lane and let’s get to our evolution of understanding hypertrophic cardiomyopathy… [our understanding] follows the parable of the six blind men and the elephant. Each of the six blind man approached it from different angles, its tusk, its ear, its tail, and they all try to convince each other what an elephant is … because none of them can see the big picture.”

• Dr. Kittleson on the history of HCM and coming to a unifying diagnosis

 “The next time you are sitting there mashing your teeth because you have to memorize what the HCM murmur does squat to stand, Valsalva, or handgrip … remember you are standing on the shoulder of Giants. They [Drs. Braunwald and Morrow] pioneered surgical myectomy based on physical exam and cath lab findings”

• Dr. Kittleson on the physical exam guiding HCM management

Takeaways from Case #1

Before we round, we think it is important to get on the same page regarding the nomenclature around HCM.

1. Since the original characterization of hypertrophic cardiomyopathy (HCM) more than 60 years ago (see the Braunwald Chronicles for the origin stories!), different terms have been used to describe the disease. These include idiopathic hypertrophic subaortic stenosis, hypertrophic obstructive cardiomyopathy (HoCM), and “burnt out HCM” when heart failure develops.
2. The 2020 guideline committee recommended a common language to avoid confusion: since left ventricular (LV) outflow tract obstruction (LVOTO) occurs in >60% of patients over time, but one-third remain non-obstructive, the recommendation is t0 call the disease state HCM with or without outflow tract obstruction.
3. Dr. Kittleson added that when heart failure develops we should characterize the pathology as HCM with heart failure rather than “burnt out HCM.”

 Do we use HCM to describe any LV that has thick walls?

• Some clinicians will use HCM to describe all disease states that can lead to increased LV wall thickness, including those associated with systemic disorders such as RASopathies, mitochondrial myopathies, glycogen/lysosomal storage diseases, Fabry’s disease, hemochromatosis, Danon disease, and amyloidosis (especially in adults).
• However, the pathophysiologic mechanisms, genetic underpinnings, and treatment of these diseases are different. Secondary causes of left ventricular hypertrophy (LVH) – such as athlete’s heart and hypertensive disorders – can also cause confusion with identifying the correct terminology and diagnosis.
• As Dr. Kittleson (and the guidelines) made clear, the clinical definition of HCM is a disease state in which (1) the morphologic expression is restricted to the heart, characterized primarily by LVH in the absence of another systemic; (2) a metabolic or cardiac cause; (3) and for which a disease-causing sarcomere (or sarcomere-related) variant is identified or genetic etiology remains undetermined.
• See some of our original CardioNerds episodes to review the clinical manifestations, diagnosis and treatment of HCM!

Ok. We are with you on the terminology! But as you mentioned there are many disease states that can look like HCM. What are phenocopies?

1. As alluded to above, there are multiple genes that can lead to the phenotypic appearance of HCM, but rather these are “phenocopies” masquerading as HCM.
2. Dr. Kittleson noted that many of these phenocopies are diagnosed in childhood (e.g., glycogen storage diseases, Friedrich ataxia, Danon disease); however, for adult cardiologists, particular attention should be given to recognizing amyloidosis (see our Amyloidosis page).
3. We should remain alert for “LVH+” states: when we see left ventricular hypertrophy but also systemic signs including peripheral neuropathy, renal dysfunction, and skin changes, which could clue us into a systemic pathology like Amyloidosis. After all, Imitation is the sincerest form of flattery!
4. The classic pathologic findings of HCM include myocyte disarray (where individual cardiomyocytes vary in size, shape and form), abnormal intercellular connections, expansion of the interstitial compartment and areas of replacement fibrosis, and small vessel disease (in which intramural vessels are narrowed by medial hypertrophy).

So back to this case. It is possible the patients’ mother had a HCM phenocopy. And the pathology was not classic for HCM. What do the guidelines say regarding genetic screening in general?

1. It was not until the 1990s when DNA sequencing of HCM pedigrees led to the discovery of variants in genes coding for sarcomere proteins were co-inherited in patients with LVH. Thus, HCM since has been regarded as a monogenic cardiac disease.
2. The two most common genes with damaging variants are beta myosin heavy chain (MYH7) and myosin-binding protein C3 (MYBPC3).70% of variant-positive patients have gene variants in these genes; however, it is important to recognize that many patients with HCM are currently without any identifiable pathogenic genetic etiology to their disease (40 to 60% of patients depending on the study).
3. Thus, genetic testing is crucial to the diagnosis and management of HCM, especially to inform cascade testing in family member and preconception and prenatal genetic counseling. As has been discussed previously on the CardioNerds podcast, appropriate pre- and post-test genetic counseling is necessary to ensure patients and their families understand the medical, social, psychological, ethical and professional implications of having a genetic disease, underscoring the value of multidisciplinary HCM centers.

How do we apply the guidelines regarding genetic screening to our patients?

• As was done in this case, a detailed family history of at least three generations regarding HCM and SCD events should be taken. Typically, genetic testing for HCM is first done in the family member with clear phenotypic evidence of HCM – the index case. The 2020 ACC/AHA HCM guidelines nicely outline subsequent testing based on whether a variant is pathologic (Figure 1) Please remember to review the Guidelines yourself as it is a comprehensive text that provides key details not covered here!
• However, the index case could not afford genetic testing and the pathology available to us was not definitive for HCM. Postmortem testing for HCM-associated variants using blood or tissue samples collected at autopsy is possible, but access to a molecular autopsy and insurance coverage can vary significantly based on jurisdiction.
• Our patients (the brothers in their 20s) were arriving without genetics to inform their screening. In this circumstance we utilize Figure 2 (below) from the guidelines and would consider the index patient (the mother) phenotype negative. And since no variant was identified in the index patient, we would likely offer screening ECG/Echo (or cardiac MRI) to the brothers and follow up with clinical surveillance with imaging/ECG every 3-5 years.

How do we decide if a variant is pathogenic?

1. The pathogenicity of variants is based on American College of Medical Genetics and Genomics criteria and can actually change over time. As Dr. Kittleson noted, there are fewer quality genetic data in non-white HCM populations.
2. The five highest frequency variants for HCM in the Human Gene Mutation Database of the NHLBI Exome sequencing Project were more frequent in Black Americans vs. White Americans which could lead to false positive diagnoses of HCM in Blacks. Furthermore, a lack of diverse racial/ethnic control populations could lead to a misclassification of benign variants
3. As Dr. Kittleson noted on #CardsRounds, this again highlights the importance of multidisciplinary HCM clinics that have the expertise to periodically re-evaluate the pathogenicity of variants. If they a particular variant has been reclassified (either upgraded or downgraded), it would affect cascade testing and clinical surveillance in families.

Case #2 Synopsis:

In this second case on HCM #CardsRounds, we saw a young woman in her 20s who was seeking a 2nd opinion regarding primary prevention ICD. She was diagnosed with HCM three years ago after a murmur was discovered on exam. Her echo demonstrated a septal wall thickness of 1.9 cm, LVOT gradient at 23 mmHg at baseline and 126 mmHg with treadmill stress. She was eventually referred for myectomy where 11 grams of myocardium was resected and her gradients improved significantly. She did well for two years and then had multiple syncopal episodes in the setting of a GI illness. Her repeat echo showed a maximal wall thickness of 2.6 cm, no LVOT obstruction at rest or provocation. She was referred for an ICD but wanted a 2nd opinion. You discover she does have a likely pathologic variant in the MYH7 gene, and both her mother and son have the variant. Her mother had NSVT and so will be receiving an ICD. She had a maternal half-brother who passed away from possible overdose but autopsy was suggestive of HCM (with genetic testing still in the works). She underwent a 7-day Holter with no NSVT. Just before this visit she had an MRI which suggested 8-12% late gadolinium enhancement, a hypertrophied septum and LV apical wall thinning (likely not a true aneurysm).

Case #2 Quotes:

“Let’s talk about Sudden Death risk stratification in HCM, or basically, how do you predict the future?”

• Dr. Kittleson reviewing the 2020 guidelines

 “If something doesn’t make sense. You go to the source! Speak to your whole team. Help me, help you, help the patient!”

• Dr. Kittleson On utilizing multidisciplinary HCM team to inform patient care

 “One fantastic component of the 2020 HCM guidelines is the explicit recommendation for shared decision-making with a full disclosure of risks, benefits, anticipated outcomes and the patient expresses their goals and concerns. But let us not forget, that shared decision-making is not an excuse to abdicate medical decision making. It is still your responsibility to provide a medical recommendation … and then work with the patient to see how that medical opinion fits in with the patient’s values and goals.”

• Dr. Kittleson on shared decision-making on ICD placement

 Takeaways Case #2

How do we make a decision for ICD in HCM patients? How do the new guidelines differ?

1. HCM is considered the most common cause of SCD in young people in North America, and thus much research has gone into defining the clinical features that would justify a primary prevention ICD in HCM patients.
2. There are important differences between the 2011 and 2020 guidelines in regards to clinical factors to consider, as outlined below.
3. Similar in Both Guidelines (Typically applying to Adults <60 years old*)
   1. A history of sudden cardiac death, ventricular fibrillation or sustained VT is a Class I indication for secondary prevention ICD in patients with HCM in both guidelines.
   1. Family history of SCD from HCM (Class IIa in 20211 and 2020) is defined as sudden death attributable (or likely attributable) to HCM in ≥ 1 first-degree or close relatives who are ≤ 50 years of age. Close relatives are generally considered to be second-degree relatives.
   1. Massive LVH (Class IIa in 2011 and 2020), in adults patients is defined as wall thickness ≥ 30 mm in any segment by echo or cardiac MRI
   1. Unexplained Syncope (Class IIa in 2011 and 2020) is defined as ≥ 1 unexplained episodes of syncope, unlikely to be of neurocardiogenic etiology or attributable to LVOTO
   1. Apical Aneurysm (Class IIa in 2011 and 2020) is defined as a discrete thin-walled dyskinetic or akinetic segment of the most distal portion of the LV
4. Differences in the Guidelines (Typically applying to Adults <60 years old*)
   1. Previously in the 2011 guidelines, the presence of abnormal BP response to exercise + either (1) genetic mutations and/or (2) LVOTO > 30 mmHg was considered a Class IIa indication for an ICD. These criteria have been removed from the 2020 guidelines.
   1. In the 2020 guidelines, there is a new emphasis on systolic dysfunction with EF < 50% by echo or cardiac MRI, and it is given a Class IIa indication for an ICD.
   1. NSVT – defined as frequent (≥3), longer (≥10 beats), and fast (≥200 bpm) occurring usually over 24 to 48 hours – was a Class IIa indication for an ICD in the 2011 guidelines and has been de-emphasized in the 2020 guidelines as a Class IIb.
   1. Extensive late gadolinium enhancement (LGE) on CMR is defined as diffuse and extensive LGE quantified or estimated as compromising ≥ 15% of the LV mass

 How often should we screen for clinical factors that would increase risk for SCD? What are some nuances we should be aware of?

1. As with most decisions in medicine, the patient should be at the center of the decision-making process regarding ICD. For some patients, they may want a quantifiable estimate of their SCD risk, which can be estimated with a 5-year SCD Risk Calculator. Of note, certain contemporary SCD risk markers are not included in these calculators, including systolic dysfunction, LGE on MRI, or LV apical aneurysm.
2. SCD risk assessment should occur at the initial visit and then be repeated every 1 to 2 years as part of the ongoing clinical surveillance of HCM. Of note, the data suggests a lower SCD event rate in older patients with HCM (>60 years of age), and thus the decision regarding continuing risk assessment in this population is individualized.
3. As noted above, several criteria are dependent on imaging – including LV wall thickness. This may be underestimated on echocardiography compared to cardiac MRI and MRI adds the additional component of assessing LGE

 Based on the above criteria, how would you advise our patient?

1. She does not meet a Class I indication for ICD.
2. In regards to Class IIa recommendations, she does not have massive LVH, unexplained syncope, likely does not have an apical aneurysm, and has a normal LVEF.
3. The family history is questionable given her half-brother’s death under unclear circumstances with morphologic evidence of HCM on autopsy. Given the concerning family history, she may have a Class IIa reason to pursue an ICD.
4. However, she also does not have NSVT and does not have extensive LGE – though this is in the setting of being post-surgical myectomy.
5. After shared-decision making, given the constellation of findings it would be reasonable to offer her an ICD.

Case #3 Synopsis:

A woman in her early 30s comes to an HCM Center of Excellence to establish care. She was diagnosed with HCM without obstruction one year prior. She initially presented with exertional dyspnea, and eventually MRI revealed HCM without obstruction, maximal wall thickness with 2.5 cm and no LGE. Her father passed away at age 50 from an “MI.” Her genotyping was negative. Soon after she was having recurrent episodes of syncope and a loop recorder was placed. She came for follow was now 4 months pregnant. Just before the visit she felt pre-syncopal and Loop revealed SVT at rates of 150s. Then at 6 months pregnant, patient had one 10-beat run of NSVT at rate of 180 bpm. How would you advise this patient?

 Case #3 Quotes:

“One of my most important ways of preventing burnout in medicine – is to phone a friend, to ask for help, to talk about cases with trusted colleagues.”

• Dr. Kittleson on how to approach complex cases

Case #3 Takeaways:

 How does HCM care differ in pregnant patients per the guidelines?

1. In most pregnant women with HCM, selected beta-blockers should be given for symptoms related to LVOTO or arrhythmias with monitoring of fetal growth (Class I). Note atenolol has some evidence of potential fetal risk.
2. In terms of delivery, Valsalva during labor has generally been shown to be well tolerated. Cesarean section should typically only be done for obstetric reasons or for emergency cardiac/maternal reasons. As discussed in our Cardio-Ob series, a delivery plan should be developed by a multi-disciplinary team by the end of the second trimester
3. Most antiarrhythmic medications are contraindicated during pregnancy because of the potential teratogenic effects, and typically many are not recommended for patients with HCM. Cardioversion can typically be performed safely in pregnancy with minimal risk to the fetus and thus may be preferred for restoring sinus rhythm in symptomatic pregnant women with HCM.

How would you advise this patient regarding ICD?

1. It appears she may have a Class IIa recommendation for ICD if you believe the family history is actually positive for sudden cardiac death, otherwise she likely does not have an indication for ICD. The NSVT was present but it was one episode, not at a fast rate (<200 bpm) and thus likely does not reach to the level of recommending an ICD. Furthermore, the syncope appears attributable to SVT rather than ventricular arrhythmia.
2. Implantation ICD for primary prevention can typically wait until after pregnancy

Figure 1:

Figure 2

1. Ommen SR, Mital S, Burke MA et al. 2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2020 Dec 22;142(25):e558-e631. doi: 10.1161/CIR.0000000000000937. Epub 2020 Nov 20. Erratum in: Circulation. 2020 Dec 22;142(25):e633. PMID: 33215931.
2. Maron BJ. Clinical Course and Management of Hypertrophic Cardiomyopathy. N Engl J Med. 2018 Aug 16;379(7):655-668. doi: 10.1056/NEJMra1710575. PMID: 30110588.
3. Manrai AK, Funke BH, Rehm HL et al. Genetic Misdiagnoses and the Potential for Health Disparities. N Engl J Med. 2016 Aug 18;375(7):655-65. doi: 10.1056/NEJMsa1507092. PMID: 27532831; PMCID: PMC5292722.
4. Gersh BJ, Maron BJ, Bonow RO, et al. 2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Developed in collaboration with the American Association for Thoracic Surgery, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2011 Dec 13;58(25):e212-60. doi: 10.1016/j.jacc.2011.06.011. Epub 2011 Nov 8. PMID: 22075469.
5. Maron BJ, Casey SA, Olivotto I et al. Clinical Course and Quality of Life in High-Risk Patients With Hypertrophic Cardiomyopathy and Implantable Cardioverter-Defibrillators. Circ Arrhythm Electrophysiol. 2018 Apr;11(4):e005820. doi: 10.1161/CIRCEP.117.005820. PMID: 29625970.

• Karan Desai, MD
• Natalie Stokes, MD
• Amit Goyal, MD
• Daniel Ambinder, MD