CardioNerds (Amit and Dan) join Dr. Maria Pabon (cardiology fellow), Dr. Kevin Bersell (cardiology fellow), Dr. Saad Sultan Ghumman (interventional cardiology fellow), and Dr. Rhanderson Cardoso (cardiovascular imaging fellow) from Brigham and Women’s Hospital. Together, they explore a complex case of STEMI that was further complicated by ventricular free wall rupture. Additionally, Dr. Ajar Kochar, Program Director for Interventional Cardiology at Brigham and Women's Hospital, provides an insightful "ECPR" segment, adding a unique perspective to the case. Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah.

This is the case of a patient who presented with STEMI and was found to have a moderate pericardial effusion with echogenic material within the pericardial space concerning for thrombus. Urgent CTA/CT surgery was engaged due to concern for dissection, but no evidence of dissection, rupture or intramural hematoma was found. The patient underwent an urgent pericardiocentesis which yielded 350cc of hemorrhagic fluid, leading to an improvement in hemodynamic status. A coronary angiogram was performed which showed a 100% thrombotic occlusion of OM 1, the culprit lesion for the STEMI. Due to the possibility of a delayed STEMI and high suspicion for mechanical complication of MI, aspirin and IV cangrelor were chosen as the preferred antiplatelet strategy. However, cangrelor was held and cardiac surgery was consulted, as LV free wall rupture was suspected. The patient underwent urgent repair of the LV free wall rupture, with an uneventful post-op recovery and discharge on day 8 to cardiac rehab.

CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ).

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Case Media

Pearls - When Infarction Brings the Walls Down - Brigham and Women’s Hospital

In the era of primary PCI, mechanical complications of MI are relatively rare.

Timely recognition using multi-modality imaging and prompt surgical intervention can result in favorable outcomes.

An approach that involves a Heart Team can be advantageous in optimizing outcomes in such complex cases.

Show Notes - When Infarction Brings the Walls Down - Brigham and Women’s Hospital

Incidence of post AMI LV free wall rupture:

0.1-1%

Risk factors for LV Free wall Rupture:

Older age

Female sex

Prior HTN

1st lateral or Anterior Wall MI

Protective factors towards free wall rupture:

LV hypertrophy

CHF

Hx of prior infarcts

Chronic ischemic heart disease

Early use of beta blockers post MI

Timely intervention

Incidence of Mortality associated with mechanical rupture related to AMI:

8-10%

When to suspect a mechanical complication of AMI:

AMI with shock/hypotension

New murmur

New pericardial effusion > 10mm on bedside echo

Other etiologies that can cause free wall rupture:

Trauma

Cardiac infection

Aortic dissection

Cardiac tumors

Infiltrative diseases

Iatrogenic from PCI or surgical procedures

References - When Infarction Brings the Walls Down - Brigham and Women’s Hospital

Varghese S, Ohlow MA. Left ventricular free wall rupture in myocardial infarction: A retrospective analysis from a single tertiary center. JRSM Cardiovasc Dis. 2019 Jan-Dec;8:2048004019896692. doi: 10.1177/2048004019896692. PMID: 31970072.

Pineda-De Paz, D.O.,

CardioNerds (Dr. Amit Goyal), Dr. Sonu Abraham (CardioNerds Ambassador from Lahey Hospital and Medical Center, Burlington, MA) discuss left ventricular assist devices (LVAD) and the implications of renal dysfunction with Dr. Brian Houston and Dr. Nisha Bansal. This episode will focus on the intersection of left ventricular assist devices and renal dysfunction. Patients with a combination of heart failure and renal dysfunction overall have a guarded prognosis and their management poses unique challenges to the clinician. We initially discuss the basics of an LVAD and general approach to LVAD candidacy evaluation. We then discuss specific implications of acute kidney injury, presence of preexisting CKD, and end stage renal disease in patients with/being considered for an LVAD. Risk factor identification and prognostication allows for appropriate selection of the right candidates for an LVAD in the context of renal disease. Dr. Brian Houston is the Director of the Mechanical Circulatory Support program at Medical University of South Carolina. Dr. Nisha Bansal is an Associate Professor and the Arthur Stach Family Endowed Professor in the Division of Nephrology, an investigator at the Kidney Research Institute, the Director of Nephrology Clinical and Research Education, and the Director of the Kidney-Heart Service at the University of Washington. Notes were drafted by Dr. Sonu Abraham and episode audio was edited by student Dr. Chelsea Amo-Tweneboah.

Check out the CardioNerds Failure Heart Success Series Page for more heart success episodes and content!

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Pearls - Left Ventricular Assist Devices and Renal Dysfunction

End stage renal disease (CKD on dialysis) is considered an absolute contraindication for LVAD implantation. Select young patients who are being considered for heart-kidney transplantation in the near future may be candidates for an LVAD as a bridge to heart-kidney transplantation.

LVAD implantation can improve kidney function in the short term in patients with AKI primarily caused by cardio-renal syndrome.

Patients with pre-existing CKD (not dialysis dependent) have a greater risk of developing AKI after LVAD implantation.  

Several dialysis modalities including in-center hemodialysis, home hemodialysis, and peritoneal dialysis are available for LVAD patients. However, there are several challenges associated with each modality.

An AV graft is a useful vascular access option in LVAD patients undergoing hemodialysis due to a lower risk of infection and ease of immediate use.

Causes for anemia in patients with an LVAD and renal dysfunction include anemia of chronic disease, gastrointestinal bleeding, and pump thrombosis leading to hemolysis.

Show notes - Left Ventricular Assist Devices and Renal Dysfunction

Notes: (drafted by Dr. Sonu Abraham)

What is a left ventricular assist device (LVAD) and what are its components?

An LVAD supports circulation by unloading the left ventricle and providing increased cardiac output to help support organ perfusion. Use in properly selected patients is associated with improved quality of life and increased survival. The current iteration of LVADs offer continuous flow, as opposed to the older versions which employed pulsatile flow.

Components of the LVAD:

Inflow cannula (sucks blood from the LV)

Pump

Outflow cannula (dumps blood into the aorta)

Percutaneous driveline

Electrical controller

How is a patient evaluated for LVAD candidacy?

The 2 main questions to be answered during the evaluation of a patient for an LVAD are:

            1. Are they sick enough? Do they have end stage heart failure?

            2. Do we expect the benefits of an LVAD to outweigh the risks?

...

CardioNerds (Amit and Dan) join Dr. Khaled Abdelrahman, Dr. Gurleen Kaur, and Dr. Danny Pipilas from the Brigham and Women’s Hospital Residency Program for Italian food and cannolis at the North End in Boston as they discuss the case of an elderly man with primary cardiac lymphoma. They review an approach to intracardiac masses, discuss advantages and disadvantages of various imaging modalities for the evaluation of intracardiac masses, and also delve into anthracycline toxicity. The E-CPR segment is provided by Dr. Ron Blankstein, Associate Director of the Cardiovascular Imaging Program and Director of Cardiac Computed Tomography at Brigham and Women’s Hospital. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig.

A 76-year-old man with a history of hyperlipidemia presented with one month of progressively worsening fatigue, weight loss, and dyspnea on exertion. Physical exam was notable for a 3/6 systolic murmur at the left upper sternal border, a flopping sound along the sternum heard throughout the cardiac cycle, and JVP elevated to the level of the mandible. TTE revealed a large heterogeneous echodensity in the right ventricular (RV) free wall that extended into the pericardium and into the RV myocardium with mobile components in the RV cavity and obstruction of the RV outflow tract. Nongated CT chest showed a solid nodule in the periphery of the left lower lung lobe. Gated cardiac CTA revealed a large heterogenous mass in the right atrioventricular groove that encased the proximal thoracic aorta and pulmonary artery and invaded the RV myocardium and RV outflow tract along with a large pericardial effusion. On cardiac MRI, the mass was isointense to the myocardium on T1-weighted images, hyperintense on T2-weighted images, and had heterogenous enhancement on late gadolinium enhancement images. Overall, the imaging findings were highly suspicious for cardiac lymphoma which was confirmed with biopsy of the lung nodule; pathology showed a large B cell lymphoma. The patient was treated with R-CHOP therapy (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone), and TTE after 6 cycles of chemotherapy demonstrated resolution of the RV mass.

CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ).

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Case Media

1.  There is a large homogeneous mass in the right atrioventricular groove that extends anterior to the right ventricular outflow tract, pulmonary artery, and ascending aorta, measuring up to 9.4 x 7.1 cm (axial) x 13 cm (craniocaudal). The mass encases the proximal thoracic aorta and pulmonary artery. The mass invades the right ventricular myocardium, the right ventricular outflow tract, the pulmonary artery, and proximal main pulmonary artery. There is severe stenosis of the right ventricular outflow tract due to obstruction by the mass. The mass encases the right coronary artery, without compression of the artery. There is enhancement of this mass on delayed contrast imaging. Collectively, these findings suggest cardiac lymphoma. 2.  There is a large pericardial effusion, circumferential, measuring up to 2.2 cm adjacent to the right atrium and up to 2.3 cm anterior to the intraventricular septum. There is pericardial enhancement, indicative of pericardial inflammation. 3.  This study was not optimized for the assessment of the coronary arteries. However,

CardioNerds co-founder Amit Goyal, Dr. Dinu Balanescu, Dr. Teodora Donisan, and Dr. Anjali Agarwalla get the cardiologist perspective of Cancer Therapy-Related Cardiac Dysfunction (CTRCD) from Dr. Joerg Hermann. We previously learned from the oncologist perspective with Dr. Susan Dent in Episode #261! In this episode, we discuss the history of cancer therapies and our developing understanding of how these life-saving medications can cause cardiac toxicities. As we manage patients in the CardioNerds CardioOncology clinic, we ask Dr. Hermann how the general cardiologist should approach patients with a cancer diagnosis, when should a patient be referred to a cardiooncology specialist, and what are the common cardiotoxicities to look out for. We’ll also place a quick consult to our guest expert’s goldendoodle! Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah.

This episode is supported by a grant from Pfizer Inc.

This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. 

Pearls • Notes • References • Production Team

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Pearls and Quotes - Cancer Therapy-Related Cardiac Dysfunction (CTRCD) – The Cardiologist Perspective with Dr. Joerg Hermann

Patients with malignancy will incur several “hits” in addition to their malignancy and its subsequent treatment — these include their genetics, environment, and comorbidities. The role of the cardiologist is to identify how the combination of these “hits” can bring cardiovascular disease to the forefront and where we can intervene upon it.

The sooner we recognize cardiotoxicity, the better the outcome for our patients. Patients should receive baseline risk assessment with TTE and biomarkers with routine surveillance.

You cannot assign a percentage to cardiac risk in cancer. Patients require a multidisciplinary approach with constant monitoring and surveillance.

Consider exercise testing when conducting pre-treatment risk assessment and during monitoring. Peak VO2 abnormalities is often the first marker of cardiotoxicity — though note that it correlates well with global longitudinal strain (GLS).

If someone develops a cardiovascular complication of chemotherapy, this should prompt referral to cardiooncology.

Show notes - Cancer Therapy-Related Cardiac Dysfunction (CTRCD) – The Cardiologist Perspective with Dr. Joerg Hermann

What types of cardiovascular pathology occur in the setting of cancer and its treatment?

We conventionally thought of cardiotoxicities as being of two types:

Type 1: irreversible cardiac injury that does not improve despite withdrawal of offending chemotherapeutic (protype = classic anthracycline cardiotoxicity)

Type 2: reversible cardiac dysfunction that improves with discontinuation of chemotherapeutic (prototype = classic traztuzumab cardiotoxicity)

However, we have begun moving away from this thought process as it has become more evident that injuries historically thought of as “type 1” may not be as relentless as previously understood, and that patients with type 2 dysfunction may not actually be returning to completely normal after the offending agent is withdrawn. As such, this episode proposes two other ways to frame our understanding of cardiotoxicities: a clinical/practical approach, based on symptoms (symptomatic vs asymptomatic — this is the approach used by the ESC guidelines), and a mechanistic approach: direct effect on cardiac myocytes, indirect effects (e.g., effect on coronaries), and inflammatory effects.

Join CardioNerds Co-Founder Dr. Dan Ambinder, Dr. Nino Isakadze (EP Fellow at Johns Hopkins Hospital), Dr. Karan Desai (Cardiology Faculty at Johns Hopkins Hospital and Johns Hopkins Bayview) and student Dr. Shivani Reddy (Medical Student at Western Michigan University Homer Stryker SOM), as they discuss how digital health in changing the landscape of CV Disease Management with Dr. Dipti Itchhaporia (Past President of the ACC). The overall goal of this episode is to broadly describe the current landscape of digital health for cardiovascular disease, define “digital health tools” and describe their role in cardiovascular disease management. Episode audio was edited by student Dr. Shivani Reddy and show notes were developed by Dr. Nino Isakadze.

In this series, supported by an ACC Chapter Grant and in collaboration with Corrie Health, we hope to provide all CardioNerds out there a primer on the role of digital heath in cardiovascular medicine. Use of versatile hardware and software devices is skyrocketing in everyday life. This provides unique platforms to support healthcare management outside the walls of the hospital for patients with or at risk for cardiovascular disease. In addition, evolution of artificial intelligence, machine learning, and telemedicine is augmenting clinical decision making at a new level fueling a revolution in cardiovascular disease care delivery. Digital health has the potential to bridge the gap in healthcare access, lower costs of healthcare and promote equitable delivery of evidence-based care to patients.

This CardioNerds Digital Health series is made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Nino Isakadze and Dr. Karan Desai.  

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

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Pearls and Quotes

COVID 19 pandemic accelerated the digital transformation of healthcare.

Digital health tools exist for disease prediction, diagnosis and management.

Digital health can increase access to care and lower overall cost expenditure.

Clinicians, policy makers, and insurance providers should be involved to facilitate rapid and effective adoption of digital health interventions to better patient and population health.

Notes

1. How did the COVID-19 pandemic accelerate the process of adopting digital health tools in healthcare including cardiovascular disease management?

Although technological advances and technological transformation have been implemented in many aspects of our lives, their adoption in healthcare, including cardiovascular disease management has lagged behind.

The COVID-19 pandemic was a force that led to the Tech-celeration as we adopted telemedicine and remote patient monitoring platforms in a short time to preserve access to healthcare.

Technology became essential not to replace but to support face to face interactions.

Reimbursement models were rapidly created that fit digital healthcare delivery; however it remains unclear whether these models will continue to be in effect in the post pandemic era.

2.  Can you discuss broadly the current landscape of evidence-based digital health tools available for cardiovascular disease management?

Three components of digital health landscape can be broken down as follows:Virtual care/telehealth platformsRemote patient monitoring systems including implanted devices, patches, wearables, smartphone applications and more

Artificial intelligence to allow meaningful use of the big data obtained from remote patient monitoring systems in therapeutic and disease management pathways

   3.

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.

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. 

Challenging Cases - Atrial Fibrillation with Dr. Hugh Calkins

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Show notes - Hemodynamics and Mechanical Circulatory Support

Case Synopsis:

Case SynopsisWe 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

Dr. Burkhoff took us through the hemodynamics of VSR with pressure-volume loops to better understand the pathology and impact of various MCS options. Of note, there are no MCS devices specifically approved to treat acute ventricular septal rupture.

In regards to the acute hemodynamic effects of a VSR (an abrupt left to right shunt), there are several aspects to note. First, the effective LV afterload is reduced; however, there is less “forward flow” as well and as a consequence, decreased left-sided cardiac output (“Qs”) and blood pressure. At the same time, flow through the pulmonary artery increases (the “Qp”). Additionally, due to the abrupt shunt flow, there is increased RV “loading” with increasing central venous pressure and pulmonary artery pressure.

The hemodynamic priorities in treating patients with cardiogenic shock and VSR are to normalize blood pressure, cardiac output, and oxygen delivery, while attempting to minimize shunt flow to allow healing. However, medications and MCS are unlikely to completely normalize hemodynamics. For instance, if the patient was placed on peripheral VA ECMO, while total CO and BP may increase, flow across the VSR could also increase at high ECMO flows (e.g., by introducing more LV afterload).

In patients with persistent cardiogenic shock and VSR, short-term MCS to divert flow away from the shunt can be an effective strategy. LV-to-aorta or LA-to-arterial MCS may provide the best single-device hemodynamic profiles by decreasing shunt flow, reducing pulmonary capillary wedge pressure, and improving blood pressure.

Surgical and percutaneous VSD repair are the definitive treatment options. If able to stabilize patients and pursue delayed repair,

The following question refers to Section 9.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. 

The question is asked by Western Michigan University medical student & CardioNerds Intern Shivani Reddy, answered first by Brigham & Women’s medicine resident and Director of CardioNerds Internship Dr. Gurleen Kaur, and then by expert faculty Dr. Shashank Sinha.

Dr. Sinha is an Assistant Professor of Medical Education at the University of Virginia School of Medicine and an advanced heart failure, MCS, and transplant cardiologist at Inova Fairfax Medical Campus. He currently serves as both the Director of the Cardiac Intensive Care Unit and Cardiovascular Critical Care Research Program at Inova Fairfax. He is also a Steering Committee member for the multicenter Cardiogenic Shock Working Group and Critical Care Cardiology Trials Network and an Associate Editor for the Journal of Cardiac Failure, the official Journal of the Heart Failure Society of America.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

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

Question #12

Mr. Shock is a 65-year-old man with a history of hypertension and non-ischemic cardiomyopathy (LVEF 25%) who is admitted with acute decompensated heart failure. He is currently being diuresed with a bumetanide drip, but is only making 20 cc/hour of urine. On exam, blood pressure is 85/68 mmHg and heart rate is 110 bpm. His JVP is at 12 cm and extremities are cool with thready pulses. Bloodwork is notable for a lactate of 3.5 mmol/L and creatinine of 2.5 mg/dL (baseline Cr 1.2 mg/dL). What is the most appropriate next step?

A

Augment diuresis with metolazone

B

Start sodium nitroprusside

C

Start dobutamine

D

Start oral metoprolol

E

None of the above

Answer #12

Explanation

The correct answer is C – start dobutamine.

 

In this scenario, the patient is in cardiogenic shock given hypotension and evidence of end-organ hypoperfusion on exam and labs. The patient’s cool extremities, low urine output, elevated lactate, and elevated creatinine all point towards hypoperfusion.

 

In patients with cardiogenic shock, intravenous inotropic support should be used to maintain systemic perfusion and preserve end-organ function (Class 1, LOE B-NR). Further, in patients with cardiogenic shock whose end-organ function cannot be maintained by pharmacologic means, temporary MCS is reasonable to support cardiac function (Class 2a, LOE B-NR).

 

The SCAI Cardiogenic Shock Criteria can be used to divide patients into stages. Stage A is a patient at risk for cardiogenic shock but currently not with any signs or symptoms, for example, a patient presenting with a myocardial infarction without present evidence of shock. Stage B is “pre-shock” – this may be a patient who has volume overload, tachycardia, and hypotension but does not have hypoperfusion based on exam and lab evaluation. Stage C is classic cardiogenic shock – the cold and wet profile. Bedside findings for Stage C shock include cool extremities, weak pulses, altered mental status, decreased urine output, and/or respiratory distress. Lab findings include impaired renal function, increased lactate, increased hepatic enzymes, and/or acidosis. Stage D is deteriorating with worsening hypotension and hypoperfusion with escalating use of pressors or mechanical circulatory support.

The following question refers to Section 8.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. 

The question is asked by Western Michigan University medical student & CardioNerds Intern Shivani Reddy, answered first by Brigham & Women’s medicine resident and Director of CardioNerds Internship Dr. Gurleen Kaur, and then by expert faculty Dr. Prateeti Khazanie.

Dr. Khazanie is an Associate Professor and Advanced Heart Failure and Transplant Cardiologist at the University of Colorado. She was an undergraduate at Duke University as a B.N. Duke Scholar. She spent two years at the NIH in the lab of Dr. Anthony Fauci and completed a dual MD-MPH program at Duke Medical School. When she started residency, she thought she was going to be an ID doctor, but she fell in love with cardiology at Stanford where she was an intern, resident, and then chief resident. She went back to Duke for her general cardiology and advanced heart failure/transplant fellowships as well as research training at the DCRI. Dr. Khazanie joined the University of Colorado in 2015 as a health services clinician researcher with a focus on improving health equity and bioethics in advanced heart failure care. She mentors medical students, residents, and fellows and is a faculty mentor for the University of Colorado Cardiology Fellows “House of Cards” mentoring group. She has research funding from the NIH/NHLBI K23, NIH Ethics Grant, and Ludeman Center for Women’s Health Research. Dr. Khazanie is an author on the 2022 ACC/AHA/HFSA HF Guidelines, the 2021 HFSA Universal Definition of Heart Failure, and multiple scientific statements.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

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

Question #11

A 64-year-old woman with a history of chronic systolic heart failure secondary to NICM (LVEF 15-20%) s/p dual chamber ICD presents for routine follow-up. She reports several months of progressive fatigue, dyspnea, and peripheral edema. She has been hospitalized twice in the past year with acute decompensated heart failure. Efforts to optimize guideline directed medical therapy have been tempered by episodes of lightheadedness and hypotension. Her exam is notable for an elevated JVP, an S3 heart sound, and a III/VI holosystolic murmur best heard at the apex with radiation to the axilla. Labs show Na 130 mmol/L, Cr 1.8 mg/dL (from 1.1 mg/dL 6 months prior), and NT-proBNP 1,200 pg/mL. ECG in clinic shows sinus rhythm and a nonspecific IVCD with QRS 116 ms. Her most recent TTE shows biventricular dilation with LVEF 15-20%, moderate functional MR, moderate functional TR and estimated RVSP of 40mmHg. What is the most appropriate next step in management?

A

Refer to electrophysiology for upgrade to CRT-D

B

Increase sacubitril-valsartan dose

C

Refer for advanced therapies evaluation

D

Start treatment with milrinone infusion

Answer #11

Explanation

The correct answer is C – refer for advanced therapies evaluation.

Our patient has multiple signs and symptoms of advanced heart failure including NYHA Class III-IV functional status, persistently elevated natriuretic peptides, severely reduced LVEF, evidence of end organ dysfunction, multiple hospitalizations for ADHF, edema despite escalating doses of diuretics, and progressive intolerance to GDMT. Importantly, the 2018 European Society of Cardiology revised definition of advanced HF focuses...

The following question refers to Section 7.7 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by St. George's University medical student and CardioNerds Intern Chelsea Tweneboah, answered first by Baylor College of Medicine Cardiology Fellow and CardioNerds Ambassador Dr. Jamal Mahar, and then by expert faculty Dr. Michelle Kittleson.Dr. Kittleson is Director of Education in Heart Failure and Transplantation, Director of Heart Failure Research, and Professor of Medicine at the Smidt Heart Institute, Cedars-Sinai. She is Deputy Editor of the Journal of Heart and Lung Transplantation, on Guideline Writing Committees for the American College of Cardiology (ACC)/American Heart Association, is the Co Editor-in-Chief for the ACC Heart Failure Self-Assessment Program, and on the Board of Directors for the Heart Failure Society of America. Her Clinician’s Guide to the 2022 Heart Failure guidelines, published in the Journal of Cardiac Failure, are a must-read for everyone!The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #10

Ms. Heffpefner is a 54-year-old woman who comes to your office for a routine visit. She does report increased fatigue and dyspnea on exertion without new orthopnea or extremity edema. She was previously diagnosed with type 2 diabetes, morbid obesity, obstructive sleep apnea, and TIA. She is currently prescribed metformin 1000mg twice daily, aspirin 81mg daily, rosuvastatin 40mg nightly, and furosemide 40mg daily. In clinic, her BP is 140/85 mmHg, HR is 110/min (rhythm irregularly irregular, found to be atrial fibrillation on ECG), and BMI is 43 kg/m2. Transthoracic echo shows an LVEF of 60%, moderate LV hypertrophy, moderate LA enlargement, and grade 2 diastolic dysfunction with no significant valvulopathy. What is the best next step?

A

Provide reassurance

B

Refer for gastric bypass

C

Refer for atrial fibrillation ablation

D

Start metoprolol and apixaban

Answer #10

ExplanationThe correct answer is D – start metoprolol and apixaban.Ms. Hefpeffner has a new diagnosis of atrial fibrillation (AF) and has a significantly elevated risk for embolic stroke based on her CHA2DS2-VASc score of 6 (hypertension, diabetes, heart failure, prior TIA, and female sex). The relationship between AF and HF is complex and the presence of either worsens the status of the other. Managing AF in patients with HFpEF can lead to symptom improvement (Class 2a, LOR C-EO). However, large, randomized trial data are unavailable to specifically guide therapy in patients with AF and HFpEF. Generally, management of AF involves stroke prevention, rate and/or rhythm control, and lifestyle / risk-factor modification. With regards to stroke prevention, patients with chronic HF with permanent-persistent-paroxysmal AF and a CHA2DS2-VASc score of ≥2 (for men) and ≥3 (for women) should receive chronic anticoagulant therapy (Class 1, LOE A). When anticoagulation is used in chronic HF patients with AF, a DOAC is recommended over warfarin in eligible patients (Class 1, LOE A).The decision for rate versus rhythm control should be individualized and reflects both patient symptoms and the likelihood of better ventricular function with sinus rhythm. For patients with HF and symptoms caused by AF,

The following question refers to Section 7.6 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. 

The question is asked by premedical student and CardioNerds Intern Pacey Wetstein, answered first by Baylor College of Medicine Cardiology Fellow and CardioNerds Ambassador Dr. Jamal Mahar, and then by expert faculty Dr. Nancy Sweitzer.

Dr. Sweitzer is Professor of Medicine, Vice Chair of Clinical Research for the Department of Medicine, and Director of Clinical Research for the Division of Cardiology at Washington University School of Medicine. She is the editor-in-chief of Circulation: Heart Failure. Dr. Sweitzer is a faculty mentor for this Decipher the HF Guidelines series.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

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

Question #9

Mr. Flo Zin is a 64-year-old man who comes to discuss persistent lower extremity edema and dyspnea with mild exertion. He takes amlodipine for hypertension but has no other known comorbidities. In the clinic, his heart rate is 52 bpm and blood pressure is 120/70 mmHg. Physical exam reveals mildly elevated jugular venous pulsations and 1+ bilateral lower extremity edema. Labs show an unremarkable CBC, normal renal function and electrolytes, a Hb A1c of 6.1%, and an NT-proBNP of 750 (no prior baseline available). On echocardiogram, his LVEF is 44% and nuclear stress testing was negative for inducible ischemia. What is the best next step in management?

A

Add furosemide BID and daily metolazone

B

Start empagliflozin and furosemide as needed

C

Start metoprolol succinate

D

No change to medical therapy

Answer #9

Explanation

The correct answer is B – start empagliflozin and furosemide as needed.

The patient described here has heart failure with mildly reduced EF (HFmrEF), given LVEF in the range of 41-49%.

In patients with HF who have fluid retention, diuretics are recommended to relieve congestion, improve symptoms, and prevent worsening HF (Class 1, LOE B-NR). For patients with HF and congestive symptoms, addition of a thiazide (eg, metolazone) to treatment with a loop diuretic should be reserved for patients who do not respond to moderate or high-dose loop diuretics to minimize electrolyte abnormalities (Class 1, LOE B-NR). Therefore, option A is not correct as he is only mildly congested on examination, and likely would not require such aggressive decongestive therapy, particularly with normal renal function. Adding a thiazide diuretic without first optimizing loop diuretic dosing would be premature.

The EMPEROR-Preserved trial showed a significant benefit of the SGLT2i, empagliflozin, in patients with symptomatic HF, with LVEF >40% and elevated natriuretic peptides. The 21% reduction in the primary composite endpoint of time to HF hospitalization or cardiovascular death was driven mostly by a significant 29% reduction in time to HF hospitalization, with no benefit on all-cause mortality. Empagliflozin also resulted in a significant reduction in total HF hospitalizations, decrease in the slope of the eGFR decline, and a modest improvement in QOL at 52 weeks. Of note, the benefit was similar irrespective of the presence or absence of diabetes at baseline. In a subgroup of 1983 patients with LVEF 41% to 49% in EMPEROR-Preserved, empagliflozin, an SGLT2i, reduced the risk of the primary composite endpoint of cardiovascular death or hospitalization f...