Episodes Archives - Cardionerds

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Episodes Archives - Cardionerds episodes

March 28, 2023277. Case Report: When Infarction Brings the Walls Down – Brigham and Women’s Hospital
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).
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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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., Hernández-del Rio, J.E., González-Padilla, C. et al. Left ventricular free-wall rupture, a potentially lethal mechanical complication of acute myocardial infarction: an unusual and illustrative case report. BMC Cardiovasc Disord 19, 80 (2019). https://doi.org/10.1186/s12872-019-1063-x
Yip HK, Wu CJ, Chang HW, Wang CP, Cheng CI, Chua S, Chen MC. Cardiac rupture complicating acute myocardial infarction in the direct percutaneous coronary intervention reperfusion era. Chest 2003;124:565–71. doi: 10.1378/chest.124.2.565. PMID: 12907558.
Sutherland FW, Guell FJ, Pathi VL, Naik SK. Postinfarction ventricular free wall rupture: strategies for diagnosis and treatment. Ann Thorac Surg 1996;61:1281–5. doi: 10.1016/0003-4975(95)00953-6. PMID: 8627055.
Meta-analysis of corticosteroid treatment in acute myocardial infarction. Am J Cardiol 2003;91:1055–9. doi: 10.1016/S0002-9149(03)00216-4. PMID: 12745097.
1 hr 6 min
March 22, 2023276. Left Ventricular Assist Devices and Renal Dysfunction with Dr. Brian Houston and Dr. Nisha Bansal
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!
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
CardioNerds Heart Success Series Page
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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?
Presence/absence of right ventricular failure
Other life limiting organ failure: Kidney failure/lung disease/liver failure/vascular disease
Anatomic concerns (ex. LV size)
Surgical risk (ex. Prior sternotomies, calcified aorta, etc)
Psychosocial aspects
Shared decision making (Does the patient want the device?)
What are the outcomes of patients with end stage renal disease (chronic kidney disease on dialysis) after LVAD implantation?
Patients with ESRD have a high burden of comorbidities. 40% of dialysis patients have heart failure.
The combination of heart failure and ESRD propounds a poor prognosis. Patients with ESRD without heart failure have a 40% survival in 5 years. Conversely, those with ESRD and heart failure have a < 20% survival in 5 years.
A retrospective analysis of the United States Renal Data System revealed that 50% patients on dialysis who received an LVAD died during the index hospitalization, compared to those not on dialysis whose in hospital mortality was <10%. The median survival was ~3 weeks. By 6 months after LVAD implantation, ~70% of patients on dialysis had died.
Based on INTERMACS data, kidney function is one of the strongest predictors of outcomes in patients with an LVAD.
What are the specific situations in which an LVAD might be offered to a patient with ESRD?
We may consider LVAD implantation in ESRD patients under specific circumstances.
Young patients with good functional status and good end organ function otherwise, who may be a candidate for heart-kidney transplantation in the near future, may be considered for LVAD implantation as a bridge to heart-kidney transplantation.
If it is felt that the patient’s renal dysfunction can be improved by augmenting cardiac output and the hemodynamics suggest cardio-renal syndrome, in very select patients on recently initiated dialysis LVAD implantation may be considered. Renal imaging showing absence of scarring and the absence of proteinuria suggest a better prognostic sign and may suggest cardio-renal syndrome.
In patients with acute kidney injury (with no prior history of CKD) being evaluated for LVAD implantation, what is the effect of an LVAD on kidney function?
Effect of an LVAD on kidney function: There is typically an initial improvement in kidney function, particularly in the first month post-implantation, due to restoration of normal hemodynamics with improvement in cardiac output and relieving renal venous congestion. Long term data, however, suggests gradual deterioration of kidney function in the long term. This is possibly due to kidney insults from the LVAD itself. The continuous flow of the LVAD can lead to periarteritis, hyperplasia of the renal arterial smooth muscle cells, and neurohormonal activation of the RAAS system leading to kidney injury over time.
Creatinine may not be the best marker of kidney function in these patients. Cystatin C and tubular kidney injury markers, soon to be commercially available, may be better markers of kidney function.
Does having chronic kidney disease (not dialysis dependent) increase the risk of worsening kidney function after LVAD implantation?
The occurrence of AKI after LVAD worsens outcomes. The presence of CKD prior to LVAD implantation increases this risk of AKI after LVAD implantation. Patients with CKD stage 3 or more have a 1-year mortality of >30% after LVAD implantation. In patients who have AKI after LVAD implantation, 30-day mortality is 18% and 1 year mortality is 40% with increased risk of infection, multisystem organ failure, and longer length of stay.
Common causes of AKI after LVAD implantation include:
Right ventricular failure
Bleeding requiring blood products and crystalloids, contributing to congestion.
Longer cardio-pulmonary bypass
Hemolysis
Based on a 10-year case series from the Mayo clinic, 15% of patients with LVAD require renal replacement therapy. If GFR<45 and there is proteinuria, the risk increased to 40%.
The 4 risk factors to predict AKI and RRT requirement after LVAD:
Presence of a low GFR
Proteinuria
Increased RA pressure
Longer cardio-pulmonary bypass time
The HEARTMATE III Risk Score provides individual survival prediction at 1- and 2-years post LVAD implantation – includes BUN and sodium levels
What are the options available to patients in terms of long-term dialysis once LVAD patients are dialysis dependent?
There are 3 main options for long term RRT:
In-center hemodialysis
Home hemodialysis
Peritoneal dialysis
Considerations:
In center Hemodialysis:
Challenges: large ultrafiltration rates can lead to lower MAPs, anticoagulation considerations (bleeding complications), high risk of infection (central venous catheter), pragmatic challenges (technical expertise of the dialysis staff, comfort of the attending nephrologist, transportation issues).
Peritoneal dialysis:
Benefits: decreased risk of infection (however anatomical considerations with respect to proximity to the driveline should be taken into account), more physiological and less hemodynamic instability, no need for anticoagulation.
Challenge: home based therapy (burden on the patient and family members)
What are the options in terms of vascular access in patients with an LVAD who are started on hemodialysis?
Central venous HD catheters – high risk of infection and therefore, not preferred.
AV fistula – low rates of infection, however, it takes 2-3 months for fistula maturation.
AV graft – preferred due to lower risk of infection, ability to use immediately.
What are the causes for anemia in patients with an LVAD and renal dysfunction?
Anemia of chronic disease
Increased risk of gastrointestinal bleed
Anticoagulation requirement
Acquired Von Willebrand deficiency
Higher burden of arterio-venous malformations
Pump thrombosis can lead to hemolysis
What are the implications of blood transfusions and use of erythropoietin stimulating agents (ESAs) in these patients?
Judicious use of blood transfusions is advised particularly in patients waiting for a heart transplantation due to increased risk of antigen sensitization which can limit their potential donor pool.
Those who receive ESAs have a dose-dependent increased risk of pump thrombosis and all-cause mortality. This was however, studied in patients with a HEARTMATE II (axial flow device) as opposed to the currently most commonly used pump which is the HEARTMATE III (centrifugal flow device) known to have an overall lower risk of pump thrombosis.
References
Peritoneal Dialysis Following Left Ventricular Assist Device Placement and Kidney Recovery: A Case Report Kidney Med. 2021;3(3):438-441. Published 2021 Feb 17. doi:10.1016/j.xkme.2020.12.009
Bansal N, Hailpern SM, Katz R, et al. Outcomes Associated With Left Ventricular Assist Devices Among Recipients With and Without End-stage Renal Disease. JAMA Intern Med. 2018;178(2):204-209. doi:10.1001/jamainternmed.2017.4831
Butler J, Geisberg C, Howser R, et al. Relationship between renal function and left ventricular assist device use. Ann Thorac Surg. 2006;81(5):1745-1751. doi:10.1016/j.athoracsur.2005.11.061
Haglund NA, Feurer ID, Dwyer JP, et al. Does renal dysfunction and method of bridging support influence heart transplant graft survival?. Ann Thorac Surg. 2014;98(3):835-841. doi:10.1016/j.athoracsur.2014.05.059
Jawaid O, Gaddy A, Omar HR, Guglin M. Ventricular Assist Devices and Chronic Kidney Replacement Therapy: Technology and Outcomes. Adv Chronic Kidney Dis. 2021;28(1):37-46. doi:10.1053/j.ackd.2021.01.002
Ootaki C, Yamashita M, Ootaki Y, et al. Reduced pulsatility induces periarteritis in kidney: role of the local renin-angiotensin system. J Thorac Cardiovasc Surg. 2008;136(1):150-158. doi:10.1016/j.jtcvs.2007.12.023
Patel AM, Eduardo Rame J, Rudnick MR. How does the nephrologist manage an LVAD patient on chronic maintenance dialysis?. Semin Dial. 2014;27(3):284-288. doi:10.1111/sdi.12229
Roehm B, Vest AR, Weiner DE. Left Ventricular Assist Devices, Kidney Disease, and Dialysis. Am J Kidney Dis. 2018;71(2):257-266. doi:10.1053/j.ajkd.2017.09.019
Sandner SE, Zimpfer D, Zrunek P, et al. Renal function and outcome after continuous flow left ventricular assist device implantation. Ann Thorac Surg. 2009;87(4):1072-1078. doi:10.1016/j.athoracsur.2009.01.022
Wettersten N, Estrella M, Brambatti M, et al. Kidney Function Following Left Ventricular Assist Device Implantation: An Observational Cohort Study. Kidney Med. 2021;3(3):378-385.e1. Published 2021 Apr 2. doi:10.1016/j.xkme.2021.01.009
Yalcin YC, Muslem R, Veen KM, et al. Impact of Continuous Flow Left Ventricular Assist Device Therapy on Chronic Kidney Disease: A Longitudinal Multicenter Study. J Card Fail. 2020;26(4):333-341. doi:10.1016/j.cardfail.2020.01.010
Yoshioka D, Sakaguchi T, Saito S, et al. Predictor of early mortality for severe heart failure patients with left ventricular assist device implantation: significance of INTERMACS level and renal function. Circ J. 2012;76(7):1631-1638. doi:10.1253/circj.cj-11-1452
58 min
March 20, 2023275. Case Report: A Rare Cause Of Fatigue, Dyspnea, And Weight Loss In An Elderly Man – Brigham and Women’s Hospital
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).
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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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, there are severe coronary artery calcifications. There is possible severe stenosis of the mid LAD.
4. Aneurysmal dilatation of the thoracic aorta, with measurements as reported in the narrative.

1. Normal left ventricular size and function.

2. There is a large homogenous, soft-tissue intensity mass in the right atrioventricular groove infiltrating the right ventricle free wall and cranially extending anterior to the aorta and main pulmonary artery. The mass encases the main pulmonary artery, the aortic root, the right coronary artery, and the left main coronary artery. The mass invades the right ventricular outflow tract and proximal main pulmonary artery, resulting in severe luminal narrowing at the level of the RVOT/pulmonary artery valve. For the dimensions of the mass, please refer to cardiac CT from 12/1/2021. The mass is isointense to myocardium on T1-weighted images and hyperintense on T2-weighted images. The mass avidly enhances on first-pass perfusion images. There is heterogeneous enhancement of the mass on late gadolinium enhancement images.

3. There is a large circumferential pericardial effusion, measuring up to 2.3 cm.
The left ventricular cavity size and wall thickness are normal. Left ventricular systolic function is normal. There are no segmental left ventricular wall motion abnormalities noted. The estimated ejection fraction is 60%. The right ventricular size is normal. Right ventricular systolic function is mildly decreased. Mildly dilated ascending aorta. Mild AI. Mild MR. There is large heterogenous echodensity in the RV free wall that extends into the parietal pericardium and also into the RV myocardium with mobile components in the RV cavity apical to the tricuspid valve and immediately adjacent to the pulmonic valve. There is obstruction of flow out of the RVOT with a peak and mean gradient of 27 and 16 mmHg respectively. There appears to be some vascularity to this structure (seen best on clips 17 and 18) and overall findings are highly suspicious for tumor. There is a small to moderate pericardial effusion. Anterior to the RV there is a larger collection that is probably pleural in etiology. Recommend cross-sectional imaging for further evaluation. There is no RV chamber collapse to suggest tamponade physiology.

1. Intensely FDG avid infiltrative mediastinal most likely high-grade lymphoma..
2. Additional discrete mediastinal and hilar nodes, and left lower lobe nodule, most likely additional areas of lymphomatous involvement. Moderate uptake along right adrenal nodule may represent additional site of lymphomatous involvement
3. Small bilateral pleural effusions and small to moderate pericardial effusion.
Pearls – A Rare Cause Of Fatigue, Dyspnea, And Weight Loss In An Elderly Man – Brigham and Women’s Hospital
In the diagnostic approach for cardiac masses, consider: 1) age of patient at time of presentation, 2) epidemiologic likelihood and clinical probability, 3) location of tumor, and 4) tissue characterization of the mass on CMR.
CMR allows for better characterization of soft tissues and can assess mass morphology, dimensions, homogeneity, and infiltration into surrounding tissues.
On CMR, cardiac lymphoma typically shows isointensity on T1 imaging and hyperintensity on T2 images.
Cardiac CT allows for high spatial and temporal resolution, and can be useful to define cardiac masses that involve the coronary arteries; compared to CMR, cardiac CT has a greater ability to assess calcifications within a mass itself.
Cardiac lymphomas have a predilection of right heart chambers, especially right atrium and can affect the AV groove, encasing the right coronary artery.
Global systolic longitudinal myocardial strain on TTE is an indicator of early anthracycline-induced cardiomyopathy before overt reduction in ejection fraction.
Show Notes – A Rare Cause Of Fatigue, Dyspnea, And Weight Loss In An Elderly Man – Brigham and Women’s Hospital
What is the approach to an enlarged cardiac silhouette noted on chest x-ray?
Cardiothoracic ratio of greater than 50%.
Two possible “buckets” of diagnoses to consider are enlargement of heart related to cardiomegaly as opposed to a pericardial process like a pericardial effusion.
For cardiomegaly, it can be from dilated or hypertrophic cardiomyopathy with most common causes including coronary artery disease, hypertension, valvular heart disease, and arrythmia-induced cardiomyopathy. Other buckets to consider are inflammatory causes, either infectious or autoimmune, as well as infiltrative diseases like amyloid or sarcoid, toxins (alcohol, cocaine, medications), endocrine, and nutritional causes (like a B1 or selenium deficiency).
The most sensitive sign of a pericardial effusion on chest x-ray is enlargement of cardiac silhouette with a sensitivity of around 71%, but low specificity (1).
With pericardial effusion, symmetric expansion of the heart contour leads to a globular appearance which is commonly referred to as flask-shaped or the water bottle sign (1).
What is the approach to intracardiac masses?
First, consider the age of the patient at the time of presentation since certain clinical entities like rhabdomyomas and fibromas are more common in the pediatric population (2).
Second, consider the epidemiologic likelihood and clinical probability. In a patient with a recent anterior wall MI and akinetic ventricular apex, a cardiac mass on echo would raise concern for an intracardiac thrombus (2).
Third, consider the location of the tumor. If the mass is on the valves, consider thrombus or a vegetation. While masses in the chambers can still represent thrombus, would also consider myxomas, lymphomas, and metastases (2).
Fourth, consider the tissue characterization of the mass on further diagnostic imaging such as CMR (2).
What is the role of multimodality imaging in the evaluation of intracardiac masses?
TTE is the first modality utilized in evaluation of a cardiac mass. TEE is useful specifically when valvular lesions are suspected or in patients with atrial masses or with mobile valvular lesions. It can help to characterize size, morphology, attachment site, extension, and hemodynamic effects.
CMR allows for better characterization of soft tissue and can assess mass morphology, dimensions, homogeneity, infiltration in surrounding tissues. These can all help differentiate different types of masses and whether a mass is benign or malignant. Signal characteristics gathered from T1, T2, early gadolinium enhancement, and late gadolinium enhancement sequences can further assess fatty infiltration, necrosis, hemorrhage, and vascularity within a mass (3, 4).
Cardiac CT is another option and offers high spatial and temporal resolution, multiplanar image reconstruction capabilities, and fast acquisition times. The large field of view also allows for assessment of chest and lung tissue, vascular structures, and assessment for other masses in the chest. CT may also be more helpful in defining surgical approaches and assessing how masses may involve the coronary arteries and assess for coronary artery calcifications or obstructive coronary disease (4).
FDG-PET is also another valuable imaging option which offers evaluation of metabolic activity of tumors. PET imaging can also help guide biopsy location, staging, and planning for cancer therapy.
What are key features of Primary Cardiac Lymphoma?
Diffuse large B-cell lymphoma is the most common subtype, though others like Burkitt lymphoma, low grade B –cell lymphoma, and T-cell lymphoma have also been described.
They occur more commonly in immunocompromised individuals and in immunocompetent patients, only account for 1.3% of primary cardiac tumors
Presenting symptoms are usually nonspecific. They may manifest as dysrhythmias like heart block, syncopal episodes, or even restrictive cardiomyopathy.
Approximately 20% of patients may develop acute heart failure before other symptoms.
On echocardiogram, these tumors appear homogeneous, with predilection of right heart chambers, especially right atrium. The AV groove can be affected, potentially encasing the right coronary artery (5).
On CMR, tissue appears isointense on T1-weighted imaging. On T2-weighted imaging, lesions are mildly hyperintense due to diffuse edema (5).
What are risk factors associated with anthracycline toxicity and what are strategies for preventing and monitoring for cardiotoxicity when anthracycline therapy is planned?
Up to 35% of patients receiving anthracycline therapy develop some form of cardiotoxicity (6).
The risk of developing anthracycline induced cardiotoxicity is directly proportional to the dose of anthracycline received, and after studies demonstrated HF incidence of 26% with doxorubicin dose of 550mg/m2 as compared to 5% with dose of 400mg/m2, efforts have been made to limit cumulative anthracycline doses to 400 to 450mg/m2. In addition, hypertension, DM, and obesity are all associated with increased risk (6).
There are two primary prevention strategies: using cardioprotective agents, and aiming to reduce potency of the anthracyclines. For cardioprotection, dexrazoxane is an FDA-approved cardioprotective agent for anthracycline induced cardiotoxicity (7).
TTE is the most common modality used for detection and monitoring of anthracycline toxicity on the heart. While LV dysfunction is most commonly detected, recent investigations suggest that RV function is also significantly affected by anthracycline toxicity (8).
Global systolic longitudinal myocardial strain on TTE has also emerged as a reproducible indicator of early anthracycline-related myocardial dysfunction and future reduction in LVEF (9).
Enjoy Episodes 261 and 274 about CTRCD (cancer therapy related cardiac dysfunction) as part of the Cardio-Oncology Series.
References – A Rare Cause Of Fatigue, Dyspnea, And Weight Loss In An Elderly Man – Brigham and Women’s Hospital
https://www.acc.org/latest-in-cardiology/articles/2019/09/09/10/46/chest-radiograph-signs-suggestive-of-pericardial-disease
Tyebally S, Chen D, Bhattacharyya S, Mughrabi A, Hussain Z, Manisty C, Westwood M, Ghosh AK, Guha A. Cardiac Tumors: JACC CardioOncology State-of-the-Art Review. JACC CardioOncol. 2020 Jun 16;2(2):293-
Motwani M, Kidambi A, Herzog BA, Uddin A, Greenwood JP, Plein S. MR imaging of cardiac tumors and masses: a review of methods and clinical applications. Radiology. 2013 Jul;268(1):26-43.
Lopez-Mattei JC, Lu Y. Multimodality Imaging in Cardiac Masses: To Standardize Recommendations, The Time Is Now! JACC Cardiovasc Imaging. 2020 Nov;13(11):2412-2414.
Jeudy J, Kirsch J, Tavora F, Burke AP, Franks TJ, Mohammed TL, Frazier AA, Galvin JR. From the radiologic pathology archives: cardiac lymphoma: radiologic-pathologic correlation. Radiographics. 2012 Sep-Oct;32(5):1369-80.
Henriksen PA. Anthracycline cardiotoxicity: an update on mechanisms, monitoring and prevention. Heart. 2018 Jun;104(12):971-977.
Vejpongsa P, Yeh ET. Prevention of anthracycline-induced cardiotoxicity: challenges and opportunities. J Am Coll Cardiol. 2014 Sep 2;64(9):938-45
Liu JE. Anthracycline-Induced Cardiotoxicity: Remembering the Forgotten Ventricle. JACC CardioOncol. 2020;2(1):23-25.
Potter E, Marwick TH. Assessment of Left Ventricular Function by Echocardiography: The Case for Routinely Adding Global Longitudinal Strain to Ejection Fraction. JACC Cardiovasc Imaging. 2018 Feb;11(2 Pt 1):260-274.
43 min
March 16, 2023274. Cardio-Oncology: Cancer Therapy-Related Cardiac Dysfunction (CTRCD) – The Cardiologist Perspective with Dr. Joerg Hermann
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.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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.
The 2021 International Cardiooncology Society (ICOS) consensus statement defines five major forms of cancer therapy related cardiac dysfunction (CTRCD):
Cardiac dysfunction/heart failure:
Asymptomatic: defined by changes in ejection fraction. This may be mild (LVEF >50% AND either new decline in GLS by >15% from baseline or new rise in troponin or NTproBNP), moderate (new LVEF reduction by ≥10 percentage points to 40 – 49% AND either new decline in GLS by >15% from baseline or new rise in troponin or NTproBNP), or severe (new LVEF reduction to < 40%).
Symptomatic: defined by severity of symptoms and intensity of treatment required. This may be mild (mild HF symptoms, no intensification of therapy required), moderate (need for outpatient intensification of diuretic and HF therapy), severe (HF hospitalization), or very severe (requiring inotropic or mechanical circulatory support, consideration for transplant).
Vascular toxicity: namely, myocardial infarction or stroke. Three primary forms:
Vasospasm
Thrombosis
Atherosclerosis
Arrhythmia/QTc prolongation
Hypertension
Myocarditis: made especially prominent by immune checkpoint inhibitors

Note that the definitions for these toxicities require a baseline assessment of LVEF, global longitudinal strain, and cardiac biomarkers. As such, these should be considered part of pre-treatment risk assessment for any patient planned to undergo therapy known to be cardiotoxic.
Who are the “usual suspects” in CTRCD?
The “five pillars” of cancer therapy can each cause a form of cardiotoxicity. These pillars are:
Conventional chemotherapeutics: designed to stop highly proliferative cells from proliferating by inhibiting DNA synthesis.
Anthracyclines, such as doxorubicin, etoposide. Mechanism: intercalates into DNA, disrupting topoisomerase-mediated DNA repair and replication. Primary form of cardiotoxicity: cardiomyopathy (can also cause arrhythmia).
Alkylating agents, such as cyclophosphamide. Mechanism: cross-links DNA. Primary form of cardiotoxicity: high doses can cause hemorrhagic pericarditis; we also see arrhythmia, cardiomyopathy, and arterial vascular disease.
Antimetabolites, such as 5-fluorouracil, gemcitabine. Mechanism: replaces base pairs, preventing synthesis. Primary form of cardiotoxicity: cardiomyopathy, arterial vascular disease.
Targeted therapies: monoclonal antibodies that inhibit cell signaling pathways that are pivotal in tumor cells.
HER2 inhibitors
Tyrosine kinase inhibitors
VEGF inhibitors, such as bevacizumab. Mechanism: inhibits angiogenesis via VEGF inhibition. Primary form of cardiotoxicity: hypertension, thrombosis, and occasionally cardiomyopathy.
Immune therapies: immunologic therapies that are “targeted” at receptors identified on specific tumor receptors
CAR-T cell therapy
Immune checkpoint inhibitors
Radiation therapy
Surgery

The first three of these — conventional chemotherapeutics, targeted therapies, and immune therapies — are the three classes we think about as causing CTRCD.
Pearls from the ESC 2022 guidelines
Cardiovascular risk in patients with cancer is a dynamic variable that requires a multidisciplinary team approach.
All patients with cancer who are scheduled to receive a potentially cardiotoxic anticancer therapy should receive a baseline cardiovascular risk assessment that includes transthoracic echocardiography with measurement of global longitudinal strain as well as baseline cardiac biomarkers.
In patients who are at high risk or very high risk of CTRCD as based on the risk stratification provided in the guidelines, efforts should be made to minimize the use of cardiotoxic agents (including the consideration of dexrazoxane and liposomal anthracyclines) and to initiate cardioprotective agents (like ACE-i/ARB, beta blockers, and statins).
In patients who develop asymptomatic, mild decreases in LVEF, especially in the setting of HER2 inhibitors, chemotherapy should be continued with the addition of cardioprotective therapy.
After the completion of chemotherapeutics, cardioprotective medications should be de-escalated in patients at low risk of future cardiovascular events.
Pearl from the ACC.23 meeting (March 4-6, 2023, New Orleans, LA) The STOP-CA trial is a multicenter, randomized, double-blind, placebo-controlled study presented at ACC.23. The study analyzed 286 patients with lymphoma undergoing treatment with anthracyclines. Baseline left ventricular ejection fraction (LVEF) was 63%. Patients were randomized into a group receiving atorvastatin 40 mg daily and a group receiving placebo. The primary endpoint of LVEF decline ≥10% at 12 months was seen in 9% of patients in the atorvastatin group and 22% of patients in the placebo group, with no difference in rates of adverse events. In conclusion, statins may have an important role in the prevention of anthracycline-associated cardiac dysfunction in lymphoma patients. For more on the STOP-CA trial, check out the ACC Fits-On-The-Go coverage by CardioNerds CardioOncology series co-chair Dr. Teodora Donisan, with lead authors Dr. Tomas Neilan and Dr. Marielle Scherrer-Crosbie. The STOP-CA trial was presented after the recording of this episode and is thus not addressed in the episode.
References – Cancer Therapy-Related Cardiac Dysfunction (CTRCD) – The Cardiologist Perspective with Dr. Joerg Hermann
Herrmann J, McCullough KB, Habermann TM. How I treat cardiovascular complications in patients with lymphoid malignancies. Blood. 2022;139(10):1501-1516. doi:10.1182/blood.2019003893
Herrmann J, Lenihan D, Armenian S, et al. Defining cardiovascular toxicities of cancer therapies: an International Cardio-Oncology Society (IC-OS) consensus statement. Eur Heart J. 2022;43(4):280-299. doi:10.1093/eurheartj/ehab674
Lyon AR, López-Fernández T, Couch LS, et al. 2022 ESC Guidelines on cardio-oncology developed in collaboration with the European Hematology Association (EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS). Eur Heart J. 2022;43(41):4229-4361. doi:10.1093/eurheartj/ehac244
Ewer MS, Ewer SM. Cardiotoxicity of anticancer treatments: what the cardiologist needs to know. Nat Rev Cardiol. 2010;7(10):564-575. doi:10.1038/nrcardio.2010.121
Yu AF, Flynn JR, Moskowitz CS, et al. Long-term Cardiopulmonary Consequences of Treatment-Induced Cardiotoxicity in Survivors of ERBB2-Positive Breast Cancer. JAMA Cardiol. 2020;5(3):309-317. doi:10.1001/jamacardio.2019.5586

Herrmann J. Adverse cardiac effects of cancer therapies: cardiotoxicity and arrhythmia. Nat Rev Cardiol. 2020;17(8):474-502. doi:10.1038/s41569-020-0348-1

Chang HM, Moudgil R, Scarabelli T, Okwuosa TM, Yeh ETH. Cardiovascular Complications of Cancer Therapy: Best Practices in Diagnosis, Prevention, and Management: Part 1 [published correction appears in J Am Coll Cardiol. 2018 Feb 6;71(5):587]. J Am Coll Cardiol. 2017;70(20):2536-2551. doi:10.1016/j.jacc.2017.09.1096
Chang HM, Okwuosa TM, Scarabelli T, Moudgil R, Yeh ETH. Cardiovascular Complications of Cancer Therapy: Best Practices in Diagnosis, Prevention, and Management: Part 2. J Am Coll Cardiol. 2017;70(20):2552-2565. doi:10.1016/j.jacc.2017.09.1095
Meet Our Collaborators
International Cardio-Oncology Society ( IC-OS). IC-OS exits to advance cardiovascular care of cancer patients and survivors by promoting collaboration among researchers, educators and clinicians around the world. Learn more at https://ic-os.org/.
55 min
March 14, 2023273. Digital Health: The Digital Transformation of Cardiovascular Medicine with Dr. Dipti Itchhaporia
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 platforms
Remote 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. How can we balance benefits and burden of digital health tools?
The pure definition of digital transformation is using digital tools to make lives of patients and clinicians better.
The data we derive from digital health technologies is only useful insofar that it can be used to affect change. We need analytical tools like AI to create actionable information and summary sheets to summarize data in meaningful ways.
While developing digital health tools, companies should engage in co-designing processes with end users. In the case, clinicians should receive iterative feedback so that tools that are developed meet user needs.
4. What are the ways to ensure inclusiveness in design and delivery of digital health tools for disease management to every patient, including those from underrepresented racial and ethnic groups?
We need to improve access to infrastructure needed to operate digital health tools. This requires engagement with institutions, organizations and legislators.
Digital health tools need to be co-designed with a diverse set of users including those with low tech literacy as well as multiple stakeholders.
We need to communicate with community members when translating science to make sure that the process is transparent to address any trust issues or skepticism.
5. How do we ensure data privacy, especially when health data is stored on different servers?
There are gaps in federal legislation that need to be addressed.
IT health standards for handling data collected outside hospital settings with digital health tools should be developed in an iterative manner. When health IT standards are developed, we need to enforce them and ensure that they are working well with feedback systems.
Individuals need to control how their data is health systems and other entities use and store their data.
Clinicians need to trust that data is stored in a secure manner when appropriate channels are utilized.
Data management should be a transparent process.
Confidentiality is going to be fundamental and all entities involved should be subject to HIPPA rules.
6. How can big organizations help advocate for updated reimbursement models and policy changes to allow for greater adoption of digital health tools?
Big professional organizations have pivotal roles in promoting the digital transformation, and implementing digital re-design.
Big professional organizations can act as conduits between different stakeholders, promote digital literacy in public as well as among professionals.
They can create standards and guidelines on proper use of digital health technology, facilitate robust studies to test clinical impact, and advocate for reimbursement and policy changes.
7. What are the near future and long-term opportunities of digital health tools in cardiovascular disease management?
Digital transformation is in progress, and we need clinicians to be at the center of innovation to drive development of care pathways and care delivery models.
Digital solutions should promote health equity, add value to healthcare systems, and promote wellbeing of clinicians
References
Bayoumy K, Gaber M, Elshafeey A, et al. Smart wearable devices in cardiovascular care: where we are and how to move forward. Nat Rev Cardiol. 2021 Aug;18(8):581-599. doi: 10.1038/s41569-021-00522-7. Epub 2021 Mar 4. PMID: 33664502.
Cowie MR, Lam CSP. Remote monitoring and digital health tools in CVD management. Nat Rev Cardiol. 2021 Jul;18(7):457-458. doi: 10.1038/s41569-021-00548-x. PMID: 33824486; PMCID: PMC8023506.
Itchhaporia D. Navigating the Path to Digital Transformation. J Am Coll Cardiol. 2021 Jul 27;78(4):412-414. doi: 10.1016/j.jacc.2021.06.018. PMID: 34294274.
30 min
March 12, 2023272. CardioNerds Rounds: Challenging Cases – Hemodynamics and Mechanical Circulatory Support with Dr. Daniel Burkhoff
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.
Challenging Cases – Atrial Fibrillation with Dr. Hugh Calkins
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Show notes – Hemodynamics and Mechanical Circulatory Support
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
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, it may lead to better outcomes by allowing for better tissue substrate for a more effective repair.
Enjoy this ACC.org Expert Analysis by Goyal and Menon to learn more about post-myocardial infarction ventricular septal rupture.
References
Pahuja M, Schrage B, Westermann D et al. Hemodynamic Effects of Mechanical Circulatory Support Devices in Ventricular Septal Defect. Circ Heart Fail. 2019 Jul;12(7):e005981. doi: 10.1161/CIRCHEARTFAILURE.119.005981.
TEACH Videos via Harvi.Org: https://harvi.org/book/data/00%20-%20TeachVideos/TeachVideos.html
Production Team
Karan Desai, MD
Natalie Stokes, MD
Amit Goyal, MD
Daniel Ambinder, MD
33 min
March 08, 2023 271. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #12 with Dr. Shashank Sinha

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. Finally, stage E is extremis with refractory hypotension and hypoperfusion, with circulatory collapse. Our patient in the question stem is in SCAI stage C, or classic cardiogenic shock.

Choice A is incorrect. Augmenting diuresis with metolazone can be useful in a patient with diuretic resistance and decompensated heart failure. However, this patient is hypotensive and fits the wet and cool profile and will benefit from inotropic support to increase end organ perfusion.

Choice B is incorrect. Sodium nitroprusside can be used to increase cardiac output in cardiogenic shock and is particularly useful in patients with high systemic vascular resistance. Indeed, intravenous nitroglycerin and nitroprusside have a Class 2a indication (LOE B-NR) in patients who are admitted with decompensated HF without systemic hypotension as an adjuvant to diuretic therapy for relief of dyspnea. However, our patient is hypotensive and so vasodilators would not be appropriate at this time.

Choice C is incorrect. Metoprolol, a negative inotropic agent, should not be used in this patient with cardiogenic shock.

Relevant to this question is the use of invasive hemodynamic monitoring to guide therapy. The use a PA line has a Class 2b indication (LOE B-NR) in patients presenting with cardiogenic shock to define hemodynamic subsets and appropriate management strategies. Obtaining hemodynamic data via a PA line can also be particularly useful when escalating to mechanical circulatory support, when there is diagnostic uncertainty, or when a patient in shock is not responding to empiric initial shock measures. While the use of PA catheters has been controversial since the ESCAPE trial which showed no benefit in decompensated HF, the trial did not actually enroll patients with cardiogenic shock. Several observational studies have shown association between PA catheter use and improved outcomes in cardiogenic shock, particularly in conjunction with short-term MCS. PA catheters are a diagnostic tool and are best utilized when hemodynamic information can be translated into appropriate interventions, such as determining response to medical and MCS therapy, weaning off of MCS support, or uncovering right ventricular failure to guide appropriate therapy.

In the case of cardiogenic shock, studies have shown benefit with multidisciplinary teams of HF and critical care specialists, interventional cardiologists, and cardiac surgeons. Such teams should also be capable of providing appropriate palliative care. There is a Class 2a (LOE B-NR) recommendation for management of patients with cardiogenic shock by an experienced multidisciplinary team.
Main Takeaway
In summary, it is important to recognize cardiogenic shock early based on clinical criteria of hypotension and hypoperfusion and begin prompt initiation of IV inotropic agents such as dobutamine and/or MCS to optimize end-organ perfusion. When there is insufficient clinical improvement with initial measures, invasive hemodynamic assessment is recommended.
Guideline Loc.
Section 9.5
Tables 22-24

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17 min
March 07, 2023 270. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #11 with Dr. Prateeti Khazanie

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 on refractory symptoms rather than cardiac function and more clearly acknowledges that advanced HF can occur in patients without severely reduced LVEF, such as in those with isolated RV dysfunction, uncorrectable valvular or congenital heart disease, and in patients with preserved and mildly reduced LVEF.
In such patients with advanced heart failure, when consistent with the patient’s goals of care, timely referral for HF specialty care is recommended to review HF management and assess suitability for advanced HF therapies (eg, LVAD, cardiac transplantation, palliative care, and palliative inotropes) (Class I, LOE C-LD).
Clinical indicators of advanced heart failure should prompt a possible referral to an advanced HF specialist and can be remembered by the INEEDHELP acronym:
·       I – IV inotropes
·       N – NYHA IIIb-VI or persistently elevated natriuretic peptides
·       E – End-organ dysfunction
·       E – EF ≤ 35%
·       D – Defibrillator shocks
·       H – Hospitalizations > 1 in past year
·       E – Edema despite escalating diuretics
·       L – Low systolic blood pressure (≤90) or high heart rate
·       P – Prognostic medication; progressive intolerance or down-titration of GDMT
It would not be appropriate to refer to EP for CRT-D upgrade as this is a Class 3 recommendation (LOE B-R) in patients with QRS duration <120 ms for no benefit.
Increasing the dose of sacubitril-valsartan would not be appropriate in this setting as the patient would be likely unable to tolerate a higher dose given her complaints of lightheadedness and episodes of hypotension.
Initiating treatment with IV inotropes would not be appropriate in this setting. Although the use of IV inotropes is given a Class 1 recommendation (LOE B-NR) for the treatment of cardiogenic shock, the patient described in the question stem does not meet clinical criteria for cardiogenic shock.
Main Takeaway
Clinical indicators for advanced heart failure can be remembered by the I-Need-Help acronym, and there is a Class 1, LOE C recommendation for these patients to be referred to HF specialists for further management and assessment for advanced therapies, when consistent with the patient’s goals of care.
Guideline Loc.
Section 8.1
Tables 16-18

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19 min
February 28, 2023 269. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #10 with Dr. Michelle Kittleson

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

Explanation
The 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, AF ablation is reasonable to improve symptoms and QOL (Class 2a, LOE B-R). However, referring for catheter ablation would be premature before first attempting rate control and instituting anticoagulation therapy.

Traditionally, beta-blockers and nondihydropyridine calcium channel blockers are used as first-line agents for rate control in AF. Interestingly, a small open-label trial, RATE-AF in elderly patients with AF and symptoms of HF (mostly with preserved LVEF), compared bisoprolol to digoxin. Although the primary endpoint of quality of life at 6 months was similar between the 2 groups, several secondary QOL endpoints, functional capacity, and reduction in NT-proBNP favored digoxin at 12 months, with similar rate reductions in both groups. More side effects (such as dizziness, lethargy, and hypotension) were seen with bisoprolol than with digoxin. However, digoxin has a narrow therapeutic window and needs to be monitored more closely.
Option A (provide reassurance) is inappropriate as this patient has heart failure with preserved EF, defined by signs and symptoms of HF in patients with an LVEF of 50% or more. Echocardiogram hints in this case include LV hypertrophy and diastolic dysfunction. Our patient also has comorbidities frequently associated with HFpEF such as hypertension, diabetes, OSA, and obesity. Other common comorbidities include CAD, CKD, and atrial arrhythmias. When diagnosing HFpEF, care must be taken to rule out mimicking conditions such as pulmonary hypertension or amyloidosis. A large portion of the management of HFpEF includes managing comorbid conditions such as hypertension, OSA, and atrial fibrillation. At this time, she is symptomatic with atrial fibrillation and rapid ventricular response, and warrants both rate control and stroke prophylaxis.

Although gastric bypass should be considered for patients with a BMI >35 kg/m2 with comorbidities (such as HTN or diabetes) and patients with a BMI > 40 kg/m2 independent of comorbid conditions, this is not the best next step at this time. First, she should receive anticoagulation to reduce the risk of stroke and achieve better control of her HR and BP.

Patients with HFpEF and hypertension should have medication titrated to attain blood pressure targets in accordance with published clinical practice guidelines to prevent morbidity (Class 1, LOE C-LD). Although the optimal BP goal and antihypertensive regimen in patient with HFpEF is not known, HFpEF trials so far have shown that RAAS antagonists including ACEi, ARB, MRA and possibly ARNi could be first-line agents to treat HTN in patients with HFpEF. Beta blockers may be used to treat hypertension in patients with a history of
MI, symptomatic CAD, or AF with rapid ventricular response. These effects need to be balanced with the potential contribution of chronotropic incompetence to exercise intolerance in some patients.
Main Takeaway
In patients with HFpEF, the diagnosis and management of comorbidities are very important, especially the treatment of HTN (Class 1, LOE C-LD) and AF (Class 2a, LOE C-EO).
Guideline Loc.
Section 7.7.1, Figure 12
Section 10.2

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12 min
February 22, 2023 268. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #9 with Dr. Nancy Sweitzer

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 for HF. Therefore, in patients with HFmrEF, SGLT2i can be beneficial in decreasing HF hospitalizations and cardiovascular mortality (Class 2a, LOE B-R). Furthermore, by inhibiting glucose reabsorption in the kidney, they have a diuretic effect which may help ease congestion and limit loop diuretic dosing. SGLT2i are beneficial to the vast majority of cardiovascular patients but are contraindicated in patients with type 1 diabetes or prior episodes of diabetic ketoacidosis as they may cause euglycemic DKA.
Option C is incorrect. Among patients with current or previous symptomatic HFmrEF (LVEF, 41%–49%), use of evidence-based beta blockers for HFrEF, ARNi, ACEi, or ARB, and MRAs may be considered to reduce the risk of HF hospitalization and cardiovascular mortality, particularly among patients with LVEF on the lower end of this spectrum (Class 2b, LOE B-NR). However, the patient’s heart rate is already low and so initiating a beta blocker would be inappropriate. Switching his calcium channel blocker to ARNi may be considered.
Option D is not correct as we can help counsel him on lifestyle and medication changes which can relieve his symptoms and reduce his risk of HF hospitalizations and mortality.
Main Takeaway
In patients with HFmrEF, diuretics are useful for decongestion and symptomatic improvement (Class 1) and there is a role for GDMT including SGLT2i (Class 2a) and BB, ARNI, ACEi/ARB, MRA (Class 2b).
Guideline Loc.
Section 7.6.1, Figure 11

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13 min

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