Advanced Heart Failure and Transplant Cardiology Fellow Texas Heart Institute at Baylor College of Medicine Houston, Texas, United States
Disclosure(s):
Omar Fakhreddine, MD: No financial relationships to disclose
Background: Acute right heart failure (RHF) classically follows a large right coronary artery distribution myocardial infarction. Its development after a left coronary system myocardial infarction is unexpected, particularly in patients on LVAD support We describe two LVAD-supported patients who developed acute RHF following left coronary artery distribution myocardial infarction and revascularization.
Methods: We report a two-patient case series of individuals who developed acute RHF following non-ST-segment myocardial infarctions involving the left coronary system while on HeartMate 3 LVAD support. Data were collected retrospectively from the electronic medical record, including presenting symptoms, electrocardiography, cardiac biomarkers, coronary angiography, invasive hemodynamics, transthoracic echocardiography, LVAD parameters, management strategies, and short-term outcomes. Particular emphasis was placed on the timing of revascularization, post-procedural hemodynamic changes, diagnostic criteria for RHF, and clinical response to therapy
Outcome: Case 1 was a 62-year-old female with nonischemic cardiomyopathy due to cardiac sarcoidosis on HeartMate3 support as BTT, and Case 2 was a 58-year-old male with ischemic cardiomyopathy on HeartMate3 support as DT. Both patients presented with acute chest pain and elevated cardiac troponin I. Both had right-dominant circulation. Culprit lesions involved the left anterior descending artery in Case 1 and the left main coronary artery in Case 2 with no significant disease involving the right coronary artery. Time from presentation to revascularization was within 12 hours for Case 1 and within 6 hours for Case 2.
Both patients underwent coronary angiography with successful revascularization. Within 24–48 hours, each developed acute clinical deterioration characterized by hypotension, reduced estimated LVAD flows, and elevated CVP. RHF was diagnosed based on a combination of clinical, hemodynamic and echocardiographic data. In both patients, RHC demonstrated elevated RA pressures and RA/PCWP. Echocardiographic demonstrated right ventricular dilation with with severe systolic dysfunction and deviation of the intraventricular septum towards the LV cavity.
Management included inotropic support and aggressive diuresis as well as LVAD speed reduction. Right ventricular function and LVAD flows recovered within 48–72 hours, and both patients survived to discharge without recurrent RHF.
Conclusion: Left coronary system myocardial infarction may precipitate acute RHF in LVAD-supported patients despite preserved LVAD function and absence of right coronary artery occlusion, potentially reflecting combined effects of altered ventricular interdependence, acute RV afterload increase, and relative RV ischemia. Early RV surveillance may enable prompt recognition and successful medical management.
