A Case of Suspected Covid 19 Related Cardiomyopathy

BACKGROUND: The novel SARS-CoV-2 virus causing COVID-19 has been associated with diverse cardiovascular pathology. We present a case of cardiomyopathy due to possible COVID-19 resulting in cardiogenic shock. CASE: A 54 year-old male presented to the hospital with 4 weeks of progressive dyspnea, leg swelling, and weight gain. His symptoms began 4 weeks after experiencing influenza-like symptoms after a trip to China during the height of their COVID-19 outbreak. He was admitted to the COVID unit in cardiogenic shock and was later intubated for acute hypoxic respiratory failure. Laboratory data demonstrated acute kidney injury, elevated transaminases, lactic acidosis, elevated pro-BNP N-Terminal to 3932pg/mL, and high sensitivity troponin to 72ng/L. Transthoracic echocardiogram showed severe biventricular failure with a LVEF of 10% and a LVIDd 5.2cm. SARS-CoV-2 RNA was negative twice, but SARS-CoV-2 IgG AB and SARS-CoV-2 IgA AB were positive. Urgent right and left heart catheterization was performed demonstrating non-obstructive coronary artery disease and hemodynamics consistent with cardiogenic shock. While supported with an intra-aortic balloon pump (IABP) and norepinephrine, he had a fick cardiac output 3.1 L/min, fick cardiac index 1.6 L/min/m(2), pulmonary capillary wedge pressure 37mmHg, right atrial pressure 25mmHg, and pulmonary arterial pressures 65/40mmHg. Given persistent cardiogenic shock on IABP and inotropes, he was later transitioned to Veno-Arterial Extracorporeal Membrane Oxygenation (VA ECMO) and an Impella CP for left ventricular unloading. He continued to have persistent INTERMACS I shock and underwent successful implantation of a HeartMate 3 LVAD with percutaneous temporary right ventricular assist device (RVAD). Pathology of the left ventricular apical core demonstrates polyclonal endocardial infiltration of B-Cells, CD4 and CD8 positive T-Cells, eosinophils, macrophages, and plump reactive endothelial cells (Figure 1). He is currently recovering in the ICU off of vasoactive support with subsequent removal of percutaneous RVAD. CONCLUSION: This is a suspected case of COVID-19 associated cardiomyopathy presenting as new on-set heart failure with reduced ejection fraction complicated by cardiogenic shock. There is still much to learn about the cardiac manifestations of COVID-19 and further studies are needed to determine appropriate diagnostics and management of such cases.