The new β-coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) appears to exhibit cardiovascular pathogenicity through use of angiotensin-converting enzyme 2 (ACE2) for cell entry and the development of a major systemic inflammation. Furthermore, cardiovascular comorbidities increase susceptibility to SARS-CoV-2 infection and the development of a severe form of COronaVIrus Disease 2019 (COVID-19).
We describe the case of a COVID-19 patient whose inaugural presentation was a refractory cardiac arrest secondary to the destabilization of known, non-significant coronary artery disease. Patient was supported by venoarterial extracorporeal life support. After 12 h of support, cardiac function remained stable on low vasopressor support but the patient remained in a coma and brainstem death was diagnosed.
Myocardial injury is frequently seen among critically unwell COVID-19 patients and increases the risk of mortality. This case illustrates several potential mechanisms that are thought to drive the cardiac complications seen in COVID-19. We present the potential role of inflammation and ACE2 in the pathophysiology of COVID-19.