Fig 1.

Cardiac Injury as a Result of Multiple Mechanisms, Triggered by SARS-COV2. SARS-COV2 incites a host response which stimulates pro-inflammatory and pro-thrombotic pathways with potential adverse effects on the cardiac microenvironment. SARS-CoV2 viral particles have also been identified in the heart of some with severe COVID-19, raising the possibility that dissemination of the virus to the heart may mediate cardiac injury. Given the cardio-protective role of ACE2 for homeostatic maintenance of the cardiac microenvironment, additional damage may occur through depletion of ACE2. In those with severe acute illness, hemodynamic and cardiometabolic stressors also likely contribute to the adverse cardiovascular effects. Thus, cardiac injury may represent a common final pathway, reflecting multiple pathways triggered by the SARS-COV2 and the host response, leading to compromised cardiovascular performance.