Direct viral invasion of myocardial cells via angiotensin-converting enzyme 2 (ACE2) receptors, dysregulation of the renin-angiotensin-aldosterone system (RAAS), systemic inflammation, cytokine storm, endothelial dysfunction, and hypercoagulable states have been proposed as potential contributors to cardiac injury and dysfunction. This evidence concerns the gene ACE2 and endothelial dysfunction.