Other proposed mechanisms of cardiac damage in patients with myocardial injury include complement activation and complement-mediated coagulopathy and microangiopathy; the downregulation of the ACE-2, with the dysregulation of the renin–angiotensin–aldosterone system; autonomic dysfunction; endothelial cell infection with endotheliitis and inflammation-triggered progression; and/or the destabilization of atherosclerotic plaques [6,29,30,31,32]. This evidence concerns the gene ACE2 and Abnormal autonomic nervous system physiology.