COVID-19 is a viral respiratory illness caused by the SARS-CoV-2 infection. In addition to lung disease, clinical complications of COVID-19 include myocardial damage and ischemia-related vascular disease. Severe manifestations and poor prognosis in these patients are associated with a hypercoagulable state predisposing to thrombotic-related complications and eventually death. However, these clinical features can also occur in other forms of pneumonia, such as community-acquired pneumonia (CAP), which, is also complicated by vascular diseases and characterized by platelet activation. Platelets play a pivotal role in these settings as bacteria and viruses may induce activation via Toll-like receptors (TLRs) in CAP patients and different and multiple pathways, including ACE2-AngII axis and/or TLRs, in COVID-19 patients. Despite evidence confirming the implication of platelet activation in both settings, their contribution to the thrombotic process is still under investigation. Thus, in this review, we (1) compare the thrombotic features of SARS-CoV-2 infection and CAP, (2) analyze the putative mechanisms accounting for venous and arterial thrombosis in SARS-CoV-2 infection, and (3) discuss the potential anticoagulant armamentarium to counteract thrombosis.
Keywords: COVID-19; SARS-CoV-2 infection; anticoagulation; platelets; thrombosis.