COVID-19 and Acute Coronary Syndromes: From Pathophysiology to Clinical Perspectives

Figure 1

Pathophysiology of ACS in COVID-19. Mechanisms involved in the pathophysiology of ACS in patients with COVID-19. SARS-CoV-2, by binding the ACE2 receptors expressed on the surface of the host cell, may infect pneumocytes, macrophages, and endothelial cells. The respiratory impairment related to the pulmonary involvement, ranging from pneumonia to ARDS in severe forms, causes hypoxia and type 2 MI due to the oxygen supply/demand mismatch. Also, the infection promotes an aberrant inflammatory response resulting in the release of cytokines and proinflammatory molecules such as IL-1, IL-6, IL-7, TNFα, and IFNγ. Cytokines have the potential to damage the endothelial function with increased production of oxidative stress agents and prothrombotic factors. SARS-CoV-2 may also exert a direct cellular effect by interacting with molecules expressed on the surface of the endothelial cells. In turn, the inflammatory environment enhances the instability of preexisting atheromatous plaques, promotes platelets activation and aggregation, and upregulates the sympathetic nervous system resulting in increased vasomotility and coronary spasm. The interplay of all these mechanisms may favor plaque rupture and thrombosis leading to type 1 MI. ACS: acute coronary syndrome; ACE2: angiotensin-converting enzyme 2; COVID-19: coronavirus disease 2019; IFNγ: interferon γ; IL-1: interleukin 1; IL-6: interleukin 6; IL-7: interleukin 7; MI: myocardial infarction; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2; TNFα: tumor necrosis factor α.