Cardiovascular disease (CVD) is the most common co-morbidity associated with COVID-19 and the fatality rate in COVID-19 patients with CVD is higher compared to other comorbidities, such as hypertension and diabetes. Preliminary data suggest that COVID-19 may also cause or worsen cardiac injury in infected patients through multiple mechanisms such as ‘cytokine storm’, endotheliosis, thrombosis, lymphocytopenia etc. Autopsies of COVID-19 patients reveal an infiltration of inflammatory mononuclear cells in the myocardium, confirming the role of the immune system in mediating cardiovascular damage in response to COVID-19 infection and also suggesting potential causal mechanisms for the development of new cardiac pathologies and/or exacerbation of underlying CVDs in infected patients. In this review, we discuss the potential underlying molecular mechanisms that drive COVID-19-mediated cardiac damage, as well as the short term and expected long-term cardiovascular ramifications of COVID-19 infection in patients. Graphical abstract Unlabelled Image
【저자키워드】 COVID-19, Neutrophils, Monocytes, Cytokine storm, SARS-CoV2, macrophages, immunopathology, heart failure, myocarditis, ARDS, acute respiratory distress syndrome, CRP, C-reactive protein, CRS, Cytokine release syndrome, TMPRSS2, Transmembrane Protease Serine 2, ACE, angiotensin-converting enzyme, CVD, cardiovascular disease, MERS-CoV, Middle East Respiratory Syndrome associated coronavirus, SARS-CoV-2, Severe Acute Respiratory Syndrome associated coronavirus, NT-proBNP, N-terminal pro-B-type natriuretic peptide, hs-TnI, high sensitivity cardiac troponin I, Myofibroblasts,