Endothelialitis plays a central role in the pathophysiology of severe COVID-19 and its cardiovascular complications.

This clinical review paper discusses the pathophysiology of the pulmonary and cardiovascular manifestations of a SARS-CoV-2 infection and the ensuing implications on acute cardiovascular care in patients presenting with a severe COVID-19 syndrome admitted to an intensive acute cardiac care unit. The high prevalence of old age, obesity, diabetes, hypertension, heart failure, and ischaemic heart disease in patients who develop a severe to critical COVID-19 syndrome suggests shared pathophysiological mechanisms. Pre-existing endothelial dysfunction and an impaired innate immune response promote the development by the viral infection of an acute endothelialitis in the pulmonary microcirculation complicated by abnormal vasoconstrictor responses, luminal plugging by inflammatory cells, and intravascular thrombosis. This endothelialitis extends into the systemic circulation what may lead to acute myocardial injury, myocarditis, and thromboembolic complications both in the arterial and venous circulation. Ever since the first case reports from the city of Wuhan in China in December of 2019, coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) continues as a raging pandemic causing significant morbidity and mortality [1]. In this paper we provide a review of the epidemiological characteristics and the pathophysiology of SARS-CoV-2 infection, and formulate the hypothesis that endothelialitis may play a key role in the pathogenesis of the pulmonary and cardiovascular complications of COVID-19.