COVID-19 and the cardiovascular system

Abstract

The COVID-19 pandemic is raging on, with impressive numbers of cases and deaths. As of 19 May 2020, there are 4,731,458 confirmed cases of COVID-19 in the world, of which 112,637 in the last 24 hours; number of deaths is 316,169 , of which 4 322 in the day before last (1) . Regions most affected are the Americas, with 2, 082,945 cases, or 44% of all cases in the world, and Europe, with 1,909,592 cases, or 40% of all reported cases. Mortality rates are, so far, 6% and 8.8%, in the Americas and Europe, respectively (1). The new coronavirus, SARS-CoV-2, causes an acute upper respiratory tract infection in around 80% of patients; in 5 to 20% it may cause severe disease, especially involving the lungs, leading to hypoxemia and acute respiratory failure (2, 3). The disease COVID-19 manifested as a critical condition, leading to intensive care treatment, in 5% of Chinese patients, and in 14% of patients in New York, USA (2-3). In this subset of critically ill patients, multiple organ failure was seen, including cardiac dysfunction and decreased vascular tone, leading to hypotension. Risk factors for development of complications of Covid-19 include older age (e.g., >65 years), prior cardiovascular disease, chronic lung disease, hypertension, diabetes, and obesity (2, 3). The cardiovascular complications of COVID-19 deserve especial attention. Myocardial injury, usually defined as increased troponin levels, with or without additional electrocardiographic or echocardiographic data suggesting cardiac damage, has been associated with adverse outcomes (4-8). The etiology of troponin

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