COVID-19 and cardiovascular consequences: Is the endothelial dysfunction the hardest challenge? Serena Del Turco 1, Annamaria Vianello 2, Rosetta Ragusa 3, Chiara Caselli 3, Giuseppina Basta 4 Affiliations
1Institute of Clinical Physiology, CNR, San Cataldo Research Area, Via Moruzzi, 1, 56124 Pisa, Italy. Electronic address: email@example.com.
2Department of Information Engineering, Telemedicine Section, University of Pisa, Italy.
3Institute of Clinical Physiology, CNR, San Cataldo Research Area, Via Moruzzi, 1, 56124 Pisa, Italy.
4Institute of Clinical Physiology, CNR, San Cataldo Research Area, Via Moruzzi, 1, 56124 Pisa, Italy. Electronic address: firstname.lastname@example.org.
Abstract A Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) has become a pandemic disease named Coronavirus Disease-19 (COVID-19) of epochal dimension. The clinical spectrum of COVID-19 is wide, ranging from asymptomatic forms to severe pneumonia, sepsis and multiple organ dysfunction syndromes resulting in poor outcomes. Among the various consequences of severe COVID-19, cardiovascular (CV) collapse appears the most serious and potentially lethal. On the other hand, pre-existent CV comorbidities are also associated with higher mortality. The most reliable hypothetical pathogenetic mechanism for CV complications and cardiac injury in severe COVID-19 patients appears to be a sustained endothelial dysfunction, caused by the interplay of inflammation and coagulation. In this review, we survey papers addressing issues related to severe COVID-19, characterized by enhanced lung microvascular loss, hypercytokinemia, hypoxemia and thrombosis. We discuss about how the virus-induced downregulation of the angiotensin converting enzyme-2 (ACE2) receptor, used to enter the host cell, could affect the renin-angiotensin system, attempting to clarify the doubts about the use of ACE inhibitors and Angiotensin-II receptor blockers in COVID-19 patients. Finally, we point out how the delicate and physiological homeostatic function of the endothelium, which turns into a disastrous battlefield of the complex interaction between “cytokine and coagulative storms”, can be irreparably compromised and result in systemic inflammatory complications. Keywords: COVID-19; Cardiac injury; Endothelial dysfunction; Inflammation; Thrombosis. Copyright © 2020. Published by Elsevier Ltd.