Hypercoagulability phenomenon in patients with COVID-19

Abstract

SARS-CoV-2 is the virus responsible for respiratory infection of the lower tract, also known as severe acute respiratory syndrome. Considering the severe clinical manifestations, it is estimated that 20-30% will have complications at the cardiovascular level and 30-50% at the renal level. Initially, SARS-CoV-2 infects our cells through an angiotensin-converting enzyme receptor 2 (ECA2 or ACE-2) in the pulmonary alveoli. There is sensitization of defense cells with consequent release of cytokines in the blood, entitled for the pathology as “cytokine storm”, including interleukins 1 and 6 (pro-inflammatory), tumor necrosis factor and γ-interferon. It is observed in this pathology the occurrence of events of hypercoagulability and ischemia due to hypoxia. Then, to reverse this clinical condition, the hypothesis of the use of anticoagulants in the pathophysiology of critically ill patients with COVID-19 has been emerging. After an immunological response, an inflammatory event occurs with consequent endothelial damage. The inflammation mediators mentioned above activate procoagulating factors. Among them, extrinsic and intrinsic factors. Based on this premise, all patients hospitalized with COVID-19 should receive anticoagulants if they are not at risk of bleeding. However, randomized studies with unfractionated and low molecular weight heparin are necessary to prove the inhibitory activity of SARS-CoV-2, in addition to presenting a perspective on causing conformational changes in the virus, making them a possibility pharmacological. From the studies analyzed, it was concluded that the use of anticoagulants in the pathophysiology of COVID-19 is quite effective, in relation to the hypercoagulability mechanism that the disease promotes.