الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
The coronavirus disease pandemic that was reported by the World Health Organization in 2019, was caused by the severe acute respiratory syndrome coronavirus. It led to enormous deaths around the whole world with a mortality rate of about 30% of ICU patients.
Multiple studies have found a rise in the occurrence of thrombotic complications in COVID-19 patients, carried on changes in levels of D-dimer, antithrombin, and fibrinogen degradation products therefore a prothrombotic state of COVID-19 pathogenesis have been considered.
COVID-induced coagulopathy may be related to platelet over-reactivity, hypercoagulability, hypo-fibrinolysis, complement system activation, and derangement in the RAAS system in the presence of endothelial injury caused by the underlying inflammation.
The SARS-CoV-2 virus enters the infected patient cells where it binds to the ACE2 receptor which is present in the endothelium of many tissues. ACE2 functions as a peptidase that cleaves angiotensin-II. Elevated levels of angiotensin (Ang-II) increase oxidative stress and dysfunction of the endothelial cell through the production of superoxide anion. So the binding of the virus to ACE2 may lead to Angiotensin induced injury of the endothelial wall that has been detected in the autopsies of COVID-19 patients’ lungs.