Abstract
The link between severe forms of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection and cardiovascular diseases has been well documented by various studies that indicated a higher risk of cardiovascular complications in COVID-19 patients, in parallel with a higher risk of mortality in COVID-19 patients with underlying cardiovascular diseases. It seems that inflammation, which is a major pathophysiological substrate for both acute myocardial infarction and severe forms of COVID-19, may play a pivotal role in the interrelation between these two critical conditions, and hypercoagulability associated with SARS-CoV-2 infection could be responsible for acute cardiovascular complications. The neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) proved to be independent predictors for prognosis in acute coronary syndromes and systemic inflammatory diseases; therefore, they may be used as independent prognostic markers of disease severity in COVID-19 infection. The aim of this review is to present the most recent advances in understanding the complex link between SARS-CoV-2 infection, inflammation and alteration of blood coagulability and hemorheology, leading to major cardiovascular events.
Highlights
COVID-19 pandemic has caused a huge economic and health burden worldwide
It has been found that COVID-19-infected people are more likely to present with acute coronary syndrome (ACS), and the risk of heart failure has increased in a significant proportion of cases even before hospitalization for COVID-19 infection [2,4,5,6]
It seems that venous thromboembolism and arterial thrombosis are more frequent associated with COVID-19 coagulopathy than with sepsis-induced coagulopathy [46,48]
Summary
COVID-19 pandemic has caused a huge economic and health burden worldwide. The new coronavirus causes respiratory disease and affects the cardiovascular system. As indicated by recent data, inflammation caused by COVID-19 may be associated with alteration of coagulation parameters, leading to an increased risk of thromboembolic complications It seems that a direct association exists between COVID-19 and blood hypercoagulability, since elevated levels of D-dimers and fibrin degradation products, as well as prolongation of prothrombin time, have been documented in severe forms of COVID-19 and are significantly associated with increased mortality [1,7,8,9,10,11]. COVID-19 infection causes an overwhelmed inflammatory response with high levels of inflammatory cytokines, primarily tumor necrosis factor-α (TNF-α), interleukins (IL-2, IL-6, IL-7) and chemokines resulting in cytokine storm This inflammatory reaction may trigger hemorhelogic alterations and blood hypercoagulability, predisposing to arterial and venous thrombosis. This may lead to severe cardiovascular complications, such as acute myocardial infarction, deep vein thrombosis and pulmonary embolism
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