The Link between SARS-CoV-2 Infection, Inflammation and Hypercoagulability-Impact of Hemorheologic Alterations on Cardiovascular Mortality

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.

Prognostic value of neutrophile-to-lymphocyte ratio (NLR) and lactate dehydrogenase (LDH) levels for geriatric patients with COVID-19

“…COVID-19 was associated with systemic inflammation and hypercoagulability which can also be accompanied by cytokine storm that alters the hematological parameters. Thus, the link between COVID-19 and cardiovascular diseases was investigated by several studies and NLR might be used as an independent prognostic marker for COVID-19 in terms of disease severity [ 9 ]. In addition to this, NLR had also been evaluated for the septic patients that it can be useful as a prognostic parameter via having a correlation with mortality prediction scores such as APACHE-II and SOFA [ 10 ].…”

Coagulation disorders and vascular diseases of the liver in patients with COVID-19

“…In this interplay, inflammation and coagulation act together to block the spread of the pathogen [25]. Another significant process involved in COVID-19 related thrombosis is excessive complement activation that favors tissue damage and intravascular thrombosis [26].…”

“…Indeed COVID-19 infection can cause a massive inflammatory response with high levels of inflammatory cytokines (tumor necrosis factor α [TNF-α], interleukin 2, 6, 7) and chemokines, resulting in the cytokine storm. This inflammatory reaction is directly related to hypercoagulability [26]. An important confounding factor which is recently recognized is the pathological angiogenesis, as implied by the overexpression of proangiogenic factors (VEGF, FGF) in COVID-19 patients (Fig.…”

Sinus venous thrombosis as a complication of COVID-19-associated hypercoagulability

“…We do not agree with the statement that hypercoagulability is a complication of COVID-19 only if there is concomitant arterial hypertension or diabetes [ 1 ]. Hypercoagulability is a common complication not only of severe, but also of mild or moderate COVID-19 [ 2 ] and explained by (1) direct activation of platelets, enhancing coagulation; (2) direct infection and indirect activation of endothelial cells by the cytokine storm, shifting endothelium from an anti-thrombotic to a pro-thrombotic state, and (3) direct activation of complement pathways, promoting thrombin generation [ 3 ]. Since SARS-CoV-2 activates the immune system, autoimmune disease is a frequent complication [ 4 ], including immune thrombocytopenia, which may further enhance the thrombogenic state in COVID-19 patients [ 5 ].…”