Anticoagulant treatment in COVID-19: a narrative review

Abstract

The actual Coronavirus Disease (COVID 19) pandemic is due to Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a member of the coronavirus family. Besides the respiratory involvement, COVID 19 patients frequently develop a pro-coagulative state caused by virus-induced endothelial dysfunction, cytokine storm and complement cascade hyperactivation. It is common to observe diffuse microvascular thrombi in multiple organs, mostly in pulmonary microvessels. Thrombotic risk seems to be directly related to disease severity and worsens patients' prognosis. Therefore, the correct understanding of the mechanisms underlying COVID-19 induced prothrombotic state can lead to a thorough assessment of the possible management strategies. Hence, we review the pathogenesis and therapy of COVID 19-related thrombosis disease, focusing on the available evidence on the possible treatment strategies and proposing an algorithm for the anticoagulation strategy based on disease severity. Keywords COVID-19 • SARS-CoV-2 • Thrombosis • Anticoagulation Highlights • SARS-CoV-2 induced complement hyperactivation, endothelial dysfunction and cytokine storm have a prothrombotic effect. • COVID 19 patients develop a pro-coagulative state directly related to disease severity. • In COVID 19 critical patients, thrombotic lesions in pulmunary microvessels have a prevalence twice higher than critical non-COVID 19 patients. • Anticoagulant treatment is associated with lower mortality. Hence, we propose an algorithm for the anticoagulation strategy based on disease severity.

RT-PCR Mediated Identification of SARS-CoV-2 Patients from Particular Regions of Bangladesh and the Multi-factorial Analysis Considering Their Pre and Post Infection Health Conditions

“…Among all the patients (n=205), there was no case of sudden death due to myocardial infarction, venous thromboembolism or pulmonary embolism. Though, research conducted by Carfora et al (2020) showed similar findings [40], thromboprophylaxis was recommended for preventing thromboembolic events by Ribes et al (2020) [41]. However, therapeutic and prophylactic doses of anticoagulants are still clouded and different hospitals are using different regimens amidst concurrent death of patients [42].…”

Herz-Kreislauf-Erkrankungen und COVID-19

“…Pathologische Herzveränderungen, Verletzungen des vaskulären Endothels und Mikroangiopathien sind bei COVID-19-Patienten eine häufige Komplikation [ 9 , 10 ]. Myokardschädigungen werden bei etwa 20 % der COVID-19-Patienten beobachtet und sind mit einem erhöhten Mortalitätsrisiko verbunden [ 3 , 11 , 12 ]. Auffallend häufig ist dabei v. a. die rechtsventrikuläre (RV) Dilatation (39 %), gefolgt von einer linksventrikulären (LV) diastolischen Dysfunktion (16 %), wie man sie bei einer floriden Virusmyokarditis im Anfangsstadium auch sieht; mit etwa 10 % eher selten sind systolische LV-Funktions-Störungen.…”

“…So zeigten z. B. post-mortem-Untersuchungen an Lungengewebe von an COVID-19 verstorbenen Patienten massive Schädigungen des vaskulären Endothels mit Mikroangiopathien und Thromben, die ein deutlich stärkeres Ausmaß aufweisen, als das bei Influenzainfektionen oder bei anderen schwer kranken Patienten ohne SARS-CoV-2-Infektion beobachtet wird [ 11 , 12 ]. Möglicherweise spielt dabei eine verstärkte Komplementaktivierung im vaskulären Endothel eine Rolle, die dann zu Endothelitis und Hypoxie in verschiedenen Organen führt [ 4 ].…”

Cardiovascular System in COVID-19: Simply a Viewer or a Leading Actor?

“…The pathogenic mechanism of a high prevalence of thromboembolic events may be linked to the hypercoagulative state observed in COVID-19 patients. COVID-19 has been described as causing a proinflammatory state due to cytokine-mediated diffuse microvascular damage [44][45][46][47]. Some authors observed a close interaction between high D-dimer values and adverse events in COVID-19 [26,48,49].…”