COVID-19 Infection: Viral Macro- and Micro-Vascular Coagulopathy and Thromboembolism/Prophylactic and Therapeutic Management

Abstract

Coronavirus-2019 (COVID-19) predisposes patients to arterial and venous thrombosis commonly complicating the clinical course of hospitalized patients and attributed to the inflammatory state, endothelial dysfunction, platelet activation and blood stasis. This viral coagulopathy may occur despite thromboprophylaxis and raises mortality; the risk appears highest among critically ill inpatients monitored in the intensive care unit. The prevalence of venous thromboembolism in COVID-19 patients has been reported to reach ∼10-35%, while autopsies raise it to nearly 60%. The most common thrombotic complication is pulmonary embolism, which though may occur in the absence of a recognizable deep venous thrombosis and may be due to pulmonary arterial thrombosis rather than embolism, resulting in thrombotic occlusion of small- to mid-sized pulmonary arteries and subsequent infarction of lung parenchyma. This micro-thrombotic pattern seems more specific for COVID-19 and is associated with an intense immuno-inflammatory reaction that results in diffuse occlusive thrombotic micro-angiopathy with alveolar damage and vascular angiogenesis. Furthermore, thrombosis has also been observed in various arterial sites, including coronary, cerebral and peripheral arteries. Biomarkers related to coagulation, platelet activation and inflammation have been suggested as useful diagnostic and prognostic tools for COVID-19-associated coagulopathy; among them, D-dimer remains a key biomarker employed in clinical practice. Various medical societies have issued guidelines or consensus statements regarding thromboprophylaxis and treatment of these thrombotic complications specifically adapted to COVID-19 patients. All these issues are detailed in this review, data from meta-analyses and current guidelines are tabulated, while the relevant mechanisms of this virus-associated coagulopathy are pictorially illustrated.

COVID-19 and liver disease: mechanistic and clinical perspectives

“…However, it is plausible that pulmonary venothromboembolic disease, a hallmark of critical COVID-19, has a contributory role given the additional hypercoagulable state associated with cirrhosis. Whilst routine thromboprophylaxis is universally recommended in hospitalized patients with COVID-19, unified risk stratification models and treatment algorithms have yet to emerge, with wide variation in clinical practice and between international guidelines 107 , 108 . However, given the coagulopathy associated with both cirrhosis and COVID-19, the coexistence of these conditions might yield a cumulative risk of thrombotic complications 103 .…”

Thrombose und COVID-19

“…Für die Therapie der COVID-19-VTE werden eine Reihe von Substanzen eingesetzt – wie unfraktioniertes Heparin, niedermolekulare Heparine („low molecular weight heparin“, LMWH), direkte orale Antikoagulanzien (DOAK), Aggregationshemmer, Faktor-XII-Inhibitoren, thrombolytische Agenten, Nafamostat, Anti-Komplement und Anti-NET-Medikamente sowie IL-1-Rezeptor-Antagonist [ 45 ]. Zurzeit laufen mehrere randomisierte kontrollierte Studien (RCTs), die verschiedene Therapien, Kombinationen und Prophylaxe-Regime untersuchen.…”

Imaging in COVID-19-related myocardial injury

“…They have highlighted that SARS-CoV-2 causes endothelial dysfunction in various district [67]. Acute myocardial injuries might be due thrombotic complication [66,68]. Therefore, the term myocarditis should be used with caution in COVID-19 patients with elevated troponin levels without a specific diagnostic test.…”