tetano
Editor, Senior Moderator
Cells
. 2020 Oct 31;9(11):E2392.
doi: 10.3390/cells9112392.
Hyperthrombotic Milieu in COVID-19 Patients
Mohamed Hassan Kamel[SUP] 1 [/SUP], Wenqing Yin[SUP] 1 [/SUP], Chris Zavaro[SUP] 1 [/SUP], Jean M Francis[SUP] 1 [/SUP], Vipul C Chitalia[SUP] 1 2 3 [/SUP]
Affiliations
Abstract
COVID-19 infection has protean systemic manifestations. Experience from previous coronavirus outbreaks, including the current SARS-CoV-2, has shown an augmented risk of thrombosis of both macrovasculature and microvasculature. The former involves both arterial and venous beds manifesting as stroke, acute coronary syndrome and venous thromboembolic events. The microvascular thrombosis is an underappreciated complication of SARS-CoV-2 infection with profound implications on the development of multisystem organ failure. The telltale signs of perpetual on-going coagulation and fibrinolytic cascades underscore the presence of diffuse endothelial damage in the patients with COVID-19. These parameters serve as strong predictors of mortality. While summarizing the alterations of various components of thrombosis in patients with COVID-19, this review points to the emerging evidence that implicates the prominent role of the extrinsic coagulation cascade in COVID-19-related coagulopathy. These mechanisms are triggered by widespread endothelial cell damage (endotheliopathy), the dominant driver of macro- and micro-vascular thrombosis in these patients. We also summarize other mediators of thrombosis, clinically relevant nuances such as the occurrence of thromboembolic events despite thromboprophylaxis (breakthrough thrombosis), current understanding of systemic anticoagulation therapy and its risk-benefit ratio. We conclude by emphasizing a need to probe COVID-19-specific mechanisms of thrombosis to develop better risk markers and safer therapeutic targets.
Keywords: COVID-19; Coronavirus; SARS-CoV2; VTE; embolism; endotheliopathy; kidney failure; microvascular thrombosis; myocardial infarction; respiratory failure; strokes; thrombosis.
. 2020 Oct 31;9(11):E2392.
doi: 10.3390/cells9112392.
Hyperthrombotic Milieu in COVID-19 Patients
Mohamed Hassan Kamel[SUP] 1 [/SUP], Wenqing Yin[SUP] 1 [/SUP], Chris Zavaro[SUP] 1 [/SUP], Jean M Francis[SUP] 1 [/SUP], Vipul C Chitalia[SUP] 1 2 3 [/SUP]
Affiliations
- PMID: 33142844
- DOI: 10.3390/cells9112392
Abstract
COVID-19 infection has protean systemic manifestations. Experience from previous coronavirus outbreaks, including the current SARS-CoV-2, has shown an augmented risk of thrombosis of both macrovasculature and microvasculature. The former involves both arterial and venous beds manifesting as stroke, acute coronary syndrome and venous thromboembolic events. The microvascular thrombosis is an underappreciated complication of SARS-CoV-2 infection with profound implications on the development of multisystem organ failure. The telltale signs of perpetual on-going coagulation and fibrinolytic cascades underscore the presence of diffuse endothelial damage in the patients with COVID-19. These parameters serve as strong predictors of mortality. While summarizing the alterations of various components of thrombosis in patients with COVID-19, this review points to the emerging evidence that implicates the prominent role of the extrinsic coagulation cascade in COVID-19-related coagulopathy. These mechanisms are triggered by widespread endothelial cell damage (endotheliopathy), the dominant driver of macro- and micro-vascular thrombosis in these patients. We also summarize other mediators of thrombosis, clinically relevant nuances such as the occurrence of thromboembolic events despite thromboprophylaxis (breakthrough thrombosis), current understanding of systemic anticoagulation therapy and its risk-benefit ratio. We conclude by emphasizing a need to probe COVID-19-specific mechanisms of thrombosis to develop better risk markers and safer therapeutic targets.
Keywords: COVID-19; Coronavirus; SARS-CoV2; VTE; embolism; endotheliopathy; kidney failure; microvascular thrombosis; myocardial infarction; respiratory failure; strokes; thrombosis.