Hyperthrombotic Milieu in COVID-19 Patients
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,...
| Main Authors: | , , , , |
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| Format: | Article |
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MDPI AG
2020
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| Online Access: | https://hdl.handle.net/1721.1/128363 |
| _version_ | 1811096390361677824 |
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| author | Kamel, Mohamed Hassan Yin, Wenqing Zavaro, Chris Francis, Jean M. Chitalia, Vipul C. |
| author2 | Massachusetts Institute of Technology. Institute for Medical Engineering & Science |
| author_facet | Massachusetts Institute of Technology. Institute for Medical Engineering & Science Kamel, Mohamed Hassan Yin, Wenqing Zavaro, Chris Francis, Jean M. Chitalia, Vipul C. |
| author_sort | Kamel, Mohamed Hassan |
| collection | MIT |
| description | 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. |
| first_indexed | 2024-09-23T16:42:59Z |
| format | Article |
| id | mit-1721.1/128363 |
| institution | Massachusetts Institute of Technology |
| last_indexed | 2024-09-23T16:42:59Z |
| publishDate | 2020 |
| publisher | MDPI AG |
| record_format | dspace |
| spelling | mit-1721.1/1283632022-10-03T07:46:39Z Hyperthrombotic Milieu in COVID-19 Patients Kamel, Mohamed Hassan Yin, Wenqing Zavaro, Chris Francis, Jean M. Chitalia, Vipul C. Massachusetts Institute of Technology. Institute for Medical Engineering & Science Harvard University--MIT Division of Health Sciences and Technology 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. NIH (Grant R01 HL132325) 2020-11-05T19:20:47Z 2020-11-05T19:20:47Z 2020-10 2020-09 Article http://purl.org/eprint/type/JournalArticle 2073-4409 https://hdl.handle.net/1721.1/128363 Kamel, Mohamed Hassan et al. "Hyperthrombotic Milieu in COVID-19 Patients." Cells 9, 11 (October 2020): 2392 © 2020 The Authors http://dx.doi.org/10.3390/cells9112392 Cells Creative Commons Attribution 4.0 International license https://creativecommons.org/licenses/by/4.0/ application/pdf MDPI AG MDPI |
| spellingShingle | Kamel, Mohamed Hassan Yin, Wenqing Zavaro, Chris Francis, Jean M. Chitalia, Vipul C. Hyperthrombotic Milieu in COVID-19 Patients |
| title | Hyperthrombotic Milieu in COVID-19 Patients |
| title_full | Hyperthrombotic Milieu in COVID-19 Patients |
| title_fullStr | Hyperthrombotic Milieu in COVID-19 Patients |
| title_full_unstemmed | Hyperthrombotic Milieu in COVID-19 Patients |
| title_short | Hyperthrombotic Milieu in COVID-19 Patients |
| title_sort | hyperthrombotic milieu in covid 19 patients |
| url | https://hdl.handle.net/1721.1/128363 |
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