tetano
Editor, Senior Moderator
Clin Cardiol
. 2020 Nov 11.
doi: 10.1002/clc.23460. Online ahead of print.
COVID-19, thromboembolic risk, and Virchow's triad: Lesson from the past
Jawahar L Mehta[SUP] 1 [/SUP], Giuseppe Calcaterra[SUP] 2 [/SUP], Pier P Bassareo[SUP] 3 [/SUP]
Affiliations
Abstract
COronavirus Infectious Disease which started in 2019 (COVID-19) usually presents with the signs and symptoms of pneumonia. However, a growing number of recent reports highlight the fact that the infection may be by far more than only a respiratory disease. There is evidence of an increased thromboembolic risk in COVID-19 patients, with a variety of manifestations in terms of ischemic stroke, deep vein thrombosis, acute pulmonary embolism, acute myocardial infarction, systemic arterial embolism, and placental thrombosis. The German physician Rudolph Virchow, about two centuries ago, described three pivotal factors contributing together to thromboembolic risk: endothelial injury, hypercoagulability, and blood stasis. COVID-19-associated hypercoagulability is unique and distinctive, and has its own features involving the immune system. Many of the drugs proposed and currently undergoing evaluation for the treatment of COVID-19 have one or more of the Virchow's triad elements as a target. The three factors outlined by Virchow are still able to explain the venous and arterial hypercoagulable state in the dramatic COVID-19 setting. Nowadays, we have decidedly more sophisticated diagnostic tools than Virchow had, but many of the challenges that we are facing are the same as Virchow faced in the 19th century.
Keywords: COVID-19; SARS-CoV-2; blood stasis; endothelial injury; hypercoagulability; thromboembolism.
. 2020 Nov 11.
doi: 10.1002/clc.23460. Online ahead of print.
COVID-19, thromboembolic risk, and Virchow's triad: Lesson from the past
Jawahar L Mehta[SUP] 1 [/SUP], Giuseppe Calcaterra[SUP] 2 [/SUP], Pier P Bassareo[SUP] 3 [/SUP]
Affiliations
- PMID: 33176009
- DOI: 10.1002/clc.23460
Abstract
COronavirus Infectious Disease which started in 2019 (COVID-19) usually presents with the signs and symptoms of pneumonia. However, a growing number of recent reports highlight the fact that the infection may be by far more than only a respiratory disease. There is evidence of an increased thromboembolic risk in COVID-19 patients, with a variety of manifestations in terms of ischemic stroke, deep vein thrombosis, acute pulmonary embolism, acute myocardial infarction, systemic arterial embolism, and placental thrombosis. The German physician Rudolph Virchow, about two centuries ago, described three pivotal factors contributing together to thromboembolic risk: endothelial injury, hypercoagulability, and blood stasis. COVID-19-associated hypercoagulability is unique and distinctive, and has its own features involving the immune system. Many of the drugs proposed and currently undergoing evaluation for the treatment of COVID-19 have one or more of the Virchow's triad elements as a target. The three factors outlined by Virchow are still able to explain the venous and arterial hypercoagulable state in the dramatic COVID-19 setting. Nowadays, we have decidedly more sophisticated diagnostic tools than Virchow had, but many of the challenges that we are facing are the same as Virchow faced in the 19th century.
Keywords: COVID-19; SARS-CoV-2; blood stasis; endothelial injury; hypercoagulability; thromboembolism.