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COVID-19 and thrombosis: The role of hemodynamics
Sudeep Sastry1, Federica Cuomo1, Jayaveera Muthusamy1
1W.L. Gore and Associates, Inc., Flagstaff, AZ, USA.
Insights
Severe COVID-19 increases thromboembolic events, impacting organs. This review explores how altered blood flow dynamics, or hemodynamics, may drive thrombosis in severe coronavirus disease 2019, suggesting new therapeutic targets.
Area of Science:
- Cardiovascular Science
- Infectious Diseases
- Pathophysiology
Background:
- Severe coronavirus disease 2019 (COVID-19) is linked to a high risk of thromboembolic events, contributing to adverse outcomes.
- While endothelial injury and hypercoagulability are studied, the role of hemodynamics in COVID-19 thrombosis remains under-investigated.
- Thrombosis is influenced by hemodynamic factors like shear stress, stasis, and turbulent flow, as per Virchow's triad and platelet activation studies.
Purpose of the Study:
- To review COVID-19 thrombotic events and hypothesize the contribution of hemodynamic pathways.
- To focus on hemodynamic factors such as stasis, turbulent flow, and non-physiological shear stress in COVID-19 thrombosis.
- To discuss hemodynamics-dependent venous, arterial, and microvascular thrombosis in COVID-19 patients.
Main Methods:
- Literature review of recent studies on COVID-19 related thrombotic events.
- Analysis of established hemodynamic principles (Virchow's triad, shear stress) in the context of COVID-19 pathophysiology.
- Synthesis of information to propose hypotheses on hemodynamics' role in COVID-19 thrombosis.
Main Results:
- Endothelial injury and hypercoagulability are known contributors to COVID-19 thrombosis.
- Hemodynamic factors like stasis, turbulent flow, and altered shear stress are hypothesized to play a significant role in COVID-19 related thrombogenesis.
- The review highlights the potential for hemodynamics to explain various thrombotic complications observed in severe COVID-19.
Conclusions:
- Hemodynamic alterations may be a critical, understudied factor in the development of thrombosis in severe COVID-19.
- Understanding hemodynamics-dependent thrombosis could offer new insights into COVID-19's severe manifestations.
- Further investigation into diagnostic and therapeutic strategies targeting hemodynamic aspects of COVID-19 thrombus formation is warranted.
Abstract:
Severe coronavirus disease 2019 (COVID-19) is characterized by an increased risk of thromboembolic events, a leading cause for adverse outcomes in patients afflicted by the more serious manifestation of the disease. These thromboembolic complications expressed as sepsis-induced coagulopathy, disseminated intravascular coagulation, venous and arterial thromboembolism, pulmonary embolism, microthrombosis, and thrombotic microangiopathy have been observed to affect different organs such as the lungs, heart, kidneys, and brain. Endothelial injury and dysfunction have been identified as the critical pathway towards thrombogenesis, and contributions of other mechanisms such as hypercoagulability, cytokine storm, neutrophils have been studied. However, the contribution of hemodynamic pathways towards thrombosis in severe COVID-19 cases has not been investigated. From the classical theory of Virchow's triad to the contemporary studies on the effect of shear enhanced platelet activation, it is well established that hemodynamics plays a role in the initiation and growth of thrombosis. This article reviews recent studies on COVID-19 related thrombotic events and offers hypotheses on how hemodynamics may be responsible for some of the adverse outcomes observed in severe COVID-19 cases. While thrombogenesis through endothelial injury and the effects of hypercoagulability on thrombosis are briefly addressed, the crux of the discussion is focused on hemodynamic factors such as stasis, turbulent flow, and non-physiological shear stress and their effects on thrombosis. In addition, hemodynamics-dependent venous, arterial, and microvascular thrombosis in COVID-19 cases is discussed. We also propose further investigation of diagnostic and therapeutic options that address the hemodynamics aspects of COVID-19 thrombus formation to assess their potential in patient care.
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