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Viral Coagulopathy in Patients With COVID-19: Treatment and Care.
Kipshidze, Nickolas; Dangas, George; White, Christopher J; Kipshidze, Nodar; Siddiqui, Fakiha; Lattimer, Christopher R; Carter, Charles A; Fareed, Jawed.
  • Kipshidze N; NY Cardiovascular Research, New York, NY, USA.
  • Dangas G; Icahn School of Medicine at Mount Sinai, New York, NY, USA.
  • White CJ; Ochsner Clinical School, University of Queensland, AU and Ochsner Medical Center, New Orleans, LA, USA.
  • Kipshidze N; NYU Langone Health, New York, NY, USA.
  • Siddiqui F; Department of Pathology, Cardiovascular Research Institute, Loyola University Chicago, Health Sciences Division, Maywood, IL, USA.
  • Lattimer CR; London Northwest University Health Care NHS Trust, London, United Kingdom.
  • Carter CA; Imperial College of Science, Technology and Medicine, London, United Kingdom.
  • Fareed J; Department of Clinical Research, College of Pharmacy & Health Sciences, Campbell University, Buies Creek, NC, USA.
Clin Appl Thromb Hemost ; 26: 1076029620936776, 2020.
Article in English | MEDLINE | ID: covidwho-657787
ABSTRACT
COVID-19 has proven to be particularly challenging given the complex pathogenesis of SARS-CoV-2. Early data have demonstrated how the host response to this novel coronavirus leads to the proliferation of pro-inflammatory cytokines, massive endothelial damage, and generalized vascular manifestations. While SARS-CoV-2 primarily targets the upper and lower respiratory tract, other organ systems are also affected. SARS-CoV-2 relies on 2 host cell receptors for successful attachment angiotensin-converting enzyme 2 and transmembrane protease serine 2. Clinicopathologic reports have demonstrated associations between severe COVID-19 and viral coagulopathy, resulting in pulmonary embolism; venous, arterial, and microvascular thrombosis; lung endothelial injury; and associated thrombotic complications leading to acute respiratory distress syndrome. Viral coagulopathy is not novel given similar observations with SARS classic, including the consumption of platelets, generation of thrombin, and increased fibrin degradation product exhibiting overt disseminated intravascular coagulation-like syndrome. The specific mechanism(s) behind the thrombotic complications in COVID-19 patients has yet to be fully understood. Parenteral anticoagulants, such as heparin and low-molecular-weights heparins, are widely used in the management of COVID-19 patients. Beyond the primary (anticoagulant) effects of these agents, they may exhibit antiviral, anti-inflammatory, and cytoprotective effects. Direct oral anticoagulants and antiplatelet agents are also useful in the management of these patients. Tissue plasminogen activator and other fibrinolytic modalities may also be helpful in the overall management. Catheter-directed thrombolysis can be used in patients developing pulmonary embolism. Further investigations are required to understand the molecular and cellular mechanisms involved in the pathogenesis of COVID-19-associated thrombotic complications.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Pneumonia, Viral / Coronavirus Infections / Thrombophilia / Pandemics / Betacoronavirus Type of study: Observational study / Prognostic study Topics: Long Covid Language: English Journal: Clin Appl Thromb Hemost Journal subject: Vascular Diseases Year: 2020 Document Type: Article Affiliation country: 1076029620936776

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Pneumonia, Viral / Coronavirus Infections / Thrombophilia / Pandemics / Betacoronavirus Type of study: Observational study / Prognostic study Topics: Long Covid Language: English Journal: Clin Appl Thromb Hemost Journal subject: Vascular Diseases Year: 2020 Document Type: Article Affiliation country: 1076029620936776