{"componentChunkName":"component---src-templates-blog-post-js","path":"/blog/the-unprecedented-link-between-covid-19-mortality-rates-and-blood-clots/","result":{"data":{"contentfulBlogPost":{"title":"The Unprecedented Link Between COVID-19 Mortality Rates and Blood Clots","publishDate":"June 13th, 2020","description":{"childMarkdownRemark":{"html":"

By Kripa Krishnan

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Fever, cough, and shortness of breath are well-known clinical symptoms of COVID-19, but there are manifestations of the virus with more severe implications that should be brought to light.

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Excessive blood clotting in patients with severe COVID-19 is a rapidly emerging trend observed across different geographies and in different patients regardless of age and the presence of other notorious underlying medical conditions. Many hematologists have come forth stating that the number of clotting problems in ICUs is unprecedented. Furthermore, there are also increases in the number of strokes reported amongst severe COVID-19 patients, a lot of whom are healthy individuals. While we can draw inferences and make postulations, we lack concrete epidemiological underpinnings about the viral pathology to pinpoint the exact reasons.

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This article aims to consolidate various anecdotes and theories as well as potential interventions in an attempt to broadly disseminate information.\nCritically ill patients with COVID-19 are at a heightened risk to develop pulmonary embolism as a result of venous thrombosis. Studies have empirically shown that there is a high prevalence of acute pulmonary embolism (Grillet, et al, 2020). This can be due to a variety of reasons including, inflammation of vessel walls and endothelial injury, pre-existing co-morbidities, and/or the notorious cytokine storm (Khan, et al, 2020). Additionally, it has been postulated that the diminished function of the ACE2 enzyme upon binding to the virus can result in an imbalance of Angiotensin I and Angiotensin II, which are hormones responsible for regulating blood pressure. This can, for example, increase blood pressure thereby clogging or bursting blood vessels that subsequently predisposes one to strokes.

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In the absence of diagnostic tests, one should be weary of the clinical manifestations of blood clotting such as facial drooping, chest pain, acute limb ischemia, and etc.

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Elevated D-dimer levels are essentially markers of coagulation activation, and studies have reported that there is a positive correlation observed between elevated D-dimer levels on admission and in-hospital COVID-19 mortality (Rotzinger, et al, 2020). Thus, interventions targeting the seemingly disturbed coagulation functioning may help prevent further clinical deterioration.

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Prophylactic low molecular weight heparin (LMHW) is widely known to be used as a means of early intervention. This essentially inhibits the conversion of prothrombin to thrombin and thus the conversion of fibrinogen to fibrin strands, which hinders clot formation. Other interventions that could be investigated include the use of coagulation protease inhibitors such as PAR antagonists. There is evidence that the PAR-1 antagonist reduced levels of pro-inflammatory cytokines, neutrophilic lung inflammation and alveolar leak during bacterial pneumonia in murine models (Jose, Manuel, 2020). Further, Antithrombin and anti-factory Xa are other oral anticoagulants that can potentially inhibit the production of pro-inflammatory cytokines. Another study (Morrow, et al, 2012) demonstrated Vorapaxar, a novel anti-platelet agent, can be used to inhibit the cellular actions of thrombin.\nOther studies have shown that patients of different ethnicities display differences in coagulopathic features. As such, a deeper investigation into the genetic variability amongst infected patients may offer better insights.

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References

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https://pubs.rsna.org/doi/10.1148/radiol.2020201544\nhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7224653/\nhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7151364/\nhttps://www.nejm.org/doi/pdf/10.1056/NEJMoa1200933

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