Jack Ryan Johnson '22

In regards to COVID-19, we are in a constantly evolving situation, with new research emerging every day. However, one thing is for sure: we do not fully understand the SARS-CoV-2 virus. What we do know is that COVID-19 is more than a simple respiratory infection. In fact, it can affect almost every organ system and lead to a wide array of lethal complications. As will be discussed in this article, in recent months, it appears that COVID-19 causes strokes. Because the SARS-CoV-2 virus is novel, all research is extremely new and a significant portion of information is anecdotal or poorly understood; therefore, while this article is based on all the data and research presently available, information referenced may very well be disproved or amended in the future.

When the SARS-CoV-2 virus infects a human host, it first infiltrates the lungs. It utilizes a spike-shaped protein to connect directly to angiotensin-converting enzyme 2 (ACE2). That specific enzyme is found abundantly in type II alveolar (alveoli are the sacs inside the lungs where gas exchange with the blood occurs) cells.

As the infection spreads, the body mounts an immune response: inflammation, the body’s automatic response to any sort of harmful stimuli. It includes several complex processes involving the blood vessels, immune cells, and chemical releases. What is important, however, is that inflammation is typically a normal response to physical injury, infection, or irritation. What is abnormal is that infections with the SARS-CoV-2 virus have a rampant tendency to induce systemic hyperinflammation, also referred to as “cytokine storm,” a condition in which the body has a massive, out-of-control inflammatory response to infection.

Although it is not precisely understood why, significant inflammation, such as that caused by cytokine storm, has a close relationship with thrombosis, the process of forming blood clots. Additionally, it appears as though the SARS-CoV-2 virus may interfere directly with both with the endothelium, the cells that line blood vessel walls, and the clotting cascades themselves, the chemical process by which blood clots are formed. Regardless of the precise origin, we know that the virus causes increased thrombosis in certain patients. This is supported by elevated levels of D-dimer, a product of the degradation of blood clots, in vast numbers of COVID-19 patients.

NOTE: While elevated D-dimer levels can be indicative of a variety of conditions in patients, they were observed to support the hypothesis that COVID-19 patients were suffering from increased thrombosis in the publications below.

Extraneous and unintentional blood clots in the body are dangerous because they can become stuck in blood vessels and clog the path of blood flow. If they clog the blood vessels supplying the heart, a myocardial infarction, or heart attack, can occur. If they become stuck in the blood vessels of the lungs, the patient may suffer a pulmonary embolism. And, most notably, if they block an artery in the brain, a stroke may occur.

A stroke occurs when blood flow to brain tissue is interrupted. When it occurs as the result of a “clog” in the artery, also known as an occlusion, we call it an ischemic stroke. When the blood flow is interrupted, brain tissue immediately begins to die; brain tissue also will not regrow, which is what makes strokes so devastating. However, strokes typically occur in older patients, with only 34% of stroke hospitalization in the United States being patients under the age of 65.

A skyrocketing number of young patients infected with the SARS-CoV-2 virus are experiencing strokes. A study performed by physicians at Mt. Sinai hospital in New York City, NY, showed a 700% increase in strokes in COVID-19 positive patients under the age of 50. Another study performed by several physicians in the Netherlands found a 31% overall increase in thrombotic issues over 184 critically ill COVID-19 patients in the intensive care unit (ICU). Simply put, SARS-CoV-2 is causing young patients with few or no underlying conditions or comorbidities to experience life-threatening strokes that are highly atypical for their age.

Compounding that fact, many patients with such symptoms are not seeking medical care or actively declining treatment. According to a combination of survey data from Mt. Sinai and my own anecdotal experiences working on 911 ambulances during the pandemic, this is a function of several things: young patients do not suspect that they could be having a stroke, people are afraid of potentially catching COVID-19 from going to the hospital, and people are reluctant to “use up resources” for what they believe are non-COVID-19-related issues. I have personally dealt with patients with potentially life-threatening issues that attempt to refuse care. Their explanation tends to revolve around guilt derived from going to the hospital or accepting field treatment during a time when so many are critically ill.

The amalgamation of avoidance of medical care and a terrifying increase in strokes in young patients poses a massive health risk. Most importantly however, the emerging and evolving findings surrounding COVID-19 should humble us. There is so much we do not yet know, and to dismiss the dangers of the virus now would be a lethal action with disastrous consequences.

Works Cited

"Angiotensin-Converting Enzyme 2." Wikipedia, 19 Oct. 2020, en.wikipedia.org/wiki/Angiotensin-converting_enzyme_2. Accessed 25 Oct. 2020.

Bikdeli, Behnood, et al. "COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-Up: JACC State-of-the-Art Review." Journal of the American College of Cardiology, vol. 75, no. 23, 16 June 2020, pp. 2950-73, doi.org/10.1016/j.jacc.2020.04.031. Accessed 25 Oct. 2020.

Centers for Disease Control and Prevention. "Stroke Facts." Centers for Disease Control and Prevention, 8 Sept. 2020, www.cdc.gov/stroke/facts.htm. Accessed 25 Oct. 2020.

"D-dimer." Wikipedia, 20 Oct. 2020, en.wikipedia.org/wiki/D-dimer. Accessed 25 Oct. 2020.

Gill, Morayma Reyes, et al. "COVID-19 and D-dimer: Frequently Asked Questions." American Society of Hematology, 20 Apr. 2020, www.hematology.org/covid-19/covid-19-and-d-dimer. Accessed 25 Oct. 2020.

Klok, F. A., et al. "Incidence of Thrombotic Complications in Critically Ill ICU Patients with COVID-19." Thrombosis Research, www.thrombosisresearch.com/article/S0049-3848(20)30120-1/pdf. Accessed 25 Oct. 2020.

Long, Brit, et al. "Cardiovascular Complications in COVID-19." The American Journal of Emergency Medicine, vol. 38, no. 7, July 2020, pp. 1504-07, doi.org/10.1016/j.ajem.2020.04.048. Accessed 25 Oct. 2020.

McNamara, Damian. "COVID-19 Linked to Large Vessel Stroke in Young Adults." Medscape Medical News, Medscape, 24 Apr. 2020, www.medscape.com/viewarticle/929345. Accessed 25 Oct. 2020.

Oxley, Thomas J., et al. Large-Vessel Stroke as a Presenting Feature of Covid-19 in the Young. New England Journal of Medicine, 28 Apr. 2020. The New England Journal of Medicine, www.nejm.org/doi/full/10.1056/NEJMc2009787?query=featured_home. Accessed 25 Oct. 2020.

Smith, Matthew S., et al. "Endovascular Therapy for Patients with Acute Ischemic Stroke during the COVID-19 Pandemic: A Proposed Algorithm." Stroke, no. 51, Spring 2020, pp. 1902-09, doi.org/10.1161/STROKEAHA.120.029863. Accessed 25 Oct. 2020.

"Thrombosis and Inflammation: The Connection." North American Thrombosis Forum, 31 July 2017, natfonline.org/2017/07/thrombosis-inflammation-connection/. Accessed 25 Oct. 2020.

Verdecchia, Paolo, et al. "The Pivotal Link between ACE2 Deficiency and SARS-CoV-2 Infection." Elsevier Public Health Emergency Collection: Public Health Emergency COVID-19 Initiative, June 2020, www.ncbi.nlm.nih.gov/pmc/articles/PMC7167588/.