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COVID-19 is a respiratory illness caused by the novel coronavirus SARS-CoV-2. Symptoms of COVID-19 range from mild upper airway distress to progressive life-threatening viral pneumonia. At the time of this writing, more than 22 million people have been infected with the virus and more than 782,000 people have died. A recent article summarizes emerging data suggesting that COVID-19 is also a vascular illness that elicits deleterious effects on the cardiovascular system.

SARS-CoV-2 virus enters human cells via the ACE2 receptor. Viral particles bind to the ACE2 receptor and together they travel into the cell. These viral particles can bind to a large number of ACE2 molecules, sequestering them from the cell surface and decreasing ACE2. The accompanying loss of ACE2 function can cause serious health consequences due to ACE2’s participation in key physiological processes. Blood vessels are rich in ACE2 receptors.

Although symptoms of COVID-19 are primarily related to its effects on the respiratory system, cardiovascular-related symptoms have been reported as well, including cardiac inflammation, blood clots, stroke, and “COVID toes” – blister-like lesions that appear on the digits of some infected people.

Several peer-reviewed articles have been published documenting cardiovascular-related symptoms in COVID-19 illness. One publication describes how SARS-CoV-2 infects the endothelial cells that line blood vessels to elicit endothelial cell dysfunction and subsequent cardiovascular complications. Another publication reports how widespread evidence of blood clots and endothelial cell infection in the lungs of people who died from COVID-19. One researcher suggested that the best therapy for COVID-19 might not be antiviral therapy; rather, drugs that stabilize the vascular endothelial tissue might be more effective.

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