The following article is a part of conference coverage from the American College of Cardiology’s 70th Annual Scientific Session & Expo is being held virtually from May 15 to 17, 2021. The team at Cardiology Advisor will be reporting on the latest news and research conducted by clinicians and scientists in the field. Check back for more from the ACC 2021 .

Although human platelets do express the requisite receptors for SARS-CoV-2 to permit access to this virus, antiplatelet therapy with aspirin does not protect patients with COVID-19 from thrombotic events or mortality. These findings were presented during the American College of Cardiology Annual Meeting, held virtually from May 15 to 17, 2021.


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COVID-19 has been found to be associated with an increased risk for thrombotic events such as stroke, myocardial infarction (MI), and venous thromboembolism (VTE). It is unknown what influence activated platelets may have on COVID-19-associated thrombosis and whether antiplatelet therapies may be of benefit in patients with SARS-CoV-2 infection.

The Cleveland Clinic team in Ohio evaluated the protein expression of both ACE2 (n=20) and TMPRSS2 (n=20) in healthy human platelets via immunoblotting and confirmed the results via confocal microscopy (ACE2, n=6; TMPRSS2, n=3). For comparison, immunoblotting was used to evaluate the protein expression of ACE2 and TMPRSS2 in patients (n=10, each) with coronary artery disease.

To determine if antiplatelet therapy protects against MI, VTE, or death, researchers conducted a review of 22,072 patients who were tested for COVID-19 and matched them with 248 COVID-19-positive patients who were not exposed to the aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs) during treatment.

Both ACE2 and TMPRSS2 were found to be present on human platelets. No association was shown between the expression of ACE2 (r2=.004; P =.79) or TMPRSS2 (r2=.058; P =.30) and age. A numerically higher expression of ACE2 and TMPRSS2 was seen in patients with coronary artery disease vs patients in the control group. In the propensity-matched analyses of aspirin use, no difference was found in the incidence of MI and VTE. However, aspirin therapy was associated with increased risk for thrombotic stroke (3.6% vs 0.40%; P =.036), as well as the composite endpoint of MI, VTE, and stroke (9.3% vs 2.8%; odds ratio [OR], 3.52; 95% CI, 1.48-8.40; P =.005). NSAID therapy was similarly associated with risk for the composite endpoint (3.8% vs 1.6%; OR, 2.49; 95% CI, 0.58-1.62; P =.046). Neither aspirin therapy (OR, 0.52; 95% CI, 0.51-1.41; P =.52) nor NSAID therapy (OR, 0.97; 95% CI, 0.58-1.62; P =.90) were associated with mortality.

The investigators concluded, “Human platelets express the requisite SARS-CoV-2 receptors to permit viral access, but antiplatelet therapy consisting of aspirin does not protect from thrombotic events or mortality.”

Reference

Bhandari R, Sahai A, Elbadawi A, et al. SARS-COV-2 platelet function and thrombotic complications: effects of aspirin therapy in COVID-19. Presented at the American College of Cardiology (ACC) 2021 Annual Meeting; May 15-17, 2021. Abstract.

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