Conference Roundup troponin perturbation over the disease course of COVID-19. The response to increased inflammation associated with severe SARS-CoV-2 infections may contribute to multiorgan dysfunction and lead to long-term sequelae. Additional studies of troponin levels among patients hospitalized with COVID-19 are needed to assess whether reductions in the inflammatory response may decrease troponin levels and subsequent cardiac injury.
EFFECTS OF ASPIRIN THERAPY ON THROMBOTIC COMPLICATIONS IN PATIENTS WITH COVID-19 Antiplatelet therapy with aspirin does not protect patients with COVID-19 from thrombotic events or mortality, according to a study presented during the American College of Cardiology Annual Meeting, held May 15 to May 17, 2021. 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 COVID19-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 angiotensin-converting enzyme 2 (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, the authors evaluated the same protein expressions 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 aspirin or other
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HYPERINFLAMMATION AFFECTS TROPONIN LEVELS IN COVID-19 PATIENTS Troponin levels may be affected by beta natriuretic peptide (BNP), interleukin (IL)-6, and D-dimer concentrations among patients with COVID-19. These findings were presented during the American College of Cardiology Annual Meeting, held May 15 to May 17, 2021. Patients with severe COVID-19 are at risk for having a hyperinflammatory response such as a cytokine storm. Recent data suggest that some patients with COVID-19 experience cardiovascular damage. It remains unclear whether troponin levels during the course of a SARS-CoV-2 infection may be affected by markers of inflammation. To assess the relationship of COVID-19 and troponin, patients (N=586) admitted to Hackensack University Medical Center in New Jersey between February and June of 2020 who underwent at least 2 troponin assessments were retrospectively reviewed for hyperinflammatory responses and clinical outcomes. Mortality was associated with age, hypertension, coronary artery disease, heart failure, previous percutaneous cardiac intervention, use of beta-blockers or statins, hemodialysis, shock, concentrations of C-reactive protein, concentrations of IL-6, and change in troponin levels (all P <.05). Maximum troponin level correlated with BNP (correlation coefficient [r], 0.55; P <.05), D-dimer (r, 0.42; P <.05), and IL-6 (r, 0.30; P <.05) concentrations. Baseline troponin level was also correlated with BNP (r, 0.54; P <.05), D-dimer (r, 0.43; P <.05), and creatinine (r, 0.43; P <.05) concentrations. This study was limited by its retrospective design because there was no predetermined protocol for assessing troponin at set timepoints during patient hospitalization. These findings suggest the hyperinflammatory response may contribute to
Aspirin therapy does not protect against MI, VTE, and stroke in patients with COVID-19.
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 SARSCoV-2 receptors to permit viral access, but antiplatelet therapy consisting of aspirin does not protect from thrombotic events or mortality." ■
