Background: There is inconclusive and controversial evidence of the association between allergic diseases and the risk of adverse clinical outcomes of coronavirus disease 2019 (COVID-19). Objective: We sought to determine the association of allergic disorders with the likelihood of a positive severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) test result and with clinical outcomes of COVID-19 (admission to intensive care unit, administration of invasive ventilation, and death). Methods: A propensity-score-matched nationwide cohort study was performed in South Korea. Data obtained from the Health Insurance Review & Assessment Service of Korea from all adult patients (age, >20 years) who were tested for SARS-CoV-2 in South Korea between January 1, 2020, and May 15, 2020, were analyzed. The association of SARS-CoV-2 test positivity and allergic diseases in the entire cohort (n 5 219,959) and the difference in clinical outcomes of COVID-19 were evaluated in patients with allergic diseases and SARS-CoV-2 positivity (n 5 7,340). Results: In the entire cohort, patients who underwent SARS-CoV-2 testing were evaluated to ascertain whether asthma and allergic rhinitis were associated with an increased likelihood of SARS-CoV-2 test positivity. After propensity score matching, we found that asthma and allergic rhinitis were associated with worse clinical outcomes of COVID-19 in patients with SARS-CoV-2 test positivity. Patients with nonallergic asthma had a greater risk of SARS-CoV-2 test positivity and worse clinical outcomes of COVID-19 than patients with allergic asthma. Conclusions: In a Korean nationwide cohort, allergic rhinitis and asthma, especially nonallergic asthma, confers a greater risk of susceptibility to SARS-CoV-2 infection and severe clinical outcomes of COVID-19.

We explored whether baseline indexed epicardial fat volume (EFVi) and serial changes in EFVi were associated with increase in coronary plaque volume as assessed by multidetector computed tomography.We retrospectively reviewed 87 patients with coronary artery plaque, identified during either baseline or follow-up cardiac computed tomography (CT) examinations. Each plaque volume was measured in volumetric units using a semiautomatic software tool. EFVi was quantified by calculating the total volume of epicardial tissue of CT density −190 to −30 HU, indexed to the body surface area. Clinical cardiovascular risk factors were extracted by medical record review at the time of the cardiac CT examinations. The relationship between EFVi and coronary plaque volume was explored by regression analysis.Although the EFVi did not change significantly from baseline to the time of the follow-up CT (65.7 ± 21.8 vs 66.0 ± 21.8 cm3/m3, P = 0.620), the plaque volumes were increased significantly on the follow-up CT scans. The annual change in EFVi was not accompanied by a parallel change in coronary plaque volume (P = 0.096–0.500). On univariate analysis, smoking, hypercholesterolemia, 10-year coronary heart disease risk, obesity, and baseline EFVi predicted rapid increases in lipid-rich and fibrous plaque volumes. On multivariate analysis, baseline EFVi (odds ratio = 1.029, P = 0.016) was an independent predictor of a rapid increase in lipid-rich plaque volume.EFVi was shown to be an independent predictor of a rapid increase in lipid-rich plaque volume. However, changes in EFVi were not associated with parallel changes in coronary plaque volume.

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