Causal associations between COVID-19 and Atrial Fibrillation: A bidirectional Mendelian randomization study

BackgroundObservational studies showed that coronavirus disease 2019 (COVID-19) attacks universally and its most menacing progression uniquely endangers the elderly with cardiovascular disease (CVD). Whether COVID-19 is causally related to increasing susceptibility and severity of atrial fibrillation (AF), the main form of CVD, remains still unknown. MethodsThe study aims to investigate the bidirectional causal relations of COVID-19 with AF using two-sample Mendelian randomization (MR) analysis. ResultsMR evidence suggested genetically predicted severe COVID-19 was significantly associated with higher risk of AF (odds ratio [OR], 1.041; 95% confidence interval (CI), 1.007-1.076; P = 0.017), while genetically predicted AF was not causally associated with severe COVID-19 (OR, 0.831; 95% CI, 1.619-1.115; P=0.217). There was limited evidence to support association of genetically proxied COVID-19 with risk of AF (OR, 1.051; 95% CI, 0.991-1.114; P=0.097), and vice versa (OR, 0.163; 95% CI, 0.004-6.790; P=0.341). MR-Egger indicated no evidence of pleiotropic bias. ConclusionOverall, severe COVID-19 may causally affect AF through independent biological pathway. Survivors from severe COVID-19 might be of high risk of AF in the future.

Association of 25 hydroxyvitamin D concentration with risk of COVID-19: a Mendelian randomization study

BackgroundIn observational studies, 25 hydroxyvitamin D (25OHD) concentration has been associated with an increased risk of Coronavirus disease 2019 (COVID-19). However, it remains unclear whether this association is causal. MethodsWe performed a two-sample Mendelian randomization (MR) to explore the causal relationship between 25OHD concentration and COVID-19, using summary data from the genome-wide association studies (GWASs) and using 25OHD concentration-related SNPs as instrumental variables (IVs). ResultsMR analysis did not show any evidence of a causal association of 25OHD concentration with COVID-19 susceptibility and severity (OR=1.168, 95% CI 0.956-1.427; OR=0.889, 95% CI 0.549-1.439). Sensitivity analyses using different instruments and statistical models yielded similar findings, suggesting the robustness of the causal association. No obvious pleiotropy bias and heterogeneity were observed. ConclusionThe MR analysis showed that there might be no linear causal relationship of 25OHD concentration with COVID-19 susceptibility and severity.