ArticleBioscience reports2025
Does COVID-19 impact the QT interval prolongation? Answers from genetic causal inference.
Article in Bioscience reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Integrative multi-omics identification and functional validation of potential targets linking metabolism-immune-colorectal cancer causal pathway.Frontiers in immunology · 2025Article
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Abstract
During the COVID-19 pandemic, there has been heightened interest in the QT interval, a crucial indicator of ventricular electrical activity. Mendelian randomization (MR) is used here to investigate the genetic causation between QT interval alterations and COVID-19. Genetic proxies representing three COVID-19 phenotypes-severe, hospitalized, and COVID-19-were identified in over 1,000,000 individuals of European ancestry. Univariate two-sample MR (TSMR) and multi-exposure-adjusted multivariate MR (MVMR) were used to assess genetic causal associations between COVID-19 and QT intervals in 84,630 UK Biobank participants. The MR-robust adjusted profile score (MR-RAPS) method and radial MR frame were utilized for effective robustness and outlier variant detection, with sensitivity analyses conducted to identify horizontal pleiotropy. For every COVID-19 phenotype, univariate TSMR analysis revealed non-significant causal estimates between COVID-19 and the QT interval [COVID-19: βIVW (95% CI): -0.44 (-1.72, 0.84), P = 0.50; hospitalization: βIVW: 0.12 (-0.57, 0.80), P = 0.74; severe case: βIVW: 0.11 (-0.29, 0.51), P = 0.58]. MR-RAPS and outlier-corrected radial MR analyses further supported this null causal estimation. In confounder-adjusted MVMR analysis, this nonsignificant causality was independent of body mass index (BMI), smoking, and alcohol consumption [βBMI+Alcohol+Smoking (95% CI): -0.77 (-2.44, 0.91), P = 0.37]. Sensitivity analyses did not detect any evidence of bias from horizontal pleiotropy, abnormal data distribution, or weak instruments. These findings suggest that COVID-19 does not directly causally prolong the QT interval. Inconsistent findings in observational research may be attributed to residual confounding.
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