Abstract：
Epidemiological studies link COVID-19 to increased cardiac arrest (CA) risk, but causality remains unclear due to potential confounding factors in observational studies . We conducted a Mendelian randomization (MR) analysis using genome-wide association study (GWAS) data, employing COVID-19-associated single nucleotide polymorphisms (SNPs) with significance values smaller than 5 × 10⁻⁸. We calculated inverse-variance weighted (IVW) MR estimates and performed sensitivity analyses using MR methods robust to horizontal pleiotropy. Additionally, a reverse MR analysis was conducted using CA-associated SNPs with significance values smaller than 1 × 10⁻⁵. Results indicated that infected COVID-19 (OR = 1.12, 95% CI = 0.47-2.67, p = 0.79), hospitalized COVID-19 (OR = 1.02, 95% CI = 0.70-1.49, p = 0.920), and severe respiratory COVID-19 (OR = 0.99, 95% CI = 0.81-1.21, p = 0.945) did not causally influence CA risk. Reverse MR analysis also did not support a causal effect of CA on COVID-19. Thus, associations in observational studies may stem from shared biological factors or environmental confounding.
摘要：
流行病学研究将COVID-19与心脏骤停（CA）风险增加联系起来，但由于观察性研究中潜在的混杂因素,因果关系尚不清楚.我们使用全基因组关联研究（GWAS）数据进行了孟德尔随机化（MR）分析，采用COVID-19相关的单核苷酸多态性（SNPs），其显著性值小于5×10炭黑。我们计算了逆方差加权（IVW）MR估计值，并使用对水平多效性具有鲁棒性的MR方法进行了敏感性分析。此外,使用CA相关SNP进行反向MR分析，其显着性值小于1×10炭黑。结果表明，感染的COVID-19(OR=1.12，95%CI=0.47-2.67，p=0.79)，住院COVID-19（OR=1.02，95%CI=0.70-1.49，p=0.920），和严重的呼吸性COVID-19（OR=0.99，95％CI=0.81-1.21，p=0.945）没有因果关系影响CA风险。反向MR分析也不支持CA对COVID-19的因果关系。因此，观察性研究中的关联可能源于共同的生物因素或环境混杂。
