A bidirectional Mendelian randomization analysis between COVID-19 and cardiac arrest

Area of Science:

• Cardiovascular Epidemiology
• Infectious Disease Epidemiology
• Genetic Epidemiology

Background:

• Observational studies suggest a link between COVID-19 and cardiac arrest (CA).
• Causality is uncertain due to potential confounding factors in existing research.
• Mendelian randomization (MR) offers a method to investigate genetic causality.

Purpose of the Study:

• To investigate the causal relationship between COVID-19 and cardiac arrest (CA) using a two-sample Mendelian randomization (MR) approach.
• To assess if COVID-19 causally increases the risk of CA.
• To examine the potential reverse causality: if CA causally influences COVID-19 risk.

Main Methods:

• Utilized genome-wide association study (GWAS) data for COVID-19 and CA.
• Employed single nucleotide polymorphisms (SNPs) associated with COVID-19 and CA as instrumental variables.
• Performed inverse-variance weighted (IVW) MR analysis and sensitivity analyses to address pleiotropy.
• Conducted a reverse MR analysis to test causality from CA to COVID-19.

Main Results:

• No significant causal effect was found for infected COVID-19 (OR=1.12, p=0.79), hospitalized COVID-19 (OR=1.02, p=0.920), or severe respiratory COVID-19 (OR=0.99, p=0.945) on CA risk.
• Reverse MR analysis did not support a causal effect of CA on COVID-19.
• Sensitivity analyses confirmed the robustness of these findings.

Conclusions:

• The study provides no evidence for a causal link between COVID-19 and cardiac arrest.
• Observed associations in epidemiological studies may be attributed to shared biological pathways or environmental confounders.
• MR analysis strengthens the understanding of COVID-19's cardiovascular implications.