Dissecting the causal effects of smoking, alcohol consumption, and related DNA methylation markers on electrocardiographic indices.

ABSTRACT:

Background

Tobacco and alcohol are recognized risk factors for heart disease, yet their causal effects on electrocardiogram (ECG) signaling and mechanisms remain unclear. Previous studies may be susceptible to confounding or bias, and this study dissected the genetic architecture linking tobacco and alcohol consumption with P-wave duration, PR interval, and QT interval.

Methods

Utilizing genetic instruments for tobacco and alcohol consumption, associated methylation quantitative trait locus (mQTL), and summary-level GWAS data for ECG indices, we assessed heritability and genetic causal associations using linkage disequilibrium score regression and Mendelian randomization (MR) analysis. Fine mapping was performed via colocalization analysis and summary-data-based MR (SMR) to

SUBMITTER: Zheng Z 

PROVIDER: S-EPMC11881420 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature