Elevated lipoprotein(a) ups risk of atrial fibrillation

Lipoprotein(a) (Lp[a]) appears to play a role in the development of atrial fibrillation (AF), with its effects extending across myocardial tissues, reveals a study.

The authors examined the role of LP(a) in AF and determined whether it was independent of atherosclerotic cardiovascular disease (ASCVD) by testing for the association of measured and genetically predicted Lp(a) levels with 20,432 cases of incident AF in the UK Biobank (n=435,579). They also performed Mendelian randomization analyses using summary-level data for AF from publicly available genome-wide association studies (n=1,145,375).

In the UK Biobank, each 50-nmol/L (23 mg/dL) increase in Lp(a) correlated with an elevated risk of incident AF using measured Lp(a) (hazard ratio, 1.03, 95 percent confidence interval [CI], 1.02‒1.04; p=1.65 × 10^–8) and genetically predicted Lp(a) (odds ratio [OR], 1.03, 95 percent CI, 1.02‒1.05; p=1.33 × 10^–5).

This effect was replicated in Mendelian randomization analyses using independent data (OR, 1.04 per 50-nmol/L Lp(a) increase, 95 percent CI, 1.03‒1.05; p=9.23 × 10^–10).

Interestingly, low-density lipoprotein cholesterol or triglycerides showed no evidence of risk-conferring effects. In addition, only 39 percent (95 percent CI, 27‒73) of Lp(a) risk was mediated through ASCVD. Such finding indicated the partial influence of Lp(a) on AF independent of its known effects on ASCVD.

“Ongoing clinical trials for Lp(a)-lowering therapies should evaluate effects on AF prevention,” the authors said.

Lp(a) is a known risk factors for ASCVD, which itself raises the risk of AF, a cardiac arrhythmia associated with an increased risk of stroke, heart failure, and mortality.