# Increased prevalence of coronary heart disease among current smokers carrying APOL1 risk variants within the African American population

## TL;DR

African American smokers with certain APOL1 gene variants may have a higher risk of heart disease, especially if they carry two copies of the variant.

## Contribution

This study identifies an interaction between APOL1 risk variants and smoking in increasing coronary heart disease risk in African Americans.

## Key findings

- Current smokers with APOL1 risk variants had 3.3 times higher odds of CHD compared to nonsmokers.
- Those with two APOL1 risk alleles had 7.3 times higher odds of CHD compared to nonsmokers.
- Former smoking was associated with CHD regardless of APOL1 genotype.

## Abstract

The apolipoprotein L1 (APOL1) G1 and G2 gene variants, highly prevalent among the African American population (rare in other racial groups), are linked to increased risk of kidney disease, sepsis, and potentially coronary heart disease (CHD). Their role in tobacco-related CHD remains unclear.

To investigate the effect of APOL1 risk variants on the association between tobacco smoking and prevalent CHD in African American adults.

We conducted a cross-sectional study involving 519 African American adults recruited through the University of California San Francisco Lipid Clinic. Using multivariable logistic regression, we assessed the association between tobacco smoking and CHD, overall and with its most severe subtype, myocardial infarction (MI), among all participants and APOL1 genotype subgroups.

Among participants, 41% were current (14%) or former (27%) smokers, 54% carried APOL1 risk variants (1 or 2 alleles), and 28% had CHD, including 16% having MI. Current smokers with APOL1 risk variants had 3.3 times higher odds of CHD compared to nonsmokers (95% CI: 1.6, 6.8), with the strongest effect observed in those with 2 risk alleles (odds ratio [OR]: 7.3, CI: 1.1, 48.6) and a substantial effect in carriers of a single risk allele (OR: 3.2, CI: 1.5, 7.2). Among non-carriers, current smoking was not significantly associated with CHD (OR: 1.3). A similar trend was observed for MI. Former smoking was associated with CHD (OR: 2.0), independent of APOL1 genotype.

African American smokers with APOL1 G1 and/or G2 risk variants may be at greater risk of CHD; this relationship appears to follow an additive model.