Mustra Rakic Jelena, Pullinger Clive R, Van Blarigan Erin L, Movsesyan Irina, Stock Eveline Oestreicher, Malloy Mary J, Kane John P
Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA (Drs Mustra Rakic, Pullinger, Movsesyan, Stock, Malloy, and Kane); Center for Tobacco Control Research and Education, University of California San Francisco, San Francisco, CA (Drs Mustra Rakic, and Kane).
Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA (Drs Mustra Rakic, Pullinger, Movsesyan, Stock, Malloy, and Kane); Department of Physiological Nursing, University of California San Francisco, San Francisco, CA (Dr Pullinger).
J Clin Lipidol. 2025 Jul-Aug;19(4):1129-1138. doi: 10.1016/j.jacl.2025.04.189. Epub 2025 Apr 10.
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.
载脂蛋白L1（APOL1）G1和G2基因变异在非裔美国人中高度流行（在其他种族群体中罕见），与肾脏疾病、败血症以及潜在的冠心病（CHD）风险增加有关。它们在烟草相关冠心病中的作用仍不清楚。
研究APOL1风险变异对非裔美国成年人吸烟与现患冠心病之间关联的影响。
我们进行了一项横断面研究，纳入了通过加利福尼亚大学旧金山分校脂质诊所招募的519名非裔美国成年人。使用多变量逻辑回归，我们评估了所有参与者和APOL1基因型亚组中吸烟与冠心病及其最严重亚型心肌梗死（MI）之间的关联。
在参与者中，41%为当前吸烟者（14%）或既往吸烟者（27%），54%携带APOL1风险变异（1个或2个等位基因），28%患有冠心病，其中16%患有心肌梗死。与不吸烟者相比，携带APOL1风险变异的当前吸烟者患冠心病的几率高3.3倍（95%CI：1.6，6.8），在携带2个风险等位基因的人群中观察到最强效应（优势比[OR]：7.3，CI：1.1，4,8.6），在携带单个风险等位基因的携带者中也有显著效应（OR：3.2，CI：1.5，7.2）。在非携带者中，当前吸烟与冠心病无显著关联（OR：1.3）。心肌梗死也观察到类似趋势。既往吸烟与冠心病有关（OR：2.0），与APOL1基因型无关。
携带APOL1 G1和/或G2风险变异的非裔美国吸烟者可能患冠心病的风险更高；这种关系似乎遵循相加模型。
