Jelena Mustra Rakic PhD , Clive R. Pullinger PhD , Erin L. Van Blarigan ScD , Irina Movsesyan BSc , Eveline Oestreicher Stock MD , Mary J. Malloy MD , John P. Kane MD, PhD
{"title":"非裔美国人中携带APOL1风险变异的当前吸烟者冠心病患病率增加","authors":"Jelena Mustra Rakic PhD , Clive R. Pullinger PhD , Erin L. Van Blarigan ScD , Irina Movsesyan BSc , Eveline Oestreicher Stock MD , Mary J. Malloy MD , John P. Kane MD, PhD","doi":"10.1016/j.jacl.2025.04.189","DOIUrl":null,"url":null,"abstract":"<div><h3>BACKGROUND</h3><div>The apolipoprotein L1 <em>(APOL1</em>) 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.</div></div><div><h3>OBJECTIVE</h3><div>To investigate the effect of <em>APOL1</em> risk variants on the association between tobacco smoking and prevalent CHD in African American adults.</div></div><div><h3>METHODS</h3><div>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 <em>APOL1</em> genotype subgroups.</div></div><div><h3>RESULTS</h3><div>Among participants, 41% were current (14%) or former (27%) smokers, 54% carried <em>APOL1</em> risk variants (1 or 2 alleles), and 28% had CHD, including 16% having MI. Current smokers with <em>APOL1</em> 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 <em>APOL1</em> genotype.</div></div><div><h3>CONCLUSION</h3><div>African American smokers with <em>APOL1</em> G1 and/or G2 risk variants may be at greater risk of CHD; this relationship appears to follow an additive model.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 4","pages":"Pages 1129-1138"},"PeriodicalIF":4.6000,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Increased prevalence of coronary heart disease among current smokers carrying APOL1 risk variants within the African American population\",\"authors\":\"Jelena Mustra Rakic PhD , Clive R. Pullinger PhD , Erin L. Van Blarigan ScD , Irina Movsesyan BSc , Eveline Oestreicher Stock MD , Mary J. Malloy MD , John P. Kane MD, PhD\",\"doi\":\"10.1016/j.jacl.2025.04.189\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>BACKGROUND</h3><div>The apolipoprotein L1 <em>(APOL1</em>) 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.</div></div><div><h3>OBJECTIVE</h3><div>To investigate the effect of <em>APOL1</em> risk variants on the association between tobacco smoking and prevalent CHD in African American adults.</div></div><div><h3>METHODS</h3><div>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 <em>APOL1</em> genotype subgroups.</div></div><div><h3>RESULTS</h3><div>Among participants, 41% were current (14%) or former (27%) smokers, 54% carried <em>APOL1</em> risk variants (1 or 2 alleles), and 28% had CHD, including 16% having MI. Current smokers with <em>APOL1</em> 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 <em>APOL1</em> genotype.</div></div><div><h3>CONCLUSION</h3><div>African American smokers with <em>APOL1</em> G1 and/or G2 risk variants may be at greater risk of CHD; this relationship appears to follow an additive model.</div></div>\",\"PeriodicalId\":15392,\"journal\":{\"name\":\"Journal of clinical lipidology\",\"volume\":\"19 4\",\"pages\":\"Pages 1129-1138\"},\"PeriodicalIF\":4.6000,\"publicationDate\":\"2025-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of clinical lipidology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1933287425002648\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"PHARMACOLOGY & PHARMACY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of clinical lipidology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1933287425002648","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PHARMACOLOGY & PHARMACY","Score":null,"Total":0}
Increased prevalence of coronary heart disease among current smokers carrying APOL1 risk variants within the African American population
BACKGROUND
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.
OBJECTIVE
To investigate the effect of APOL1 risk variants on the association between tobacco smoking and prevalent CHD in African American adults.
METHODS
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.
RESULTS
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.
CONCLUSION
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.
期刊介绍:
Because the scope of clinical lipidology is broad, the topics addressed by the Journal are equally diverse. Typical articles explore lipidology as it is practiced in the treatment setting, recent developments in pharmacological research, reports of treatment and trials, case studies, the impact of lifestyle modification, and similar academic material of interest to the practitioner.
Sections of Journal of clinical lipidology will address pioneering studies and the clinicians who conduct them, case studies, ethical standards and conduct, professional guidance such as ATP and NCEP, editorial commentary, letters from readers, National Lipid Association (NLA) news and upcoming event information, as well as abstracts from the NLA annual scientific sessions and the scientific forums held by its chapters, when appropriate.