Rebecca Fisher, Nick S. Nurmohamed, Edward A. Fisher, Melissa Aquino, James P. Earls, James K Min, Chen Gurevitz, Waqas Malick, Robert Peters, Sascha N Goonewardena, Robert S. Rosenson
{"title":"Lipoprotein(a) is Associated with Increased Low-Density Plaque Volume","authors":"Rebecca Fisher, Nick S. Nurmohamed, Edward A. Fisher, Melissa Aquino, James P. Earls, James K Min, Chen Gurevitz, Waqas Malick, Robert Peters, Sascha N Goonewardena, Robert S. Rosenson","doi":"10.1101/2024.07.18.24310539","DOIUrl":null,"url":null,"abstract":"BACKGROUND: Lipoprotein(a) [Lp(a)] is an inherited risk factor for cardiovascular disease that is accompanied by a more severe coronary artery disease (CAD) phenotype and a higher risk for events. The objective of this study is to clarify the association between Lp(a) and coronary plaque characteristics in asymptomatic patients. METHODS: 373 consecutive asymptomatic patients were evaluated for primary prevention of CAD. Artificial intelligence quantitative coronary CTA (AI-QCT) was used to investigate the relationship between Lp(a) and coronary plaque characteristics. Multivariable linear regression adjusted for CAD risk factors (age, sex, race, diabetes, smoking), statin use, and body mass index were used to analyze associations between the Lp(a) (by quintile), high sensitivity C-reactive protein (hsCRP), coronary artery calcium (CAC) score, and AI-QCT findings. AI-QCT findings were defined as low-density non-calcified plaque volume (LD-NCPV). RESULTS: The mean age was 56.2±8.9 years, 71.6% were male, and 54.2% were taking statin therapy. Median LDL-C was 103(72,136)mg/dL, median Lp(a) was 31(11, 89)nmol/L, median Lp(a) corrected LDL-C was 101(64, 131)mg/dL. Median hsCRP levels were 0.8(0.4, 1.8)mg/L. Median CAC levels were 6.0(0.0,110.0). There was no association between Lp(a) concentrations and CAC(P=0.281). After adjustment for CAD risk factors, every quintile of Lp(a) increase was associated with a 0.4% increase in LD-NCPV(P=0.039). The inclusion of hsCRP to the models had no significant effect on LD-NCPV. CONCLUSIONS: Higher Lp(a) concentrations in asymptomatic patients are significantly associated with increased low-density non-calcified plaque volume.","PeriodicalId":501297,"journal":{"name":"medRxiv - Cardiovascular Medicine","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"medRxiv - Cardiovascular Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1101/2024.07.18.24310539","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
BACKGROUND: Lipoprotein(a) [Lp(a)] is an inherited risk factor for cardiovascular disease that is accompanied by a more severe coronary artery disease (CAD) phenotype and a higher risk for events. The objective of this study is to clarify the association between Lp(a) and coronary plaque characteristics in asymptomatic patients. METHODS: 373 consecutive asymptomatic patients were evaluated for primary prevention of CAD. Artificial intelligence quantitative coronary CTA (AI-QCT) was used to investigate the relationship between Lp(a) and coronary plaque characteristics. Multivariable linear regression adjusted for CAD risk factors (age, sex, race, diabetes, smoking), statin use, and body mass index were used to analyze associations between the Lp(a) (by quintile), high sensitivity C-reactive protein (hsCRP), coronary artery calcium (CAC) score, and AI-QCT findings. AI-QCT findings were defined as low-density non-calcified plaque volume (LD-NCPV). RESULTS: The mean age was 56.2±8.9 years, 71.6% were male, and 54.2% were taking statin therapy. Median LDL-C was 103(72,136)mg/dL, median Lp(a) was 31(11, 89)nmol/L, median Lp(a) corrected LDL-C was 101(64, 131)mg/dL. Median hsCRP levels were 0.8(0.4, 1.8)mg/L. Median CAC levels were 6.0(0.0,110.0). There was no association between Lp(a) concentrations and CAC(P=0.281). After adjustment for CAD risk factors, every quintile of Lp(a) increase was associated with a 0.4% increase in LD-NCPV(P=0.039). The inclusion of hsCRP to the models had no significant effect on LD-NCPV. CONCLUSIONS: Higher Lp(a) concentrations in asymptomatic patients are significantly associated with increased low-density non-calcified plaque volume.