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Journal Article
Research Support, N.I.H., Extramural
Relation of Plasma Lipoprotein(a) to Subclinical Coronary Plaque Volumes, Three-Vessel and Left Main Coronary Disease, and Severe Coronary Stenoses in Apparently Healthy African-Americans With a Family History of Early-Onset Coronary Artery Disease.
American Journal of Cardiology 2016 September 2
Serum lipoprotein(a) [Lp(a)] is a coronary artery disease (CAD) risk factor in persons of European ancestry. Levels are twofold to threefold higher in African-Americans (AAs), but reported associations with CAD have been inconsistent. The relation of Lp(a) with the extent and severity of subclinical coronary plaque has not been described in AAs. We screened 269 apparently healthy AAs for risk factors and coronary plaque using advanced coronary computed tomographic angiography. Total coronary plaque (TCP), noncalcified coronary plaque, and calcified coronary plaque volumes (mm(3)) were quantified using a validated automated method. Lp(a) was measured by ELISA. Multivariable modeling was performed with adjustment for traditional CAD risk factors and intrafamilial correlations. Mean age was 51 ± 11 years and 64% were female. Plaque was present in 41%. Lp(a) was independently associated with TCP volume [log(TCP + 1)] (p = 0.04), 3-vessel and/or left main involvement (p = 0.04), and at least 1 stenosis >50% (p = 0.006). Best-fit regression analyses showed that subjects with Lp(a) >40 mg/dl were threefold more likely to have 3-vessel and/or left main disease (95% confidence interval 1.4 to 6.8, p = 0.005) and fourfold more likely to have stenosis >50% (95% confidence interval 1.3 to 15.0, p = 0.02). In subjects with plaque (n = 110), multivariable models showed the Lp(a) level was significantly and independently associated with TCP (p = 0.009), noncalcified coronary plaque (p = 0.01), and calcified coronary plaque (p = 0.003) and affected vessel length (p = 0.01). In conclusion, high Lp(a) is strongly associated with coronary plaque volumes, extent, and severity in apparently healthy AAs. High levels of Lp(a) may be particularly important in the pathogenesis of CAD in AAs.
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