LIPOPROTEIN[A] AS A RISK FACTOR FOR PRECLINICAL ATHEROSCLEROSIS

被引:111
作者
SCHREINER, PJ
MORRISETT, JD
SHARRETT, AR
PATSCH, W
TYROLER, HA
WU, K
HEISS, G
机构
[1] METHODIST HOSP,DEPT MED,HOUSTON,TX 77030
[2] METHODIST HOSP,ATHEROSCLEROSIS CLIN LAB,HOUSTON,TX 77030
[3] NHLBI,DECA,ARIC PROJECT OFF,BETHESDA,MD 20892
[4] UNIV TEXAS,SCH MED,HOUSTON,TX 77025
来源
ARTERIOSCLEROSIS AND THROMBOSIS | 1993年 / 13卷 / 06期
关键词
LIPOPROTEIN[A; ATHEROSCLEROSIS; B-MODE ULTRASONOGRAPHY; RACE;
D O I
10.1161/01.ATV.13.6.826
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Elevated mean levels of lipoprotein[a] (Lp[a]) have been associated with symptomatic cardiovascular diseases such as clinically manifest myocardial infarction (MI), coronary artery disease, restenosis of coronary artery vein grafts after bypass, and a family history of MI. Associations of Lp[a] with arterial wall thickening in asymptomatic individuals previously have not been addressed and are evaluated in this report among participants of the Atherosclerosis Risk in Communities (ARIC) Study. Intima-media wall thickening in the extracranial carotid arteries was assessed noninvasively with B-mode ultrasonography; Lp[a] was measured as its total protein component. Individuals with wall thickening greater-than-or-equal-to 90th percentile of the population maximum far-wall thickness were pair matched to participants < 75th percentile of wall thickness by race, gender, center, 10-year age group, and time of examination. These selection criteria yielded 492 matched pairs, with 395 white pairs and 97 black pairs. The mean Lp[a] protein level for all black participants was 174.6 mug/mL compared with 77.8 mug/mL for whites. Conditional logistic regression analysis for the association of Lp[a] with case-control status yielded a statistically significant prevalence odds ratio (OR) estimate of 1.49, based on a I-SD difference in Lp[a] protein, after adjusting for age, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, fibrinogen, hypertension, and cigarette smoking. None of these risk factors significantly altered the OR, in agreement with reports that Lp[a] is unaffected by environmental influences. In addition, no differential effect of Lp[a] protein on case-control status (effect modification) was observed by race, gender, low-density lipoprotein cholesterol, or fibrinogen in this population. We conclude that Lp[a] is an independent risk factor for intima-media carotid thickening in individuals free of prevalent cardiovascular disease. Further investigation of racial effects may benefit from a population-based analysis that includes additional black participants as well as from elucidation of apolipoprotein[a] polymorph differences between races and degree of wall thickening.
引用
收藏
页码:826 / 833
页数:8
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