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  Vol. 270 No. 18, November 10, 1993 TABLE OF CONTENTS
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A Prospective Study of Lipoprotein(a) and the Risk of Myocardial Infarction

Paul M. Ridker, MD; Charles H. Hennekens, MD; Meir J. Stampfer, MD

JAMA. 1993;270(18):2195-2199.


Abstract

Objective.
—To assess prospectively the risk of myocardial infarction (Ml) associated with elevated levels of lipoprotein(a) (Lp[a]).

Design.
—Nested case-control study using prospectively collected plasma samples.

Setting.
—Participants in the Physicians' Health Study.

Participants.
—A total of 14916 male physicians aged 40 to 84 years with no prior history of Ml or stroke provided plasma samples at baseline and were followed up prospectively for an average period of 60.2 months. Samples from 296 physicians who subsequently developed Ml were analyzed for Lp(a) level together with paired controls, matched for smoking status and age.

Main Outcome Measure.
—Fatal or nonfatal acute Ml.

Results.
—The distribution of Lp(a) level among cases was virtually identical to that of controls (P=.88), and there was no significant difference between groups for median Lp(a) levels (103.0 mg/L vs 102.5 mg/L; P=.73). In analyses controlling for age and smoking status, we found no evidence of association between increasing level of Lp(a) and risk of Ml (relative risks from lowest to highest quintiles of Lp(a): 1.00, 0.97, 0.83, 0.88, and 1.07; P for trend=.93) or a threshold effect at any prespecified cutoff of Lp(a) level (relative risks associated with Lp[a] levels above the 25th, 50th, 75th, 90th, and 95th percentiles of the control distribution, respectively: 1.04,1.00,1.19,1.00, and 1.07; all Pvalues nonsignificant). Further adjustment for both lipid and nonlipid cardiovascular risk factors had no material impact.

Conclusions.
—In this prospective study of predominantly middle-aged white men, we found no evidence of association between Lp(a) level and risk of future Ml. These data do not support the use of Lp(a) level as a screening tool to define cardiovascular risk among this population.

(JAMA. 1993;270:2195-2199)



Author Affiliations

From the Divisions of Preventive Medicine (Drs Ridker and Hennekens) and Cardiology (Dr Ridker), and the Channing Laboratory (Dr Stampfer), Department of Medicine, Brigham and Women's Hospital, and the Department of Ambulatory Care and Prevention (Dr Hennekens), Harvard Medical School and the Department of Epidemiology (Dr Stampfer), Harvard School of Public Health, Boston, Mass.


Footnotes

Reprint requests to Brigham and Women's Hospital, 900 Commonwealth Ave E, Boston, MA 02215-1204 (Dr Ridker).



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