Association of small low-density lipoprotein particles with the incidence of coronary artery disease in men and women.
OBJECTIVE
To investigate the prospective association of low-density lipoprotein (LDL) particle diameter with the incidence of fatal and nonfatal coronary artery disease (CAD).


METHODS
A nested case-control study.


METHODS
Cases and controls were identified from a population-based sample of men and women combining all of the 5 cross-sectional surveys conducted from 1979 to 1990 of the Stanford Five-City Project (FCP).


METHODS
Incident CAD cases were identified through FCP surveillance between 1979 and 1992. Controls were matched by sex, 5-year age groups, survey time point, ethnicity, and FCP treatment condition. The sample included 124 matched pairs: 90 pairs of men and 34 pairs of women.


METHODS
LDL peak particle diameter (LDL size) was determined by gradient gel electrophoresis on plasma samples collected during the cross-sectional surveys (stored at 70 degrees C for 5-15 years). Established CAD risk-factor data were available from FCP baseline measurements.


RESULTS
LDL size was smaller among CAD cases than controls (mean +/- SD) (26.17 +/- 1.00 nm vs 26.68 +/- 0.90 nm; P<.001). The association was graded across control quintiles of LDL size. The significant case-control difference in LDL size was independent of levels of high-density lipoprotein cholesterol (HDL-C), non-HDL cholesterol (non-HDL-C), triglyceride, smoking, systolic blood pressure, and body mass index, but was not significant after adjusting for the ratio of total cholesterol (TC) to HDL-C (TC:HDL-C). Among all the physiological risk factors, LDL size was the best differentiator of CAD status in conditional logistic regression. However, when added to the physiological parameters above, the TC:HDL-C ratio was found to be a stronger independent predictor of CAD status.


CONCLUSIONS
LDL size was significantly smaller in CAD cases than in controls in a prospective, population-based study. These findings support other evidence of a role for small, dense LDL particles in the etiology of atherosclerosis.
Gardner
C D
CD
Stanford Center for Research in Disease Prevention and the Department of Medicine, Stanford University School of Medicine, Calif, USA.
Fortmann
S P
SP
Krauss
R M
RM
D000328:Adult; D000368:Aged; D015992:Body Mass Index; D016022:Case-Control Studies; D003327:Coronary Disease / Q000097:blood* / Q000453:epidemiology*; D003430:Cross-Sectional Studies; D004591:Electrophoresis, Polyacrylamide Gel; D005260:Female; D006801:Humans; D015994:Incidence; D016014:Linear Models; D008055:Lipids / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood / Q000737:chemistry*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012307:Risk Factors
D008055:Lipids; D008077:Lipoproteins, LDL