PREDOMINANCE OF DENSE LOW-DENSITY-LIPOPROTEIN PARTICLES PREDICTS ANGIOGRAPHIC BENEFIT OF THERAPY IN THE STANFORD CORONARY RISK INTERVENTIONPROJECT

Citation
Bd. Miller et al., PREDOMINANCE OF DENSE LOW-DENSITY-LIPOPROTEIN PARTICLES PREDICTS ANGIOGRAPHIC BENEFIT OF THERAPY IN THE STANFORD CORONARY RISK INTERVENTIONPROJECT, Circulation, 94(9), 1996, pp. 2146-2153
Citations number
31
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiac & Cardiovascular System",Hematology
Journal title
ISSN journal
0009-7322
Volume
94
Issue
9
Year of publication
1996
Pages
2146 - 2153
Database
ISI
SICI code
0009-7322(1996)94:9<2146:PODLPP>2.0.ZU;2-9
Abstract
Background LDL particles differ in size and density. Individuals with LDL profiles that peak in relatively small, dense particles have been reported to be at increased risk of coronary artery disease. We hypoth esized that response to coronary disease therapy in such individuals m ight differ from response in individuals whose profiles peak in larger , more buoyant LDL. We examined this hypothesis in the Stanford Corona ry Risk Intervention Project, an angiographic trial that compared mult ifactorial risk-reduction intervention with the usual care of physicia ns. Methods and Results For 213 men, a bimodal frequency distribution of peak LDL density (g/mL) determined by analytical ultracentrifugatio n was used to classify baseline LDL profiles as ''buoyant mode'' (dens ity less than or equal to 1.0378) or ''dense mode'' (density >1.0378). Coronary disease progression after 4 years was assessed by rates of c hange (mm/y, negative tn hen arteries narrow) of minimum artery diamet er. Rates for buoyant-mode subjects were -0.038+/-0.007 (mean+/-SEM) i n usual care (n=65) and -0.039+/-0.010 in intervention (n=56; P=.5). R ates for dense-mode subjects were -0.054+/-0.012 in usual care (n=51) and -0.008+/-0.009 in intervention (n=41, P=.007). Lipid changes did n ot account for this difference in angiographic response. Conclusions D ifferent types of LDL profile may predict different responses to speci fic therapies, perhaps because metabolic processes determine both LDL profiles and responses to therapies.