November 1, 1996
View Full PaperPredominance of Dense Low-Density Lipoprotein Particles Predicts Angiographic Benefit of Therapy in the Stanford Coronary Risk Intervention Project
Key Result
Multifactorial risk-reduction intervention significantly slowed coronary disease progression in men with dense LDL profiles (-0.008 vs -0.054 mm/y; P=0.007), but not in those with buoyant LDL.
Study Design
Type
RCT (n=213)
Structured PICO
Does multifactorial risk-reduction intervention reduce coronary disease progression differently based on baseline LDL density profiles in men?
P
Population
213 men with coronary artery disease, classified by baseline LDL density, followed for 4 years to assess angiographic disease progression.
I
Intervention
Multifactorial risk-reduction intervention over 4 years
C
Comparator
Usual care of physicians over 4 years
O
Outcome
Coronary disease progression assessed by rates of change of minimum artery diameter after 4 yearssurrogate
The predominance of dense LDL particles predicts a significant angiographic benefit from multifactorial risk-reduction intervention, suggesting LDL profile types may guide specific therapies.
Main Result
Absolute Event Rate: -0.008% vs -0.054%
p-value: p=0.007
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 hypothesized that response to coronary disease therapy in such individuals might differ from response in individuals whose profiles peak in larger, more buoyant LDL. We examined this hypothesis in the Stanford Coronary Risk Intervention Project, an angiographic trial that compared multifactorial risk-reduction intervention with the usual care of physicians. METHODS AND RESULTS: For 213 men, a bimodal frequency distribution of peak LDL density (g/mL) determined by analytical ultracentrifugation was used to classify baseline LDL profiles as "buoyant mode" (density 1.0378). Coronary disease progression after 4 years was assessed by rates of change (mm/y, negative when arteries narrow) of minimum artery diameter. Rates for buoyant-mode subjects were -0.038 +/- 0.007 (mean +/- SEM) in usual care (n = 65) and -0.039 +/- 0.010 in intervention (n = 56; P = .6). Rates 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 not account for this difference in angiographic response. CONCLUSIONS: Different types of LDL profile may predict different-responses to specific therapies, perhaps because metabolic processes determine both LDL profiles and responses to therapies.