Key result
Compared with controls, male CHD patients had significantly lower concentrations of large LpA-I alpha(1) (-35%) and pre-alpha(1-3) particles, and higher small LpA-I/A-II alpha(3) particles (P<0.001).
Why the study?
Are there differences in the distribution of ApoA-I-containing HDL subpopulations between male patients with coronary heart disease and healthy controls?
Case-Control (n=155)
Are there differences in the distribution of ApoA-I-containing HDL subpopulations between male patients with coronary heart disease and healthy controls?
p-value: p=<0.001
Patients with coronary heart disease exhibit a major rearrangement in HDL subpopulations, characterized by lower large LpA-I particles and higher small LpA-I/A-II particles, independent of total HDL-C levels.
HDL subpopulation shifts may mark CHD in men beyond HDL-C; hypothesis-generating for risk stratification or targeted therapies.
High density lipoproteins (HDLs) and their subspecies play a role in the development of coronary heart disease (CHD). HDL subpopulations were measured by 2-dimensional nondenaturing gel electrophoresis in 79 male control subjects and 76 male CHD patients to test the hypothesis that greater differences in apolipoprotein (apo)A-I-containing HDL subpopulations would exist between these 2 groups than for traditional lipid levels. In CHD subjects, HDL cholesterol (HDL-C) was lower (-14%, P<0.001), whereas total cholesterol and the low density lipoprotein cholesterol/HDL-C ratio were higher (9% [P:<0.05] and 21% [P:<0.01], respectively) compared with control levels. No significant differences were found for low density lipoprotein cholesterol, triglyceride, and apoA-I levels. In CHD subjects, there were significantly (P:<0.001) lower concentrations of the large lipoprotein (Lp)A-I alpha(1) (-35%), pre-alpha(1) (-50%), pre-alpha(2) (-33%), and pre-alpha(3) (-31%) subpopulations, whereas the concentrations of the small LpA-I/A-II alpha(3) particles were significantly (P:<0.001) higher (20%). Because alpha(1) was decreased more than HDL-C and plasma apoA-I concentrations in CHD subjects, the ratios of HDL-C to alpha(1) and of apoA-I to alpha(1) were significantly (P:<0.001) higher by 36% and 57%, respectively, compared with control values. Subjects with low HDL-C levels (</=35 mg/dL) have different distributions of apoA-I-containing HDL subpopulations than do subjects with normal HDL-C levels (>35 mg/dL). Therefore, we stratified participants according to HDL-C concentrations into low and normal groups. The differences in lipid levels between controls and HDL-C-matched cases substantially decreased; however, the significant differences in HDL subspecies remained. Our research findings support the concept that compared with control subjects, CHD patients not only have HDL deficiency but also have a major rearrangement in the HDL subpopulations with significantly lower alpha(1) and pre-alpha(1-3) (LpA-I) and significantly higher alpha(3) (LpA-I/A-II) particles.
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Asztalos et al. (2000) conducted a case-control in Coronary Heart Disease (n=155). Coronary Heart Disease vs. Control subjects was evaluated on Differences in apolipoprotein (apo)A-I-containing HDL subpopulations (p=<0.001). Compared with controls, male CHD patients had significantly lower concentrations of large LpA-I alpha(1) (-35%) and pre-alpha(1-3) particles, and higher small LpA-I/A-II alpha(3) particles (P<0.001).
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