Bf. Asztalos et al., Distribution of apoA-I-containing HDL subpopulations in patients with coronary heart disease, ART THROM V, 20(12), 2000, pp. 2670-2676
High density lipoproteins (HDLs) and their subspecies play a role in the de
velopment of coronary heart disease (CHD). HDL subpopulations were measured
by 2-dimensional nondenaturing gel electrophoresis in 79 male control subj
ects and 76 male CHD patients to test the hypothesis that,greater differenc
es in apolipoprotein (apo)A-I-containing HDL subpopulations would exist bet
ween these 2, groups than for traditional lipid levels. In CHD subjects, HD
L cholesterol HDL-C) was lower (-14%, P<0.001), whereas total cholesterol a
nd 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 signif
icant differences were found for low: density lipoprotein cholesterol, trig
lyceride, 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%) subp
opulations, whereas the concentrations of the small LpA-I/A-II alpha (3), p
articles 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 significa
ntly (P<0.001) higher by 36% and 57% respectively, compared with control va
lues. Subjects with low HDL-C levels (<less than or equal to>35 mg/dL) have
different distributions of apoA-I-containing HDL subpopulations than do su
bjects with normal HDL-C levels (>35 mg/dL). Therefore, We stratified parti
cipants according to HDL-C concentrations into low and normal groups. The d
ifferences in lipid levels between controls and HDL-C-matched cases substan
tially decreased; however, the significant differences in HDL subspecies re
mained. Our research findings support the concept that compared with contro
l 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.