P. Tornvall et al., HIGH-DENSITY-LIPOPROTEIN - RELATIONS TO METABOLIC PARAMETERS AND SEVERITY OF CORONARY-ARTERY DISEASE, Metabolism, clinical and experimental, 45(11), 1996, pp. 1375-1382
The regulation of plasma high density lipoprotein (HDL) cholesterol le
vel by the joint influence of plasma lipoprotein lipids, lipoprotein l
ipase (LPL), hepatic lipase (HL), cholesteryl ester transfer protein (
CETP), oral glucose tolerance, and postload plasma insulin and proinsu
lin levels was investigated in young postinfarction patients and healt
hy population-based control subjects. In addition, the association bet
ween HDL cholesterol and the number and severity of coronary stenoses
previously reported in this cohort of young postinfarction patients wa
s further investigated by analyzing the determinants and angiographic
relations of HDL subclasses measured by gradient gel electrophoresis.
The following parameters showed significant univariate relations with
HDL cholesterol level in the patient group: very-low-density lipoprote
in (VLDL) cholesterol and triglyceride, low-density lipoprotein (LDL)
triglyceride, and postload plasma insulin concentrations, preheparin p
lasma LPL mass, and postheparin plasma HL activity. In the control gro
up, significant correlations with HDL cholesterol concentration in add
ition to those noted among the patients were found for body mass index
(BMI), LDL cholesterol level, postload plasma intact proinsulin conce
ntration, and LPL activity in postheparin plasma. In contrast to the p
atients, no significant relations were noted for postload plasma insul
in level and preheparin plasma LPL mass. Multiple stepwise regression
analysis showed that 42% of the variability of HDL cholesterol in the
patients could be accounted for by VLDL cholesterol concentration (29%
), LDL triglyceride level (7%), and postheparin plasma HL activity (6%
), whereas the corresponding figure in controls was 35% (VLDL choleste
rol concentration [9%] and postheparin plasma HL activity [26%]). The
strength of the relationships of HDL cholesterol and HDL subclasses to
the coronary stenosis score was similar and statistically significant
(r = .25 to .36). When the metabolic parameters that correlated with
HDL cholesterol and HDL subclass concentrations in univariate analysis
were used as covariates, all relations to the coronary stenosis score
disappeared. This clearly indicates that the influence of triglycerid
e-rich lipoproteins and lipolytic enzymes needs to be considered when
assessing the association between HDL cholesterol and coronary artery
disease (CAD). Copyright (C) 1996 by W.B. Saunders Company