HIGH-DENSITY-LIPOPROTEIN - RELATIONS TO METABOLIC PARAMETERS AND SEVERITY OF CORONARY-ARTERY DISEASE

Citation
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
Citations number
33
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
00260495
Volume
45
Issue
11
Year of publication
1996
Pages
1375 - 1382
Database
ISI
SICI code
0026-0495(1996)45:11<1375:H-RTMP>2.0.ZU;2-7
Abstract
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