High Density Lipoprotein Subspecies and Coronary Disease
|Cardiovascular Diseases Coronary Disease Coronary Arteriosclerosis Heart Diseases|
|Study Design:||Observational Model: Case Control
Time Perspective: Cross-Sectional
|Official Title:||High Density Lipoprotein Subspecies and Coronary Disease|
- HDL subspecies [ Time Frame: 1992-1998 ]
|Study Start Date:||April 2000|
|Study Completion Date:||August 2005|
|Primary Completion Date:||August 2005 (Final data collection date for primary outcome measure)|
VA-HIT and FOS
VA-HIT cohort: men with established CHD and low HDL-C FOS cohort: men without CHD
Coronary heart disease (CHD) continues to be a leading cause of death and disability in the United States. Information about the contribution of different subspecies of HDL-C to increased or decreased risk for premature CHD and the extent to which common lipoprotein lipase (LPL) mutations affect HDL-C composition and subspecies could contribute to an increased understanding of the role of HDL-C in determining CHD risk.
The following parameters will be measured in blood samples collected from the VA-HIT study and the Framingham Offspring Study: apo A-I-containing HDL subspecies (prebeta, alpha, and prealpha) in plasma using two-dimensional gel electrophoresis immunoblot and image analysis, LpA-I and LpA-I/A-II in plasma using differential electroimmunoassay, and apo C-III in HDL using immunoturbidometric assay. The study hypotheses are as follow. a) Subjects from the placebo arm of VA-HIT will have significantly lower alpha l HDL subspecies, LpA-I, and apo C-III in HDL, and higher HDL/alpha l and apo A-I/alpha l ratios than subjects free of coronary heart disease from the Framingham Offspring Study. b) These parameters will also predict prospectively risk of coronary heart disease in both groups. c) In the VA-HIT study, treatment with gemfibrozil, which has been shown to be associated with a 22 percent reduction in myocardial infarction and coronary heart disease death, will be associated with increases in alpha l HDL subspecies, LpA-I, and apo C-III in HDL, as well as decreases in HDL/alpha l and apo A-I/alpha l ratios, compared to placebo. d) The hypothesis that subjects with specific mutations in the lipoprotein lipase gene have less beneficial changes in HDL subspecies with gemfibrozil than subjects with no mutations will also be tested.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00005676
|Principal Investigator:||Bela Asztalos, PhD||Tufts University|