Cardiovascular Diseases Clinical Trial
To identify genetic mechanisms controlling apolipoprotein levels and other 'non-traditional' risk factors in families ascertained through probands with premature coronary artery disease (CAD).
BACKGROUND:
Preliminary work for this project was carried out as part of the Johns Hopkins Coronary
Artery Disease study (R01-HL-34791) which provided extensive data on families ascertained
through equal numbers of white male and female probands undergoing elective angiography.
DESIGN NARRATIVE:
The study, a subproject within an Arteriosclerosis SCOR, had three components. In Component
1, the group of 203 probands under study R01HL34791 was expanded with an additional 50 black
patients undergoing angiography, meeting identical criteria. In Component 2, segregation
analysis was carried out on lipoproteins, apolipoproteins, and selected non-traditional risk
factors on families of all probands and the etiologic heterogeneity among different groups
of families was tested. In Component 3, linkage was tested between putative Mendelian loci
defined in Component 2 and markers in and around candidate loci involved in lipid
metabolism. Preliminary results provided evidence of Mendelian control for apolipoprotein A1
and B, and the candidate loci examined included apo B, lipoprotein lipase, and the
A1-CIII-A4 gene cluster. The major hypothesis was that these apolipoprotein levels and other
non-traditional risk factors might be under genetic control. Genetic analysis of these risk
factors was used to direct molecular studies to identify specific mutations.
The study completion date listed in this record was obtained from the "Completed Date"
entered in the Query View Report System (QVR).
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