Correlation of HLA types in premature coronary artery disease: an attempt to define independent genetic risk factors.
This study was designed to investigate whether isolated genetic factors, controlled by genes in the HLA chromosomal region, could be indicted as independent contributing influences in the genesis of premature coronary artery disease (CAD). Nineteen patients with fixed obstructive CAD documented by coronary angiography had no coronary risk factors with respect to age; levels of serum cholesterol, fasting triglycerides, and blood glucose; blood pressure; obesity; history of diabetes mellitus or hypertension; and cigarette-smoking history. Sixteen patients had a family history of CAD. HLA typing was restricted to antigens of the A and B loci. Control subjects (n = 1,157) were normal. At the A locus, no antigens demonstrated an observed frequency significantly higher than that expected from the control population. At the B locus, BW 38 had a statistically significant greater frequency (p less than 0.01) in the study group with CAD (21 percent) than in the control population (4 percent). The association between BW 38 and premature CAD lost its statistical significance when conservatively corrected for the number of HLA antigens tested by the Bonferroni adjustment. The relative risk for CAD if a patient had antigen BW 38 was 6.2. Our data suggest a statistically significant trend between the presence of HLA BW 38 and premature CAD. Whether the HLA tissue antigens are involved directly in the pathogenesis of CAD, act as markers for immune response genes, or serve as markers of other yet undefined genetic factors needs further study.
D000328:Adult; D001161:Arteriosclerosis / Q000276:immunology; D002874:Chromosome Mapping; D003327:Coronary Disease / Q000235:genetics*; D005260:Female; D006680:HLA Antigens / Q000235:genetics* / Q000276:immunology; D006801:Humans; D008297:Male; D008875:Middle Aged; D011247:Pregnancy; D012306:Risk; D014427:Twins
D006680:HLA Antigens