A DNA POLYMORPHISM AT THE ANGIOTENSIN-II TYPE-1 RECEPTOR (ATIR) LOCUSAND MYOCARDIAL-INFARCTION

Two hundred and thirty-five survivors of myocardial infarction (MI) we re compared to 384 controls with respect to distribution of genotypes and gene frequencies in the A1166C polymorphism at the angiotensin II type 1 receptor (AT1R) locus. No differences in allele frequencies or genotype distribution were observed when all patients were compared wi th all controls. When comparing CC homozygotes with the combined group of CA heterozygotes and AA homozygotes (CA/AA), a difference in borde rline significance between the MI group and controls was observed (p=0 .05). In males alone, this difference was much more pronounced because of the larger proportion of males with the CC genotype in MI cases th an in male controls (p=0.01). No significant differences were observed between female cases and controls. No interaction between the inserti on/deletion (I/D) polymorphism at the angiotensin I-converting enzyme (ACE) locus and the polymorphism at the AT1R locus was detected. When subdividing the subjects into a ''low-risk'' and a ''high-risk'' group , based on levels of apolipoprotein B (apoB) and body mass index (BMI) , and whether or not the person used lipid-lowering drugs, the frequen cy of CC homozygotes in male cases of the ''low-risk'' group differed significantly compared to the frequency in male controls of the ''low- risk'' group (p<0.001). No differences were observed in females, but t he number of ''low-risk'' group female cases was low (n=3). Thus, CC h omozygosity appears to be associated with MI in Norwegian males, espec ially among those with a ''low-risk'' phenotype.