GENETIC-BASIS OF LEFT-VENTRICULAR REMODELING AFTER MYOCARDIAL-INFARCTION

The purpose of the present study was to assess whether the insertion ( I)/deletion (D) polymorphism of the angiotensin converting enzyme (ACE ) gene, and the polymorphism of angiotensinogen (AGT) gene with threon ine (T) instead of methionine (M) at amino acid 235 in exon 2 (M235T) were associated with left ventricular dilatation after myocardial infa rction. In 103 patients with myocardial infarction, the left ventricul ar (LV) end-diastolic volume index (EDVI) and the end-systolic volume index (ESVI) were assessed by echocardiography at two time points, nam ely at 7 +/- 4 days and at 3.9 +/- 1.3 months (mean +/- S.D.) after th e infarction. The increases in the LVEDVI and LVESVI on the second ech ocardiogram were significantly higher in subjects with the DD and ID g enotypes than in patients with the II genotype (P < 0.05 and P < 0.005 , respectively). Multiple regression analysis revealed that the LVESVI at the first echocardiographic examination and the ACE I/D genotype w ere significant predictors of the LVEDVI and LVESVI at the second echo cardiographic examination. However, the AGT M235T genotype was elimina ted. In conclusion, the DD and ID genotypes of the ACE gene were signi ficantly associated with the progression of the LVEDVI and LVESVI afte r myocardial infarction. The presence of the deletion allele of the AC E gene may be a risk factor of congestive heart failure after a myocar dial infarction.