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 threonine (T) instead of methionine (M) at amino acid 235 in exon 2 (M235T) were associated with left ventricular dilatation after myocardial infarction. In 103 patients with myocardial infarction, the left ventricular (LV) end-diastolic volume index (EDVI) and the end-systolic volume index (ESVI) were assessed by echocardiography at two time points, namely at 7 +/- 4 days and at 3.9 +/- 1.3 months (mean +/- S.D.) after the infarction. The increases in the LVEDVI and LVESVI on the second echocardiogram were significantly higher in subjects with the DD and ID genotypes 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 were significant predictors of the LVEDVI and LVESVI at the second echocardiographic examination. However, the AGT M235T genotype was eliminated. In conclusion, the DD and ID genotypes of the ACE gene were significantly associated with the progression of the LVEDVI and LVESVI after myocardial infarction. The presence of the deletion allele of the ACE gene may be a risk factor of congestive heart failure after a myocardial infarction.
Ohmichi
N
N
First Department of Internal Medicine, Shiga University of Medical Sciences, Japan.
Iwai
N
N
Maeda
K
K
Shimoike
H
H
Nakamura
Y
Y
Izumi
M
M
Sugimoto
Y
Y
Kinoshita
M
M
D000704:Analysis of Variance; D000808:Angiotensinogen / Q000235:genetics*; D004452:Echocardiography; D005260:Female; D005838:Genotype; D006333:Heart Failure / Q000209:etiology / Q000235:genetics; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000235:genetics*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D012044:Regression Analysis; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000235:genetics
D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A