The genotype of the angiotensin-converting enzyme gene and global left ventricular dysfunction after myocardial infarction

• Published in: The American journal of cardiology Vol. 76; no. 5; pp. 326 - 329
• Main Authors: Ohmichi, Nobuyuki, Iwai, Naoharu, Nakamura, Yasuyuki, Kinoshita, Masahiko
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 15.08.1995; Elsevier; Elsevier Limited
• Subjects: Aged; Analysis of Variance; Angioplasty, Balloon, Coronary; Biological and medical sciences; Cardiac Catheterization; Cardiology. Vascular system; Cardiovascular disease; Coronary heart disease; DNA - analysis; Enzymes; Female; Follow-Up Studies; Gene Deletion; Genes; Genetics; Heart; Heterozygote; Homozygote; Humans; Male; Medical sciences; Middle Aged; Multivariate Analysis; Myocardial Infarction - complications; Myocardial Infarction - genetics; Myocardial Infarction - therapy; Peptidyl-Dipeptidase A - genetics; Polymerase Chain Reaction; Stroke Volume; Time Factors; Ventricular Dysfunction, Left - etiology; Ventricular Dysfunction, Left - genetics; Human; Infarct; Enzyme; Cardiovascular disease; Genotype; Coronary heart disease; Myocardial disease; Left ventricle; Gene; Peptidyl-dipeptidase A; Dysfunction; Myocardium; Hydrolases; Peptidyl-dipeptidases; Proteinases
• ISSN: 0002-9149; 1879-1913
• DOI: 10.1016/S0002-9149(99)80094-0

We examined the relation between the genotype of the angiotensin-converting enzyme (ACE) gene and the development of left ventricular dysfunction, as assessed by biplane left ventriculograms, after myocardial infarction. Seventy-nine patients (deletion homozygote [DD] = 13; insertion/deletion heterozygote [ID] = 38; insertion homozygote [II] = 28) underwent cardiac catheterization twice for reevaluation of percutaneous transluminal coronary angioplasty. Subjects who had their first cardiac catheterization within 2 months from the onset of myocardial infarction were enrolled. The second cardiac catheterization was performed from 4 to 7 months after the first cardiac catheterization. ACE genotypes were determined by using the polymerase chain reaction. Ejection fraction, and end-diastolic and end-systolic volume indexes at the first cardiac catheterization were not significantly different among the 3 groups. The end-diastolic volume index at the second cardiac catheterization was not significantly different among the 3 groups. Ejection fractions (mean ± SD) at the second catheterization in the 3 groups were 0.51 ± 0.15 (DD), 0.56 ± 0.12 (ID), and 0.62 ± 0.09 (II) (p = 0.02), and were significantly lower in the DD group than in the II group. The end-systolic volume indexes (mean ± SD) were 46 ± 21 (DD), 43 ± 24 (ID), and 30 ± 14 (II) ml/m 2 (p = 0.01), and were significantly greater in the DD and ID groups than in the II group. Multiple regression analysis indicated that ejection fraction at the first cardiac catheterization (r = 0.699, p = 0.0001) and the genotype of the ACE gene (dummy coding for nominal variables: DD + ID = 0, II = 1; r = 5.439, p = 0.0073) were predictors of ejection fraction at the second cardiac catheterization. In conclusion, the deletion allele for the ACE gene was associated with global left ventricular dysfunction after myocardial infarction.