Background: The development of left ventricular remodeling after acute myocardial infarction is a predictor of heart failure and mortality. The genetic influence on cardiac remodeling in the early period after acute myocardial infarction, is however, unclear. The aim ofthis study was to investigate the relationship between angiotensin-converting enzyme (ACE) gene polymorphism and left ventricular remodeling in the early period in patients with anterior myocardial infarction.
Method: The study population consisted of 142 patients with their first attack of acute anterior myocardial infarction. Echocardiographic examinations were performed within 24 h of the first attack (first evaluation) and on the fifth day of acute myocardial infarction (second evaluation). Left ventricular end systolic and diastolic diameters, left ventricular end systolic and diastolic volumes, ejection fraction, mitral flow velocities (E, A, E/A), deceleration time, isovolumic relaxation time and myocardial performance index were calculated. ACE I/D polymorphism was determined using polymerase chain reaction amplification.
Results: On the basis of polymorphism of the ACE gene, the patients were classified into the three groups: group 1, deletion/deletion (n=59) genotype, group 2 insertion/deletion (n=69), and group 3 insertion/insertion (n=14) genotype. When the first and second sets of echocardiographic results of the groups were compared, all parameters were not different among three groups. In group analysis, Left ventricular systolic diameters, left ventricular diastolic diameters, left ventricular end diastolic diameters, left ventricular ejection fraction and myocardial performance index between first and second echocardiographic results were significantly different in deletion/deletion group and only myocardial performance index and left ventricular ejection fraction in insertion/deletion group (P<0.05).
Conclusions: ACE gene polymorphism may influence early cardiac remodeling after acute myocardial infarction. Patients with the deletion/deletion-insertion/deletion genotype may be particularly more sensitive to ACE-I treatment possibly owing to the more prominent role of the renin-angiotensin system.