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Öğe Association Between A/C1166 Gene Polymorphism of the Angiotensin II Type 1 Receptor and Biventricular Functions in Patients With Acute Myocardial Infarction(Japanese Circulation Society, 2006) Ülgen, Mehmet S.; Öztürk, Önder; Yazıcı, Mehmet; Kayrak, Mehmet; Alan, Sait; Koç, Fatih; Tekes, SelahattinAlthough there have been several association studies of angiotensin II type 1 receptor (AT1R, A/C1166) gene polymorphism in clinical endpoints such as myocardial infarction (MI), hypertension, aortic stiffness, and left ventricular mass, the relationship between AT1R polymorphism and biventricular function in acute anterior MI has not been studied before. Methods and Results The study group comprised 132 consecutive patients who were admitted to the coronary care unit with their first acute anterior MI. Systolic and diastolic diameters, volumes, inflow properties, ejection fraction and myocardial performance index of both ventricles were measured. AT1R polymorphism was determined using polymerase chain reaction amplification. Based on A/C1166 polymorphism of ATIR, the patients were classified into 3 groups: group 1, A/A (n=91) genotype, group 2 A/C (n=28), and group 3 C/C (n=13) genotype. When the left ventricular and right ventricular echocardiographic functions were compared, all parameters of the 3 groups were found to be similar. No difference was detected in either the genotype distribution or allele frequencies between the patients and the controls for AT1R. Conclusions The results suggest that A/C1166 polymorphism of AT1R did not influence the risk of either acute MI or biventricular function after anterior MI.Öğe The relationship between angiotensin-converting enzyme (insertion/deletion) gene polymorphism and left ventricular remodeling in acute myocardial infarction(2007) Ülgen, Mehmet S.; Öztürk, Önder; Alan, Sait; Kayrak, Mehmet; Turan, Yaşar; Tekeş, Selahattin; Toprak, NizamettinBACKGROUND: 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. © 2007 Lippincott Williams & Wilkins, Inc.