Background

Prolongation of OT dispersion serves an independent predictor of cardiac arrhythmia in patients with miyocardial infarction(MI). ACE gene polymorphism is associated with high renin angiotensin system causing myocardial fibrosis and ventricular repolarization abnormality. Based on these finding, this study was designed to determine the association between ACE gene insertion/deletion (I/D) polymorphism and QT dispersion after acute myocardial infarction.

Methods – Results

The study included 108 patients with acute MI admitted to our clinic within sixth hour of onset of chest pain. Blood samples were obtained from all patients for genomic DNA analysis.ECGs were recorded at baseline and and the end of 6-months follow up. The OT dispersion was manually calculated.

The mean age of the patients were 57,5 ± 9,9 years (range from 36 to 70) Among the all patients, 29 (26,9%), 59 (54,6%) and 20 (18,5%) had the ACE DD, DI and II genotypes, respectively. The patients with DD genotype showed longer QT dispersion than patients with II or DI genotype at the baseline. Whereas, the patients with DI genotype showed longer QT dispersion than patients with DD or II genotype at the end of 6-months follow up (Table 1). However, the magnitude of the QT dispersion prolongation was higher in patients with carrying the ACE D allele than no carrying the ACE D allele at baseline and the end of 6-months follow up ( 52,5±2,6msn vs 47,5±2,1msn at baseline, 57±3,2msn vs 53±2,6 msn in months 6, p:0,428 and p:0,613 respectively)

Methods – Results

The study included 108 patients with acute MI admitted to our clinic within sixth hour of onset of chest pain. Blood samples were obtained from all patients for genomic DNA analysis.ECGs were recorded at baseline and and the end of 6-months follow up. The OT dispersion was manually calculated.

The mean age of the patients were 57,5 ± 9,9 years (range from 36 to 70) Among the all patients, 29 (26,9%), 59 (54,6%) and 20 (18,5%) had the ACE DD, DI and II genotypes, respectively. The patients with DD genotype showed longer QT dispersion than patients with II or DI genotype at the baseline. Whereas, the patients with DI genotype showed longer QT dispersion than patients with DD or II genotype at the end of 6-months follow up (Table 1). However, the magnitude of the QT dispersion prolongation was higher in patients with carrying the ACE D allele than no carrying the ACE D allele at baseline and the end of 6-months follow up ( 52,5±2,6msn vs 47,5±2,1msn at baseline, 57±3,2msn vs 53±2,6 msn in months 6, p:0,428 and p:0,613 respectively)