Association Between ACE Gene Polymorphism and QT Dispersion in Patients with Acute Myocardial Infarction



Zulkuf Karahan1, Murat Ugurlu1, Berzal Ucaman1, Ali Veysel Ulug1, Ilyas Kaya1, Kemal Cevik1, Mehmet Sahin Adiyaman1, Onder Oztürk1, Hikmet Iyem2, *, Ferit Ozdemir2
1 Gazi Yasargil Education and Research Hospital, Cardiology, Diyarbakir, Turkey
2 Gazi Yasargil Education and Research Hospital, Cardiovascular Surgery, Diyarbakir, Turkey


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© Karahan et al.; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Gazi Yasargil Education and Research Hospital, Cardiovascular Surgery, Diyarbakir, Turkey; Email: hikmetiyem@gmail.com


Abstract

Background:

Angiotensin converting enzyme (ACE) gene polymorphism is associated with high renin-angiotensin system causing myocardial fibrosis and ventricular repolarization abnormality. Based on these findings, this study was designed to determine the association between ACE gene insertion/deletion (I/D) polymorphism and QT dispersion after acute myocardial infarction (MI).

Objective and Methods:

The study included 108 patients with acute MI. Blood samples were obtained from all the patients for genomic DNA analysis. ECGs were recorded at baseline and at the end of a 6-month follow up. The OT dispersion was manually calculated.

Results:

The mean age of the patients was 57.5 ±9.9 years (ranging from 36 to 70). The patients with DD genotype showed longer QT dispersion than patients with II or DI genotype at the baseline, while at the end of the six-month follow up the patients with DI genotype showed longer QT dispersion than patients with DD or II genotypes. However, the magnitude of the QT dispersion prolongation was higher in patients carrying the ACE D allele than patients who were not carrying it, at baseline and at the end of six-month follow up (52.5 ±2.6 msn vs. 47.5±2.1 msn at baseline, 57±3.2 msn vs. 53±2.6 msn in months, P: 0.428 and P: 0.613, respectively).

Conclusion:

Carriers of the D allele of ACE gene I/D polymorphism may be associated with QT dispersion prolongation in patients with MI.An interaction of QT dispersion and ACE gene polymorphism may be associated with an elevation of serum type I-C terminal pro-collagen concentration, possibly leading to myocardial fibrosis, and increased action potential duration.

Keywords: ACE gene polymorphism, Coronary artery disease (CAD), Myocardial infarction, QT dispersion.