Please use this identifier to cite or link to this item:
https://hdl.handle.net/11499/4821
Title: | QT dispersion and left ventricular hypertrophy in athletes: Relationship with angiotensin-converting enzyme I/D polymorphism | Authors: | Tanrıverdi, Halil Kaftan, Havane Asuman Evrengül, Harun Dursunoğlu, Dursun Turgut, Günfer Kılıç, Mustafa |
Keywords: | ACE I/D polymorphism Athlete QT dispersion Ventricular hypertrophy dipeptidyl carboxypeptidase DNA adult article athlete controlled study echocardiography electrocardiogram female genetic polymorphism genotype heart left ventricle hypertrophy human major clinical study male training Adult Case-Control Studies Echocardiography Electrocardiography Exercise Female Genotype Heart Ventricles Humans Hypertrophy, Left Ventricular Male Peptidyl-Dipeptidase A Physical Endurance Polymorphism, Genetic Regression Analysis Sports |
Abstract: | Background - QT dispersion (QTd) is a measure of inhomogeneous repolarization of myocardium and is used as an indicator of arrhythmogenicity. QTd is increased in myocardial hypertrophy secondary to systemic hypertension. The relation between left ventricular (LV) enlargement in endurance trained subjects and QTd is unknown. The cloning of the angiotensin-converting enzyme (ACE) gene has made it possible to identify a deletion (D)-insertion (I) polymorphism that appears to affect the level of serum ACE activity. The aim of this study was to assess whether physiologic left ventricular hypertrophy as a result of physical training is associated with an increased QT length or dispersion depending on ACE I/D polymorphism. Methods - 56 endurance athletes and 46 sedentary subjects were included in this study, and they underwent both complete echocardiographic and electrocardiographic examination, the QT interval was measured manually as an average based on a 12-lead ECG. We also analysed ACE I and D allele frequencies in all patients. Results - Athletes had a significantly increased LV mass (235.1 ± 68.5 g vs. 144.9 ± 44.5 g, p < 0.001) and corrected QTd (QTcd) (55.5 ± 18.1 ms vs. 42.9 ± 17.2 ms, p < 0.001) in comparison to control subjects. There was a positive correlation between left ventricular mass index and QTcd in athletes (r = 0.3, p = 0.024). Left ventricular mass and mass index in ACE DD, DI and II genotypes were significantly different (p < 0.001). QTcd was significantly different between ACE DD (63.2 ± 12.8 ms) and ACE II (44.9 ± 17.6 ms) genotypes in athletes (p < 0.05). Conclusion - These data show that myocardial hypertrophy induced by exercise training might be associated with increased QTd as observed in systemic hypertension and might be affected by ACE I/D polymorphism. | URI: | https://hdl.handle.net/11499/4821 https://doi.org/10.2143/AC.60.4.2004987 |
ISSN: | 0001-5385 |
Appears in Collections: | PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection Tıp Fakültesi Koleksiyonu WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection |
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