Key result
AT1R and AGT polymorphisms are not linked to 4-year QTd and Tpe prolongations.
Why the study?
Do AGT [-6G > A] and AT1R [1166A > C] gene polymorphisms influence repolarization parameters (QTd and Tpe) in elderly Chinese individuals?
Cohort (n=106)
Do AGT [-6G > A] and AT1R [1166A > C] gene polymorphisms influence repolarization parameters (QTd and Tpe) in elderly Chinese individuals?
AGT [-6G > A] and AT1R [1166A > C] polymorphisms do not influence ventricular repolarization parameters in elderly Chinese individuals and are not suitable markers for susceptibility to repolarization changes.
These polymorphisms should not guide repolarization risk assessment in elderly Chinese; leaves open other genetic determinants of QTd/Tpe prolongation.
Ventricular repolarization abnormality plays a crucial role in cardiac arrhythmia. Polymorphisms in renin-angiotensin system genes are associated with occurrence of ventricular arrhythmia. We previously demonstrated that subjects carrying the angiotensin converting enzyme (ACE) D-allele but not the angiotensinogen (AGT) M235T polymorphism had a higher magnitude of QT dispersion (QTd) prolongation. The aim of this study was to test whether the AGT [-6G > A] and angiotensin II type 1 receptor (AT1R) [1166A > C] polymorphisms influence repolarization parameters, including QTd and the peak and end of the T wave interval (Tpe). Of 1,500 people screened, 106 normotensive, non-diabetic participants aged > or = 60 were recruited. ECGs were recorded at baseline and in the second and fourth years. QTd and Tpe were manually calculated. Gene polymorphisms were analyzed by polymerase chain reaction. Mean age was 72.7 +/- 4.1 years (range, 62-81 years). QTd and Tpe were significantly prolonged in the second and fourth years (all p < 0.001). Neither gene polymorphism was associated with the magnitudes of QTd and Tpe prolongations. This longitudinal study shows that the AT1R [1166A > C] and AGT [-6G > A] polymorphisms do not influence repolarization parameters in this Chinese population in Taiwan, and so are not suitable markers to identify individuals susceptible to changes in these parameters.
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Lee et al. (2008) conducted a cohort in Normotensive, non-diabetic (n=106). AGT [-6G > A] and AT1R [1166A > C] polymorphisms vs. Non-carriers was evaluated on Magnitudes of QTd and Tpe prolongations. Although QTd and Tpe were significantly prolonged over 4 years (P<0.001), neither the AT1R [1166A > C] nor AGT [-6G > A] polymorphisms were associated with the magnitude of these prolongations.
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