Abstract
Life-threatening ventricular arrhythmias have frequently been documented in patients with vasospastic angina. Moreover, the incidence of ventricular arrhythmias has been closely associated with increased QT dispersion. However, the underlying mechanism responsible for this arrhythmogenesis has not been clarified. The effects of dipyridamole and subsequent aminophylline administration on QT dispersion were examined in 35 patients with vasospastic angina and 30 patients with atypical chest pain. None of the patients enrolled in this study revealed any significant stenosis in coronary angiography. QT dispersion during dipyridamole followed by aminophylline administration was compared between the 2 groups. The baseline QT dispersion was similar in both groups (vasospastic angina: 27 ± 8 ms; atypical chest pain: 28 ± 7 ms). No significant changes in QT dispersion were observed in patients with atypical chest pain by dipyridamole (23 ± 9 ms) and subsequent aminophylline administration (23 ± 5 ms). However, the QT dispersion in patients with vasospastic angina increased significantly by dipyridamole administration (53 ± 14 ms, p <0.0001) and returned to baseline by subsequent aminophylline administration (26 ± 10 ms). Our data suggest that the disparity of ventricular repolarization in vasospastic angina may be mediated by increased endogenous adenosine.
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