Life-threatening ventricular arrhythmias have frequently been documented in
patients with vasospastic angina. Moreover, the incidence of ventricular a
rrhythmias has been closely associated with increased QT dispersion. Howeve
r, the underlying mechanism responsible for this arrhythmogenesis has not b
een clarified, The effects of dipyridamole and subsequent aminophylline adm
inistration on QT dispersion were examined in 35 patients with vasospastic
angina and 30 patients with atypical chest pain. None of the patients enrol
led in this study revealed any significant stenosis in coronary angiography
. QT dispersion during dipyridamole followed by aminophylline administratio
n 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 amin
ophylline administration (23 +/- 5 ms). However, the Qi dispersion in patie
nts with vasospastic angina increased significantly by dipyridamole adminis
tration (53 +/- 14 ms, p < 0.0001) and returned to baseline by subsequent a
minophylline administration (26 +/- 10 ms). Our data suggest that the dispa
rity of ventricular repolarization in vasospastic angina may be mediated by
increased endogenous adenosine. (C) 1999 by Excerpta Medica, Inc.