The aim of this study was to assess whether myocardial oxygen consumption can be responsible for
aminophylline resistance in
dipyridamole-induced
ischemia. We analyzed 163 consecutive patients who had a positive low-dose (0.56 mg/kg over 4 minutes)
dipyridamole-echocardiography test, requiring intravenous
aminophylline as an
antidote. All patients also performed an exercise stress test. In 141 of these patients, the signs of
ischemia were reversed by administration of intravenous
aminophylline (group I), while the remaining 22 patients were resistant to
aminophylline (240 mg/kg over 3 minutes) and received additional treatment with
nitrates to relieve
ischemia (group II). The increase in rate-pressure product (RPP = mm Hg x beats/min x 100) measured during the exercise stress test in the patients in group I was significantly greater than that determined during
dipyridamole-induced
ischemia (204 +/- 41 versus 145 +/- 33, p less than 0.01). However, the increases in RPP under both conditions were similar for the patients in group II (147 +/- 24 versus 150 +/- 20, p = ns). In patients with
dipyridamole-induced
ischemia who were resistant to
aminophylline, the rise in myocardial oxygen consumption--probably linked to reflex sympathetic activation--might maintain
ischemia independently from flow maldistribution, which should be reversed by
aminophylline.