Role of myocardial oxygen consumption in dipyridamole-induced ischemia.

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.