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Role of myocardial oxygen consumption in dipyridamole-induced ischemia
E Picano1, F Lattanzi, A Distante
1C.N.R. Institute of Clinical Physiology, Pisa, Italy.
Abstract:
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.
Insights
Myocardial oxygen consumption may cause aminophylline resistance in dipyridamole-induced ischemia. Increased oxygen demand, potentially from sympathetic activation, can sustain ischemia even after aminophylline treatment for flow maldistribution.
Area of Science:
- Cardiology
- Pharmacology
- Physiology
Background:
- Dipyridamole-echocardiography is used to diagnose myocardial ischemia.
- Aminophylline is an antidote used to reverse dipyridamole-induced ischemia.
- Aminophylline resistance can occur, necessitating alternative treatments.
Purpose of the Study:
- To investigate if increased myocardial oxygen consumption contributes to aminophylline resistance.
- To determine the role of myocardial oxygen demand in dipyridamole-induced ischemia management.
Main Methods:
- Analysis of 163 patients with positive dipyridamole-echocardiography tests.
- Comparison of rate-pressure product (RPP) during exercise stress tests and dipyridamole-induced ischemia.
- Categorization into aminophylline-responsive (Group I) and resistant (Group II) groups.
Main Results:
- Group I showed a significantly greater RPP increase during exercise than during dipyridamole stress (204 vs. 145, p<0.01).
- Group II exhibited similar RPP increases under both exercise and dipyridamole conditions (147 vs. 150, p=ns).
- Aminophylline resistance was associated with elevated myocardial oxygen consumption, possibly due to sympathetic activation.
Conclusions:
- Increased myocardial oxygen consumption may be a key factor in aminophylline resistance.
- This elevated oxygen demand, potentially linked to sympathetic response, can perpetuate ischemia independently of flow maldistribution.
- Aminophylline may not be effective when ischemia is driven by increased myocardial oxygen consumption rather than solely by flow redistribution.