Why the study?
Does intravenous dipyridamole produce a coronary steal effect and acute ischaemia in patients with ischaemic heart disease?
Does intravenous dipyridamole produce a coronary steal effect and acute ischaemia in patients with ischaemic heart disease?
Intravenous dipyridamole can induce a 'coronary steal' effect, leading to acute ischaemia and angina in patients with underlying ischaemic heart disease.
May provoke ischaemia in IHD via coronary steal; hypothesis-generating and requires prospective validation before clinical implications.
Summary: We studied thirteen patients before and after a five-minute infusion of intravenous dipyridamole (Persantin) (0.6 mg/kg). In ten patients with no evidence of ischaemic heart disease there were only modest increases in cardiac output (+17%) and heart rate (+16%), and decreases in systemic resistance (-24%), pulmonary capillary pressure (-19%), and mean blood pressure (-10%), five minutes after dipyridamole. Values returned towards control levels ten minutes later; there were no symptoms. By contrast, two patients with ischaemic heart disease developed acute coronary insufficiency after dipyridamole. ECG changes indicated acute ischaemia in the region of the previous infarct. Used diagnostically in a third patient, with the patient's consent, dipyridamole produced symptoms and haemodynamic changes of angina pectoris. We concluded that dipyridamole caused moderate peripheral vasodilatation in the patients without evidence of coronary artery disease. The findings in the patients with ischaemic heart disease are consistent with the hypothesis that dipyridamole produced a shunting of blood away from ischaemic areas in the myocardium by reducing coronary vascular resistance more in well perfused areas than in ischaemic areas–a “coronary steal” effect. Recent reports suggest that dipyridamole (Persantin) reduces platelet aggregation1–4. This effect has been the rationale for the use of dipyridamole with anticoagulants in the prevention of thromboembolic complications of prosthetic valve replacement5 and in the treatment of acute renal failure due to glomerulonephritis6 and rejection of the transplanted kidney7. It is possible that repeated attacks of “crescendo” angina pectoris and acute coronary insufficiency, which frequently culminate in myocardial infarction, could be due to recurrent embolisation of platelet aggregates forming on an atheromatous plaque in a major coronary vessel. If this hypothesis is correct, infusions of dipyridamole might be useful therapeutically. We undertook a study of the effects of dipyridamole on plateletss and in the course of this we noted important and unexpected circulatory effects of the drug in two patients with coronary artery disease. This prompted us to investigate the circulatory effects of dipyridamole and this paper reports our findings; some of the results have already been recorded briefly9,10.
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Wilcken et al. (1971) studied this question.
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