ipyridamole is an antiplatelet agent that inhibits the cellular reuptake of adenosine, leading to increased extracellular concentrations of adenosine. 1 Adenosine has cardioprotective actions: it activates adenosine receptors, resulting in attenuation of catecholamine release, -adrenoceptor-mediated myocardial hypercontraction, and Ca 2+ overload via A1 receptors, and increases coronary blood flow and inhibits platelet and leukocyte activation via A2 receptors. A meta-analysis of 13 randomized, placebocontrolled trials published between 1960 and 1992 demonstrated the beneficial effect of dipyridamole with respect to the prevention of angina pectoris, particularly with a longer duration of treatment. 2 In experimental studies, absolute coronary flow is increased when collateral circulation is not present. 3 However, dipyridamole induced myocardial ischemia that depended on collateral circulation in some patients with coronary artery disease (CAD), because dipyridamole decreased flow to collateral-dependent vascular beds through "coronary steal". [4][5][6] Coronary steal is conventionally defined as an absolute decrease in perfusion, compared with resting flow, to collateralized myocardium following coronary vasodilation. Therefore, dipyridamole and adenosine are used in diagnostic examinations for detecting myocardial ischemia, 7,8 rather than as treatment for CAD, 9 because of the coronary steal phenomenon. In recent studies, elevation of serum adenosine by administration of dipyridamole improved cardiac function in patients with heart failure; 10,11 however, there are few data regarding the long-term effects of dipyridamole on mortality and cardiovascular events in Japanese patients. The aim of this study was to assess whether the use of dipyridamole after complete revascularization affects long-term mortality in patients with impaired left ventricular (LV) systolic function.
Methods
SubjectsData from consecutive patients who had undergone surgical and/or percutaneous coronary revascularization at Juntendo University Hospital between January 1984 and December 1992 were analyzed. Patients were enrolled who met the inclusion criteria: (1) achieved complete revascularization, defined as no un-bypassed major vessels with a ≥50% stenosis, 12,13 and (2) had impaired LV systolic function, defined as a LV ejection fraction (LVEF) <50% on echocardiography at the time when complete revascularization was achieved. Patients who had other known life-threatening diseases at baseline and patients who had associated complex cardiac procedures, such as valve replacement or aneurysm repair at the time of surgical revascularization, were excluded.