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Circulation, Vol 88, 502-508, Copyright © 1993 by American Heart Association

ARTICLES

Bamiphylline improves exercise-induced myocardial ischemia through a novel mechanism of action

A Gaspardone, F Crea, M Iamele, F Tomai, F Versaci, A Pellegrino, L Chiariello and PA Gioffre
Divisione di Cardiochirurgia, Universita di Roma Tor Vergata European Hospital, Italy.

BACKGROUND. In patients with stable angina pectoris aminophylline, a nonselective antagonist of adenosine receptors, markedly improves exercise capacity. To establish the role played by A1 adenosine receptors in the anti-ischemic action of aminophylline, the effects of bamiphylline, a selective A1 antagonist, on exercise-induced ischemia were investigated in patients with stable angina pectoris. METHODS AND RESULTS. In a single-blind, placebo-controlled, randomized cross-over trial in 18 patients, oral administration of 1200 mg bamiphylline increased both the time to 1-mm ST segment depression (from 524 +/- 177 to 664 +/- 192 seconds, P < .01) and the rate-pressure product at 1-mm ST segment depression (from 159 +/- 31 to 190 +/- 34 beats per minute per mm Hg/10(2) (P < .001). End-diastolic and end-systolic left ventricular volumes, left ventricular ejection fraction, and systolic septal and posterior wall thickening investigated by two-dimensional echocardiography in 12 of the 18 patients were not affected by oral administration of bamiphylline (124 +/- 22 versus 125 +/- 20 mL, P = NS; 49 +/- 12 versus 50 +/- 13 mL, P = NS; 60 +/- 8% versus 58 +/- 7%, P = NS; 35 +/- 6% versus 36 +/- 7%, P = NS; 32 +/- 6% versus 33 +/- 6%, P = NS, respectively). In 7 of the 18 patients, the intravenous infusion of bamiphylline (5 mg/kg in 15 minutes) during cardiac catheterization did not produce any significant change of heart rate (76 +/- 10 versus 75 +/- 13 beats per minute, P = NS), mean right atrial pressure (3.8 +/- 1.7 versus 3.7 +/- 1.7 mm Hg, P = NS), mean aortic pressure (102 +/- 12 versus 99 +/- 10 mm Hg, P = NS), or left ventricular end-diastolic pressure (14 +/- 3 versus 14 +/- 4 mm Hg, P = NS) compared with baseline. Furthermore, after intravenous infusion of bamiphylline, the diameter of seven proximal and distal normal segments and of seven stenotic segments were similar to those measured at baseline (3.1 +/- 0.5 versus 3.1 +/- 0.5 mm, P = NS; 1.6 +/- 0.2 versus 1.7 +/- 0.2 mm, P = NS; 1.6 +/- 0.5 versus 1.6 +/- 0.5 mm, P = NS, respectively). CONCLUSIONS. In patients with stable angina pectoris, oral administration of bamiphylline improves exercise capacity. Its anti-ischemic action does not appear to be mediated by systemic hemodynamic effects or by stenosis dilation. Therefore, the improvement of myocardial ischemia caused by bamiphylline is probably due to redistribution of coronary blood flow toward the underperfused subendocardium. This novel anti-ischemic action would appear to be mediated by antagonism of A1 receptors.

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