Effects of aminophylline on cardiac function and regional myocardial perfusion: Implications regarding its antiischemic action

Aminophylline improves exercise capacity in patients with angina. Because this drug does not dilate epicardial coronary vessels, its beneficial effect is from either a reduction of myocardial oxygen consumption or an improvement of myocardial blood flow distribution. This study was performed to assess the effects of aminophylline on cardiac function and on regional myocardial perfusion to establish the mechanisms of its antiischemic action. In 10 patients during cardiac catheterization hemodynamic parameters and cardiac volumes were obtained during baseline and after intravenous infusion of aminophylline. Aminophylline decreased left ventricular end-diastolic pressure (from 11 ± 4 to 4 ± 2 mm Hg, p < 0.001), mean right atrial pressure (from 5 ± 2 to 2 ± 1 mm Hg, p < 0.01), and left ventricular end-diastolic volume (from 117 ± 36 to 88 ± 36 ml, p < 0.01); it increased peak dpdt (from 1931 ± 329 to 2430 ± 540 mm Hg/sec, p < 0.001) and heart rate (from 69 ± 9 to 76 ± 14 beats/min, p < 0.05) and did not modify systolic aortic pressure (138 ± 14 vs 137 ± 16 mm Hg, p = not significant [NS]). Estimated oxygen consumption during aminophylline (6.7 ± 1.3 ml/min/gm) was similar to that during baseline (6.7 ± 1.4 ml/min/gm). In another study in nine anesthetized dogs with a critical stenosis of the left anterior descending artery, myocardial perfusion was assessed by microspheres during control atrial pacing and during atrial pacing after aminophylline; left atrial pressure was kept constant throughout the study. During the second atrial pacing, total blood flow in the myocardium supplied by the left anterior descending coronary artery was similar to that observed during the control pacing (0.60 ± 0.17 vs 0.60 ± 0.16 ml/min/gm, p = NS), but the endo/epi flow ratio was higher (0.59 ± 0.29 vs 0.39 ± 0.25, p < 0.05). Left atrial pressure, mean aortic pressure, and heart rate were similar during both atrial pacings (14 ± 8 vs 15 ± 6 mm Hg, p = NS, 85 ± 9 vs 88 ± 13, p = NS, 178 ± 16 vs 178 ± 16 beats/min, p = NS, respectively). Thus aminophylline does not reduce myocardial oxygen consumption. It can improve myocardial ischemia through (1) left ventricular unloading which is likely to result in a reduction of subendocardial extravascular compression; and (2) constriction of subepicardial vessels with redistribution of blood flow toward the subendocardium.