Summary
To compare the antiischemic effects of intracoronary administration of a beta blocker, atenolol, and of a calcium antagonist, nifedipine, on the clinical and electrocardiographic signs of myocardial ischemia induced by balloon occlusion of the coronary artery, we studied 32 consecutive patients undergoing routine PTCA. In each patient at least three balloon inflations were performed: the first served to verify the occurrence of ischemia (ST segment depression/elevation >1.5 mm); the second was used as a control occlusion; the third was performed after the patients were assigned to receive either atenolol 1.0 mg IC (group 1, N=16) or nifedipine V=0.2 mg IC (group 2, N=16). In a control population of 10 patients, the time to return to baseline of the ECG tended to be progressively shorter during the three consecutive inflations, but the other clinical and ECG parameters did not change significantly. In group 1 and group 2, two patients did not show ECG signs of ischemia at the third inflation; the time to ischemia increased in group 1 (+76%, p < .001) and group 2 (+85%, p < .01; NS group 1 versus group 2); ST segment displacement at 30 seconds decreased in group 1 (-38%, p < .01) and group 2 (-36%, p < .01; NS group 1 versus group 2). In group 1, 2/16 patients were symptom free, and the time to chest pain was significantly delayed (+47%, p < .01) at the third inflation; in group 2 no patient became asymptomatic at the third inflation, and the time to chest pain did not change (+5%, NS; NS group 1 versus group 2). In conclusion, the regional cardioplegia obtained through the blockade of the slow calcium channels with IC nifedipine or of the beta receptors with IC atenolol reduced myocardial ischemia to a similar extent during ballon occlusion of the coronary artery. Atenolol was also very effective on chest pain, though not significantly more than nifedipine.
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Ghio, S., De Servi, S., Angoli, L. et al. Similar antiischemic effects of intracoronary atenolol and nifedipine during brief coronary occlusions in humans. Cardiovasc Drug Ther 6, 255–259 (1992). https://doi.org/10.1007/BF00051147
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DOI: https://doi.org/10.1007/BF00051147