In a double-blind, randomized, placebo-controlled trial, the possible antiischemic effect of metoprolol during percutaneous transluminal coronary angioplasty was tested. Electrocardiograms, hemodynamics, and metabolism were studied in 27 patients with a stenosis in the left anterior descending coronary artery. Measurements took place before angioplasty, after each of four 1-minute occlusions and 15 minutes after the last balloon deflation. Patients were randomly given placebo or metoprolol (15 mg as a bolus intravenously, followed by an infusion 0.04 mg/kg/hr). At the end of the procedure, the rate-pressure product had decreased by 15% (NS) and 23% (p=0.001) in the placebo and metoprolol groups, respectively, mainly due to similar decreases in heart rate. Metoprolol tended to lower chest pain and reduce precordial ST-segment elevation due to angioplasty, but the effects were not statistically significant. Lactate, hypoxanthine, and urate release immediately after deflation was similar in both groups. Metoprolol reduced arterial plasma hypoxanthine throughout the procedure by about 30% (p ≦ 0.02 vs. placebo). Thus, intravenous infusion of metoprolol did not significantly attenuate chest pain and ST-segment elevation, and failed to decrease cardiac lactate and oxypurine release. It did, however, reduce arterial hypoxanthine concentrations during angioplasty, possibly indicating that the beta-blocker inhibits extracardiac ATP catabolism. Cardiovascular Drugs and Therapy Cardiovascular Drugs and Therapy Look Inside 1 Citation Other actions Export citation Register for Journal Updates About This Journal Reprints and Permissions Add to Papers Share Share this content on Facebook Share this content on Twitter Share this content on LinkedIn

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doi.org/10.1007/BF00877821, hdl.handle.net/1765/65167
Cardiovascular Drugs and Therapy
Department of Cardiology

de Jong, J. W., Bonnier, H., Huizer, T., Ciampricotti, R., & Roelandt, J. (1993). Absence of beneficial effect of intravenous metoprolol given during angioplasty in patients with single-vessel coronary artery disease. Cardiovascular Drugs and Therapy, 7(4), 677–682. doi:10.1007/BF00877821