Postrevascularization recovery of fatty acid utilization in ischemic myocardium: A randomized clinical trial of potassium channel opener

Abstract

Background. Abnormal fatty acid metabolism persists in hibernating myocardium, even after reperfusion. This study was designed to determine whether the K + channel opener, nicorandil, improves fatty acid utilization after percutaneous transluminal coronary angioplasty (PTCA). Methods. Patients undergoing elective PTCA were randomly assigned to treatment (group N, n = 26) or control groups (group C, n = 22). Group N received intracoronary and intravenous nicorandil during PTCA. Myocardial fatty acid use and perfusion were quantitatively evaluated by means of iodine-123-beta-methyl-p-iodophenyl-pentadecanoic acid single photon emission computed tomography (I-123 BMIPP SPECT) and thallium-201 (Tl-201) imaging before PTCA, 72 hours after PTCA, and 3 months after PTCA. Left ventricular function was also evaluated by means of contrast ventriculography before and 3 to 6 months after PTCA. Results. The I-123 BMIPP defect score in group N significantly decreased, from 28% ± 13% to 20% ± 20% after PTCA and to 18% ± 17% 3 months later. In contrast, the I-123 BMIPP defect score in group C increased from 28% ± 20% to 36% ± 15% ( P < .05 versus group N) after PTCA, then returned to 28% ± 17% ( P < .05 versus group N) 3 months after PTCA. Recovery of left ventricular function paralleled the recovery of I-123 BMIPP uptake. Conclusions. Nicorandil improves the recovery of myocardial fatty acid utilization and cardiac function after PTCA. K channel activation may have a protective effect during coronary artery occlusion and improve subsequent recovery. (J Nucl Cardiol 2000;7:320–7.)