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 1-123 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(ATP) channel activation may have a protective effect during coronary artery occlusion and improve subsequent recovery.