Y. Kuwabara et al., Postrevascularization recovery of fatty acid utilization in ischemic myocardium: A randomized clinical trial of potassium channel opener, J NUCL CARD, 7(4), 2000, pp. 320-327
Background. Abnormal fatty acid metabolism persists in hibernating myocardi
um, even after reperfusion, This study was designed to determine whether th
e K+ channel opener, nicorandil, improves fatty acid utilization after perc
utaneous transluminal coronary angioplasty (PTCA),
Methods. Patients undergoing elective PTCA were randomly assigned to treatm
ent (group N, n = 26) or control groups (group C, n = 22), Group N received
intracoronary and intravenous nicorandil during PTCA. Myocardial fatty aci
d use and perfusion were quantitatively evaluated by means of iodine-123-be
ta-methyl-p-iodophenyl-pentadecanoic acid single photon emission computed t
omography (I-123 BMIPP SPECT) and thallium-201 (Tl-201) imaging before PICA
, 72 hours after PICA, and 3 months after PICA, Left ventricular function w
as also evaluated by means of contrast ventriculography before and 3 to 6 m
onths after PTCA,
Results. The I-123 BMIPP defect score in group N significantly decreased, f
rom 28% +/- 13% to 20% +/- 20% after PICA 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 util
ization and cardiac function after PTCA, K-ATP channel activation may have
a protective effect during coronary artery occlusion and improve subsequent
recovery.