Differential release of cardiac enzymes after percutaneous coronary intervention

We hypothesized that using calcium channel blockers (CCBs) that dilate microvasculature during percutaneous coronary intervention (PCI) would result in lower postprocedural creatine phosphokinase (CPK). PCI can be complicated by elevated CPK that has been associated with impaired microvascular perfusion. Nitroglycerin (NTG), the conventional PCI vasodilator, dilates epicardial arteries but does not affect the microvasculature. We hypothesized that using CCBs that dilate the microvasculature would result in lower postprocedural CPK values. Patients (n = 816) without evidence of acute myonecrosis undergoing PCI were divided into two groups based on whether they received intracoronary NTG or CCB during PCI. Postprocedural CPK values were compared using a repeated-measures ANOVA and a random coefficient model. By repeated-measures analysis, the NTG group had CPK values of 88%, 83%, and 89% of the CCB group's CPK values at < 8, 8-14, and > 14 hr after PCI (P = 0.0080, 0.0002, and 0.0244), respectively. In a random coefficient model, the NTG group had CPK values 84%, 84%, and 89% of the CCB group's mean CPK values at 6, 12, and 18 hr after PCI (P = 0.0003, 0.0006, and 0.0403), respectively. Peak CPK values occurred earlier with CCB, although the maximal CPK was similar in both groups. Intracoronary CCB use is associated with an accelerated release of CPK after PCI compared with NTG. This is consistent with more efficient relief of microvascular obstruction with CCB. It suggests that myonecrosis may originate with vascular trauma at the time of PCI and its enzymatic expression is modifiable with different vasodilators.