Differential release of cardiac enzymes after percutaneous coronary intervention

Area of Science:

• Cardiology
• Interventional Cardiology
• Pharmacology

Background:

• Percutaneous coronary intervention (PCI) can lead to elevated creatine phosphokinase (CPK) levels, linked to impaired microvascular perfusion.
• Nitroglycerin (NTG) dilates epicardial arteries but does not impact coronary microvasculature during PCI.
• Calcium channel blockers (CCBs) are hypothesized to dilate microvasculature, potentially mitigating post-PCI CPK elevation.

Purpose of the Study:

• To investigate the effect of intracoronary calcium channel blockers (CCBs) versus nitroglycerin (NTG) on postprocedural creatine phosphokinase (CPK) levels during percutaneous coronary intervention (PCI).
• To determine if CCBs, by dilating microvasculature, result in lower CPK values compared to conventional NTG during PCI.

Main Methods:

• A study involving 816 patients undergoing PCI without acute myonecrosis.
• Patients were divided into two groups: one receiving intracoronary NTG, the other receiving intracoronary CCB.
• Postprocedural CPK values were analyzed using repeated-measures ANOVA and a random coefficient model.

Main Results:

• The NTG group showed significantly higher CPK values compared to the CCB group at various time points post-PCI (<8, 8-14, >14 hours).
• Random coefficient modeling confirmed higher CPK values in the NTG group at 6, 12, and 18 hours post-PCI.
• While peak CPK levels were similar, CCB use was associated with an earlier CPK release, indicating more efficient microvascular obstruction relief.

Conclusions:

• Intracoronary CCB use is associated with an accelerated release of CPK after PCI compared to NTG.
• This accelerated release suggests more efficient relief of microvascular obstruction when CCBs are used.
• The findings imply that myonecrosis post-PCI may originate from vascular trauma, and its enzymatic expression can be modulated by different vasodilators.