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The effects of reperfusion of infarct-related coronary artery on serum creatine phosphokinase and left ventricular
Insights
Restoring blood flow after myocardial infarction significantly alters serum CPK levels, leading to earlier peak enzyme activity. However, serum CPK alone cannot accurately estimate infarct size or assess long-term ventricular function.
Area of Science:
- Cardiology
- Biochemistry
- Medical Imaging
Background:
- Transmural myocardial infarction requires timely intervention to restore coronary blood flow.
- Serum creatine phosphokinase (CPK) levels are a marker of myocardial injury, but their time-activity curve and relationship with ventricular function post-reperfusion require further investigation.
Purpose of the Study:
- To investigate the impact of restoring coronary blood flow on the serum CPK time-activity curve in patients with myocardial infarction.
- To examine the relationship between cumulative CPK release (CPKr) and chronic-phase left ventricular function.
Main Methods:
- Coronary arteriography was performed within 8 hours of symptom onset in 31 patients with transmural myocardial infarction.
- Patients were divided into two groups: Group A (19 patients) with successful coronary reperfusion and Group B (12 patients) with persistent coronary occlusion.
- Serum CPK time-activity curves and left ventricular function (percent abnormally contracting segment, %ACS) were analyzed.
Main Results:
- The time to peak serum CPK activity was significantly shorter in the reperfusion group (Group A) compared to the occluded group (Group B).
- While the correlation between cumulative CPKr and %ACS was not strong, a linear relationship was observed in both groups.
- The ratio of CPKr to %ACS (CPKr/%ACS) was significantly higher in Group A, suggesting altered CPK release kinetics with reperfusion.
Conclusions:
- Reperfusion of the infarct-related coronary artery alters the serum CPK time-activity curve, characterized by an earlier appearance of peak CPK levels.
- Serum CPK levels alone are insufficient for accurately estimating infarct size or predicting chronic-phase left ventricular function.
- Further research is needed to fully elucidate the complex interplay between reperfusion, CPK kinetics, and myocardial recovery.
Abstract:
In 31 patients with transmural myocardial infarction in whom coronary arteriography was performed within 8 hours after the onset of symptoms, we examined (1) the effect of restoration of coronary blood flow on serum CPK time-activity curve and (2) the relationship between cumulative CPKr and the left ventricular function in the chronic phase. We divided 31 patients into 2 groups: Group A consists of 19 patients in whom coronary reperfusion was established. Group B consists of 12 patients whose coronary artery remained occluded. In group A, the time required to reach peak serum CPK activity was significantly shorter than in group B. When comparing CPKr with percent abnormally contracting segment (%ACS) in 2 groups, correlation between CPKr and %ACS was not good, but it revealed linear relation in both group A and B. CPKr divided by %ACS (CPKr/%ACS) was significantly higher in group A than in group B. We conclude that reperfusion of infarct-related coronary artery changes serum CPK time-activity curve resulting in earlier appearance of peak serum CPK and that infarct size cannot be estimated by serum CPK level alone.