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Published on: August 8, 2013
Determination of the origin of elevated plasma CPK after cardiac catheterization
Insights
Chest pain after cardiac catheterization is usually not myocardial infarction. Elevated creatine kinase (CK) levels post-procedure reflect non-cardiac sources, while MB CK elevation reliably indicates infarction.
Area of Science:
- Cardiology
- Biochemistry
Background:
- Chest pain during cardiac catheterization can be misdiagnosed as myocardial infarction due to ECG changes and elevated serum enzymes.
- Distinguishing catheterization-related enzyme elevations from actual myocardial infarction is crucial for treatment decisions, especially before coronary revascularization.
Purpose of the Study:
- To determine if creatine phosphokinase (CPK) elevations after cardiac catheterization can be differentiated from those caused by myocardial infarction.
- To assess the diagnostic utility of CPK isoenzymes, specifically MB CPK, in patients undergoing cardiac catheterization.
Main Methods:
- Assayed CPK isoenzymes in plasma samples from 184 patients undergoing cardiac catheterization.
- Collected samples every 2 hours for 24 hours post-procedure.
- Quantified CPK isoenzymes using a kinetic fluorometric method; confirmed myocardial infarction with 99mTc pyrophosphate scan when necessary.
Main Results:
- Total plasma CPK increased in all patients post-catheterization, but MB CPK remained normal in 181 patients.
- Three patients showed elevated MB CPK, confirmed as myocardial infarction via scan.
- Control patients with acute myocardial infarction had significantly higher total CPK and elevated MB CPK.
Conclusions:
- CPK elevations following cardiac catheterization primarily originate from non-cardiac sources, not myocardial injury.
- Elevated plasma MB CPK activity is a reliable indicator of myocardial infarction in patients undergoing cardiac catheterization.
Abstract:
Episodes of chest pain are not common in patients undergoing cardiac catheterization. The diagnostic implications of this symptom may be complicated by the occasional appearance of electrocardiographic changes mimicking those seen in acute myocardial infarction, and by the frequent elevation of conventionally measured serum enzymes. Exclusion of infarction is particularly important when coronary revascularization is contemplated. Since the MB CPK isoenzyme is relatively specific to myocardium, we assayed CPK isoenzymes in plasma samples from 184 patients undergoing cardiac catheterization to determine whether CPK elevations accompanying catheterization can be distinguished from those associated with myocardial infarction. Samples were obtained every 2 hr for 24 hr, and CPK isoenzymes quantified by a kinetic fluorometric method. Total plasma CPK increased in all patients (mean peak 0.238 +/- 0.042 (SD) IU/ml) but MB CPK remained normal in 181 patients (less than 0.005 IU/ml). In three remaining patients, MB CPK was elevated and myocardial infarction was confirmed by 99mTc (SN) pyrophosphate scan. Twelve patients after catheterization, in whom no intramuscular premedication was given, exhibited only minimal elevation of total plasma CPK. In contrast, 100 control patients with acute myocardial infarction exhibited peak total CPK activity averaging 0.833 +/- 0.037 (SD), and MB CPK was elevated in all cases (0.078 +/- 0.027 (SD) IU/ml). Thus, CPK elevations after catheterization reflect release of enzyme from noncardiac sources rather than from injured myocardium. Furthermore, increased plasma MB CPK activity may be considered a reliable index of myocardial infarction in patients undergoing cardiac catheterization.
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