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Creatine phosphokinase following cardioversion
Insights
Cardioversion for supraventricular tachyarrhythmias rarely impacts diagnosing acute myocardial infarction (AMI) using creatine phosphokinase (CPK) levels. CPK levels in patients without AMI remained within normal limits post-cardioversion.
Area of Science:
- Cardiology
- Biochemistry
Background:
- Supraventricular tachyarrhythmias require treatment like cardioversion.
- Acute myocardial infarction (AMI) diagnosis relies on serial creatine phosphokinase (CPK) measurements.
- The potential impact of cardioversion on CPK levels is a diagnostic concern.
Purpose of the Study:
- To evaluate the effect of cardioversion on serum CPK levels.
- To determine if cardioversion interferes with diagnosing AMI using CPK.
- To assess CPK changes in patients undergoing cardioversion for supraventricular tachyarrhythmias.
Main Methods:
- Serial total serum CPK estimations were performed before and up to 51 hours after cardioversion.
- 12 patients without AMI undergoing cardioversion were studied.
- CPK levels were compared to normal limits and levels observed in AMI patients.
Main Results:
- The maximal CPK rise observed was 78 mU/ml (110%), not exceeding normal limits in most patients.
- Only two patients had CPK levels slightly above the normal limit (149 and 156 mU/ml).
- This contrasts with significantly higher CPK elevations (mean 900 mU/ml) observed in AMI patients.
Conclusions:
- Cardioversion for supraventricular tachyarrhythmias generally does not interfere with diagnosing AMI via serial CPK estimations within 24 hours.
- The observed CPK elevations post-cardioversion are typically minor and distinct from those seen in AMI.
- Serial CPK monitoring remains a reliable tool for AMI diagnosis even after cardioversion.
Abstract:
Serial estimations of total serum creatine phosphokinase (CPK) have been performed before and during 18-51 hours after cardioversion of supraventricular tachyarrhythmias in 12 patients without acute myocardial infarction (AMI). The maximal CPK rise was 78 mU/ml (110%) and the CPK did not exceed the upper normal limit (130 mU/ml) in more than two patients (149 respectively 156 mU/ml). The CPK rise we have observed in a series of AMI patients varied between 101 (133%) and 2 260 mU/ml (3 780%), mean 900 mU/ml (1 184%). Therefore, cardioversion performed as described seldom seems to interfere with diagnosing AMI by serial estimations of serum CPK during the next 24 hours.