Time course of creatine kinase release after termination of sustained ventricular dysrhythmias

doi:10.1016/0002-8703(91)90515-J

American Heart Journal

Volume 122, Issue 3, Part 1, September 1991, Pages 709-714

https://doi.org/10.1016/0002-8703(91)90515-J Get rights and content

Abstract

Differentiation between primary and secondary (caused by acute myocardial infarction) ventricular fibrillation has important therapeutic and prognostic implications. The diagnosis of myocardial infarction is based on clinical, ECG, and creatine kinase MB isoenzyme (MBCK) activity. Enzymatic criteria might not be able to confirm the diagnosis of myocardial infarction after recent cardioversion. The routine use of electrophysiologic studies involving the induction and termination of ventricular dysrhythmias provides a setting in which enzyme release as a result of cardioversion alone can be examined. Therefore a systematic investigation of the magnitude and time course of creatine kinase (CK) and MBCK release was performed after termination of ventricular dysrhythmias in 57 patlents undergoing electrophysiologic studies. Of patients requiring external cardioversion, only 50% had an elevation in CK and MBCK activity. Elevation when present correlated with the number of shocks and cumulative energy delivered. The magnitude of MBCK release exceeded 10% of the total CK activity in 9% of observations. Pace-termination of ventricular tachycardia did not result in enzyme release. Arrhythmia characteriatics, coronary artery disease, and left ventricular function did not affect the magnitude of the time course of enzyme release. These data suggest that cardioversion with multipile shocks may result in a component of MBCK release, and thus a false positive diagnosis of primary acute myocardial infarction may be made by relying exclusively on the enzyme release pattern.

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Cited by (15)

Cardiac troponin T and cardiac enzymes after external transthoracic cardioversion of ventricular arrhythmias in patients with coronary artery disease
2002, Chest
Citation Excerpt :
Therefore, total CK and CK-MB activity has the potential to produce false-positive results in defibrillated patients. O’Neil et al13 investigated the plasma total CK and CK-MB activity after DC shock for ventricular arrhythmias induced during electrophysiologic testing. Despite the fact that they studied the same group of patients as we did, they reported 50% elevation rate of CK and CK-MB activity after ECV.
Serum levels of cardiac troponins after external cardioversion (ECV) for atrial fibrillation and atrial flutter are widely investigated, and no increases in cardiac troponin T (cTnT) levels have been reported. However, the effect of ECV on cardiac enzyme release may depend on the type of arrhythmias. Furthermore, ventricular tachycardia (VT) or ventricular fibrillation (VF) could cause release of cardiac enzymes after ECV due to underlying myocardial ischemia, myocardial dysfunction, or more pronounced hemodynamic deterioration during arrhythmia.
The purpose of this study was to determine whether direct current (DC) shock may increase cardiac enzyme levels in patients with coronary artery disease undergoing ECV for VT or VF, so that diagnosis of acute myocardial infarction, which initially presents with VT or VF, can be excluded.
We obtained measurement of cTnT, total creatine kinase (CK), and CK MB isoenzyme (CK-MB) activity before and after ECV in 27 patients (mean ± SD age, 62 ± 13 years) with induced VT or VF (22 patients) who required ECV during provocative electrophysiologic testing and who underwent ECV due to VT (5 patients) in the cardiology department. Blood samples were drawn before, and 4 h, 8 h, and 24 h after ECV. The total energy used was 630 ± 375 J (range, 200 to 1,280 J). CK levels rose to the upper limit of reference range in seven patients (26%), and CK-MB activity was higher than the normal reference range in five patients (19%) after ECV. In contrast, cTnT concentrations remained within the normal range (< 0.1 μg/L) in all patients. Peak CK and CK-MB activity levels strongly correlated with the total energy delivered.
Elevation of cTnT level after an urgent DC shock strongly indicates the diagnosis of acute myocardial infarction presented with life-threatening arrhythmias, rather than myocardial damage caused by ECV.
Cardiac enzyme elevations after cardiac surgery: The cardiologist's perspective
2001, American Heart Journal
Evaluation of myocardial injury following repeated internal atrial shocks by monitoring serum cardiac troponin I levels
2000, Chest
Citation Excerpt :
CV of AF by DC shocks traditionally has been performed by the transthoracic technique, and controversial data have been reported on possible myocardial damage related to the procedure.1314151733 Increased amounts of CK-MB activity and CK-MB mass were found after transthoracic CV in 9.3 to 50% of patients16173435 and were related to muscular lesions induced by DC shock. The negativity of cTnI in patients with elevations of CK-MB supported this interpretation.17
Electrical shocks delivered for atrial cardioversion (CV) may cause myocardial damage. The aim of this study was to assess the extent of myocardial injury caused by repeated intracardiac shocks delivered for low-energy internal atrial CV.
Thirty-five patients with chronic persistent atrial fibrillation (AF) of different etiologies underwent CV with delivery of synchronized biphasic shocks (3.0/3.0 ms) between two catheters positioned in the right atrium and the coronary sinus. Shocks were delivered according to a step-up protocol (50 V, 180 V, then steps of 40 to 56 V up to 500 V, if necessary). In 23 patients, AF was reinduced after baseline CV, and CV was repeated. Myocardial injury was monitored by measuring cardiac troponin I (cTnI) serum concentrations in blood samples taken at baseline and at 2, 4, 8, 12, and 24 h after the procedure, by means of an immunoenzymologic assay (normal values, ≤ 0.6 ng/mL). A mean (± SD) of 6.9 ± 3.4 shocks per patient were delivered (range, 2 to 17). Shocks delivered in each patient had a maximal energy of 7.3 ± 4.0 J (range, 1.7 to 15.7). In 20 patients (57%), no evidence of myocardial injury (cTnI level, ≤ 0.6 ng/mL) was found. In 13 patients (37%), mildly elevated cTnI levels (range, 0.7 to 1.4 ng/mL) in samples taken 4 to 12 h after CV suggested minor myocardial injury. In two patients (6%), higher cTnI levels were found in samples taken 4 to 8 h after CV (peak, 1.7 and 2.4 ng/mL), indicating a necrotic damage. Patients with no cTnI elevation, with mild cTnI elevation, or with cTnI levels≥ 1.5 ng/mL did not differ significantly with respect to the total number of shocks delivered, the mean amount of energy delivered, and the cumulative amount of energy delivered. No clinical complications were observed.
Following internal CV with the delivery of repeated shocks, minor elevations of cTnI serum levels could be detected in a significant proportion of patients, and this suggests subtle asymptomatic minor myocardial injury. The elevations of cTnI levels do not appear to be related to the number of shocks or to the amount of energy delivered.
The influence of chest compressions and external defibrillation on the release of creatine kinase-MB and cardiac troponin T in patients resuscitated from out-of-hospital cardiac arrest
1998, Resuscitation
Objectives: This study sought to determine the influence of resuscitative procedures, such as chest compressions and external defibrillation, on the release of creatine kinase (CK)-MB and cardiac troponin T (cTnT). Methods: In 87 patients with out-of-hospital cardiac arrest and successful cardiopulmonary resuscitation (CPR), the initial ECG rhythm, the duration of cardiac arrest and CPR, and the number of defibrillations were assessed on arrival in the hospital. The serum CK-MB and cTnT were measured 12 h after the event. We also assessed whether the patient developed cardiogenic shock within 12 h, and if the patient had acute myocardial infarction (AMI), which was confirmed or eliminated by of typical ECG findings, thallium-201 myocardial scintigraphy, or autopsy within the hospital stay. A backward stepwise linear regression model was applied to assess the association between the markers of myocardial injury (CK-MB and cTnT) and the above clinical variables. Results: CK-MB concentrations were independently associated with the presence of AMI [B 68.5 (SE 28.5, P=0.018)], the duration of CPR (as a measure of trauma to the chest by means of chest compressions) [B 2.07 (SE 1.01, P=0.045)] and cardiogenic shock [B 52.3 (SE 23.4, P=0.03)]. The remaining clinical variables listed were excluded by the model. Cardiac troponin T concentrations were only associated with the presence of AMI [B 4.86 (SE 1.34, P=0.0005)]. There was a non-significant association between increasing serum cTnT concentrations and the presence of cardiogenic shock [B 2.51 (SE 1.46, P=0.09)]. The remaining clinical variables were excluded by the model. Conclusion: The release of CK-MB appears to be influenced by the duration of resuscitation and the presence of cardiogenic shock. This has to be considered when interpreting serum CK-MB concentrations after CPR. The release of cTnT seems to be only associated with acute myocardial infarction, but not with the duration of chest compressions, or with the number of defibrillations administered.
Predisposing factors and prognostic value of sustained monomorphic ventricular tachycardia in the early phase of acute myocardial infarction
1997, Journal of the American College of Cardiology
The purpose of the study was to analyze the factors that favor the occurrence of sustained monomorphic ventricular tachycardia in the early phase (<48 h) of acute myocardial infarction and to establish its prognostic implications.
Sustained monomorphic ventricular tachycardia early in the course of an acute myocardial infarction is an uncommon arrhythmia, and its significance has not been specifically studied.
The clinical characteristics and prognosis of sustained monomorphic ventricular tachycardia were studied in 21 (1.9%) of 1,120 consecutive patients admitted to the coronary care unit with a diagnosis of myocardial infarction.
Patients with sustained monomorphic ventricular tachycardia had a larger infarct on the basis of peak creatine kinase, MB fraction (CK-MB) isoenzyme activity (435 ± 253 IU/liter vs. 168 ± 145 IU/liter, p < 0.001) and higher mortality rate (43% vs. 11%, p < 0.001). By logistic regression analysis, independent predictors of sustained monomorphic ventricular tachycardia were CK-MB (odds ratio [OR] 11.8), Killip class (OR 4.0) and bifascicular bundle branch block (OR 3.1). Moreover, sustained monomorphic ventricular tachycardia was itself an independent predictor of mortality (OR 5.0). Compared with patients with ventricular fibrillation, those with sustained mono-morphic ventricular tachycardia had a worse Killip class (Killip class > I: 63% vs. 30%, p < 0.05), higher CK-MB activity (430 ± 260 IU/liter vs. 242 ± 176 IU/liter, p < 0.01) and higher arrhythmia recurrence rate (31% vs. 4%, p < 0.01). During the follow-up period, 5 (42%) of 12 survivors in the sustained monomorphic ventricular tachycardia group died of cardiac-related causes. Recurrence of ventricular tachycardia was seen in two patients (17%).
Sustained monomorphic ventricular tachycardia during the first 48 h of myocardial infarction is a sign of extensive myocardial damage and an independent predictor of in-hospital mortality.
Cardiac troponin I does not increase after cardioversion
1997, Chest
Serum total creatine kinase (total CK) level increases in the patients following electrical cardioversion. The same has been observed with CK-MB, an isoenzyme of the total CK with some cardiospecificity. Cardiac troponin I (cTnI), a new specific cardiac biological marker, is highly effective to discriminate myocardial and muscular injuries after noncardiac surgery.
To assess cardiac damage after cardioversion, we measured serum cTnl, myoglobin, total CK, CK-MB mass, 1, 2, 3, 4, 8, 12, and 24 h after elective cardioversion of supraventricular tachycardia in 28 patients (eight women, 20 men; mean age, 64±10 years). Cumulative energy was below 370 J in 17 patients, between 370 and 900 J in eight patients, and 1,020 J in three patients. Serum cTnI was measured using a sandwich immunoenzymologic assay. The detection limit of the assay was 0.35 µg/L and normal values range from 0.35 to 1.3 µg/L.
In all but three patients, cTnI remained below 0.35 µg/L. In these three patients, cTnI ranged between 0.35 and 0.9 µg/L. There was no correlation between cTnI and the number or the energy of cardioversion. Myoglobin and total CK increased to abnormal concentrations in 11 patients (myoglobin, 630±190 µg/L, and total CK, 2,584±780 U/L) and reached myocardial infarction-like values in five patients. Modest increases of CK-MB were then also observed. A strong correlation was observed between the total energy of direct current cardioversion and the increase of either myoglobin (r=0.87; p<001) or total CK (r=0.81; p<001).
Cardioversion in a clinical setting does not induce elevation of cTnI. Increase in total CK, CK-MB, and myoglobin may be due solely to muscular lesions and is closely related to the cumulative energy delivered.

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^☆: Supported in part by grant HL-36277 from the National Heart, Lung, and Blood Institute and by grant 87G-175 from the American Heart Association; computational assistance was provided by the CLINFO project funded by the Division of Research Resources of the National Institutes of Health under grant RR-00350.

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Time course of creatine kinase release after termination of sustained ventricular dysrhythmias☆

Abstract

Am J Cardiol

Am J Cardiol

J Thorac Cardiovasc Surg

J Am Coll Cardiol

J Biol Chem

Am Heart J

Am J Cardiol

Am J Cardiol

Am J Cardiol

Serum enzyme assays in the diagnosis of acute myocardial infarction

Ann Intern Med

Estimation of acute myocardial infarct size in man by serum CKMB measurements

Circulation