BACKGROUND: The serum concentration of cardiac enzymes may be influenced by mechanical and electrical trauma due to cardiopulmonary resuscitation (CPR) attempts. This could complicate the determination of whether an acute myocardial infarction (AMI) had occurred. In this study, only patients without any of the known confounding factors affecting cardiac enzyme release were included, and the specific time course and patterns of serum cardiac enzyme levels after resuscitation were evaluated. The purpose is to help clinicians distinguish between spontaneous myocardial damage and that induced by CPR. METHODS AND RESULTS: This prospective, observational study was performed in the emergency department on eight patients surviving cardiac arrest. They were selected for not having heart disease, chest trauma or septic shock; and not receiving defibrillation. The median (range) duration of return of spontaneous circulation (ROSC) was 13 min (5-30 min). Cardiac enzyme measurements were taken immediately after ROSC and every 6h thereafter. Although cardiac troponin I (cTnI) level reached as high as 62.6 ng/ml at 24 h in one patient, five of the eight (62.5%) patients had their cTnI level fall below the normal reference range (i.e. 2 ng/ml) by 30 h. The time to maximum and peak concentration of cTnI was 16.50+/-10.99 h and 16.85+/-21.50 ng/ml, respectively. Both MB creatine kinase (CKMB) and total creatine kinase (CK) levels were above their normal reference ranges. In addition, the CKMB/CK ratio exceeded 5% in all patients at any time point during this study. CONCLUSION: In this study, the influence of resuscitative procedures - defibrillation excluded - on the release of cardiac enzymes were examined. During 30 h after ROSC cTnI level exhibited a bell-shaped configuration, which is distinct from that after AMI; whereas the enzymatic activities of CKMB and CK, as well as CKMB/CK ratio, were constantly higher than normal. This chronological pattern of cardiac enzyme levels may help physicians differentiate primary cardiac disease from other aetiologies in out-of-hospital cardiac arrests.
BACKGROUND: The serum concentration of cardiac enzymes may be influenced by mechanical and electrical trauma due to cardiopulmonary resuscitation (CPR) attempts. This could complicate the determination of whether an acute myocardial infarction (AMI) had occurred. In this study, only patients without any of the known confounding factors affecting cardiac enzyme release were included, and the specific time course and patterns of serum cardiac enzyme levels after resuscitation were evaluated. The purpose is to help clinicians distinguish between spontaneous myocardial damage and that induced by CPR. METHODS AND RESULTS: This prospective, observational study was performed in the emergency department on eight patients surviving cardiac arrest. They were selected for not having heart disease, chest trauma or septic shock; and not receiving defibrillation. The median (range) duration of return of spontaneous circulation (ROSC) was 13 min (5-30 min). Cardiac enzyme measurements were taken immediately after ROSC and every 6h thereafter. Although cardiac troponin I (cTnI) level reached as high as 62.6 ng/ml at 24 h in one patient, five of the eight (62.5%) patients had their cTnI level fall below the normal reference range (i.e. 2 ng/ml) by 30 h. The time to maximum and peak concentration of cTnI was 16.50+/-10.99 h and 16.85+/-21.50 ng/ml, respectively. Both MB creatine kinase (CKMB) and total creatine kinase (CK) levels were above their normal reference ranges. In addition, the CKMB/CK ratio exceeded 5% in all patients at any time point during this study. CONCLUSION: In this study, the influence of resuscitative procedures - defibrillation excluded - on the release of cardiac enzymes were examined. During 30 h after ROSC cTnI level exhibited a bell-shaped configuration, which is distinct from that after AMI; whereas the enzymatic activities of CKMB and CK, as well as CKMB/CK ratio, were constantly higher than normal. This chronological pattern of cardiac enzyme levels may help physicians differentiate primary cardiac disease from other aetiologies in out-of-hospital cardiac arrests.
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