OBJECTIVES: It is often difficult to diagnose acute myocardial infarction (AMI) in patients who resuscitated after out-of-hospital cardiac arrest (OHCA) and had a delayed elevation in cardiac marker. This study explored whether elevations in cardiac marker were due to coronary artery occlusion or resulted from other causes. METHODS: The study included 19 non-ST-segment elevation patients who resuscitated after OHCA and underwent delayed coronary angiography. We checked patients' serial creatine kinase-myocardial band (CK-MB) and troponin I (cTnI) levels on arrival and 6, 12, 24, 48, 72, and 96 hours postarrest. Based on the association of elevated cTnI and the results of their delayed angiographies, the patients were retrospectively divided into 2 groups: an AMI group (n=5) and a non-AMI group (n=14). We then analyzed the serial cardiac marker measurements in each group. RESULTS: Peak marker levels were significantly higher in the AMI group than in the non-AMI group (CK-MB, 177.0±112.7 vs 66.4±85.2 ng/mL; P=.033 and cTnI, 40.4±14.5 vs 10.6±13.5 ng/mL; P=.005). After adjusting for covariates, the peak and 6-, 12-, and 24-hour cTnI and 6-hour CK-MB were significantly different between the 2 groups (P=.005, P=.004, P=.005, P=.020, and P=.007). In the non-AMI group, 3 patients had cTnI values that were within the reference range at all of the evaluated times. Most patients had only low cTnI elevations that rapidly fell back to normal. CONCLUSION: The resuscitation of patients who experience sudden OHCA but do not have an AMI may lead to elevations of cardiac markers. However, these elevations are low and normalize early.
OBJECTIVES: It is often difficult to diagnose acute myocardial infarction (AMI) in patients who resuscitated after out-of-hospital cardiac arrest (OHCA) and had a delayed elevation in cardiac marker. This study explored whether elevations in cardiac marker were due to coronary artery occlusion or resulted from other causes. METHODS: The study included 19 non-ST-segment elevation patients who resuscitated after OHCA and underwent delayed coronary angiography. We checked patients' serial creatine kinase-myocardial band (CK-MB) and troponin I (cTnI) levels on arrival and 6, 12, 24, 48, 72, and 96 hours postarrest. Based on the association of elevated cTnI and the results of their delayed angiographies, the patients were retrospectively divided into 2 groups: an AMI group (n=5) and a non-AMI group (n=14). We then analyzed the serial cardiac marker measurements in each group. RESULTS: Peak marker levels were significantly higher in the AMI group than in the non-AMI group (CK-MB, 177.0±112.7 vs 66.4±85.2 ng/mL; P=.033 and cTnI, 40.4±14.5 vs 10.6±13.5 ng/mL; P=.005). After adjusting for covariates, the peak and 6-, 12-, and 24-hour cTnI and 6-hour CK-MB were significantly different between the 2 groups (P=.005, P=.004, P=.005, P=.020, and P=.007). In the non-AMI group, 3 patients had cTnI values that were within the reference range at all of the evaluated times. Most patients had only low cTnI elevations that rapidly fell back to normal. CONCLUSION: The resuscitation of patients who experience sudden OHCA but do not have an AMI may lead to elevations of cardiac markers. However, these elevations are low and normalize early.
Authors: Alf Inge Larsen; Anders Morten Grejs; Simon Tilma Vistisen; Kristian Strand; Øyvind Skadberg; Anni Nørgaard Jeppesen; Christophe H V Duez; Hans Kirkegaard; Eldar Søreide Journal: BMC Cardiovasc Disord Date: 2022-07-30 Impact factor: 2.174
Authors: Reidun Aarsetøy; Hildegunn Aarsetøy; Tor-Arne Hagve; Heidi Strand; Harry Staines; Dennis W T Nilsen Journal: Front Cardiovasc Med Date: 2018-06-07