BJA Advance Access originally published online on January 16, 2006
British Journal of Anaesthesia 2006 96(3):303-309; doi:10.1093/bja/aei317
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CARDIOVASCULAR |
Relationship between perioperative troponin elevation and other indicators of myocardial injury in vascular surgery patients
1 Academic Unit of Anaesthesia, Leeds General Infirmary, Leeds LS1 3EX, UK. 2 University Department of Anaesthesia, Critical Care and Pain Management, Leicester Royal Infirmary, Leicester, UK. 3 Department of Anaesthesia, Critical Care and Pain Medicine, Royal Infirmary of Edinburgh, Edinburgh, UK. 4 Freeman Hospital, Newcastle-upon-Tyne, UK. 5 Northern General Hospital, Sheffield, UK. 6 Torbay Hospital, Torquay, UK. 7 Division of Cardiac, Anaesthetic and Radiological Sciences and 8 Bristol Royal Infirmary, Bristol, UK
*Corresponding author. E-mail: s.howell{at}leeds.ac.uk
Background. In 2000 the European Society of Cardiology and the American College of Cardiology published a consensus document revising the definition of myocardial infarction. The usefulness of this revised definition has been challenged. It has been suggested that, rather than any release of cardiac troponin being potentially diagnostic of myocardial infarction, a diagnostic threshold consistent with significant myocardial injury should be defined.
Methods. We studied 65 patients undergoing elective major vascular surgery to examine the relationship between the magnitude of cardiac troponin I (cTnI) and creatine kinase MB fraction (CK-MB) release and clinical signs or symptoms of myocardial injury. cTnI and CK-MB concentrations were measured preoperatively and on the first 4 postoperative days using the ACCESS® assay (Beckmann). Patients were considered to have suffered a perioperative myocardial infarction if they had either symptoms or ECG changes consistent with this diagnosis, together with cTnI release.
Results. Peak postoperative cTnI concentrations above the lower detection limit of the ACCESS® assay (0.06 µg litre–1) occurred in 26 patients. Eight of these patients displayed symptoms or ECG changes consistent with myocardial injury. A cTnI level greater than 0.68 µg litre–1 was found to be consistent with the clinical diagnosis of myocardial infarction. The optimal cut-off for the diagnosis of MI using CK-MB was 40.4 µg litre–1.
Conclusions. These data suggest that further studies are required to define the optimal cardiac troponin diagnostic threshold for the diagnosis of myocardial infarction in the non-cardiac surgery population.
Vascular Anaesthesia Society of Great Britain and Ireland.
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