Troponin T as a marker for myocardial ischemia in patients undergoing major noncardiac surgery

Thomas H. Lee, Eric J. Thomas, Lynn E. Ludwig, David B. Sacks, Paula A. Johnson, Magruder C. Donaldson, E. Francis Cook, Alex Pedan, Karen M. Kuntz, Lee Goldman

Research output: Contribution to journalArticlepeer-review

104 Scopus citations

Abstract

To assess the diagnostic performance of cardiac troponin T as a marker for myocardial injury in patients undergoing major noncardiac surgery, we prospectively collected preoperative and postoperative clinical data, including measurements for creatine kinase (CK), CK-MB, and troponin T for 1,175 patients undergoing major noncardiac surgery. Acute myocardial infarction was diagnosed in 17 patients (1.4%) by a reviewer who was blinded to troponin T data and who used CK-MB and electrocardiographic criteria to define acute myocardial infarction. Other predischarge major cardiac complications were detected for another 17 patients. Troponin T elevations (>0.1 ng/ml) occurred in 87% of patients with and in 16% of patients without myocardial infarction. Among patients without myocardial infarction, troponin T was elevated in 62% of patients with and in 15% of patients without major cardiac complications. Receiver-operating characteristic analysis indicated that troponin T had a performance for the diagnosis of acute myocardial infarction similar to CK-MB, and a significantly better correlation with other major cardiac complications in patients without definitive infarction. Future research should seek to determine the significance of troponin T elevations in patients without complications.

Original languageEnglish (US)
Pages (from-to)1031-1036
Number of pages6
JournalAmerican Journal of Cardiology
Volume77
Issue number12
DOIs
StatePublished - May 15 1996

Bibliographical note

Funding Information:
From the Section for Clinical Epidemiology, the Division of General Medicine and the Cardiovascular Division, the Departments of Medicine, Pathology, and Surgery, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts. This study was supported by a rant from the Boerhinger Mannheim Corporation, Indi-anapolrs, In cl fana. Manuscrrpt received September 20, 1995; revised manuscript received and accepted December 14, 1995 Address for reprints: Thomas H. lee, MD, Brigham and Women’s Hospital, 75 Francis Street, Boston, Massachusetts 02 1 15.

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