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Clinical Chemistry 47: 377-379, 2001;
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(Clinical Chemistry. 2001;47:377-379.)
© 2001 American Association for Clinical Chemistry, Inc.

Editorial

Myocardial Infarction Redefined: Role of Cardiac Troponin Testing

Fred S. Apple1,a and Alan H.B. Wu2

1 Department of Laboratory Medicine, and Pathology, University of Minnesota, School of Medicine, Minneapolis, MN 55415

2 Department of Pathology, Hartford Hospital, Hartford, CT 06102
a Address correspondence to this author at: Hennepin County Medical Center, Clinical Laboratories MC 812, 701 Park Ave., Minneapolis MN 55415. Fax 612-904-4229; e-mail fred.apple@co.hennepin.mn.us.

As we move into the new Millennium, "the times they are a changin" regarding the diagnostic criteria used to rule in and rule out acute myocardial infarction (AMI) (1). The purpose of this editorial is to comment on the new cardiology guidelines for the redefinition of AMI and unstable angina, as well as to compare them with previously published laboratory medicine recommendations. Some of the new recommendations made by clinical groups may appear to be in conflict with those published previously by laboratory medicine groups; thus, we document the chronology and evolution of all guidelines on the use of cardiac markers.

Consensus documents recently published by the European Society of Cardiology (ESC), the American College of Cardiology (ACC), and the American Heart Association (AHA) make specific recommendations on the use of biomarkers for the detection of myocardial infarction (MI) (2)(3)(4)(5). The redefined criteria used to classify acute coronary syndrome (ACS) patients presenting with ischemic symptoms as acute, evolving, or recent MI are heavily predicated on an increased serum/plasma cardiac troponin (I or T) concentration (2)(3)(4). Furthermore, in the new ACC/AHA guidelines for management of patients with unstable angina and non-ST-segment elevation MI (NSTEMI), an increased cardiac troponin value establishes the diagnosis of NSTEMI, whereas a normal cardiac troponin value establishes the diagnosis of unstable angina in ACS patients with ischemic discomfort (5).

The new guidelines emphasize the following clinical issues. First, increases of cardiac troponins are indicative of myocardial injury but are not synonymous with MI or an ischemic mechanism of injury. If an ischemic mechanism of injury is unlikely, other etiologies of myocardial injury should be pursued. Second, increases in cardiac troponin likely reflect irreversible rather than reversible injury, although there . . . [Full Text of this Article]


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