Can Changes in Troponin Results Be Useful in Diagnosing Myocardial Infarction?

In 1979, the WHO defined 3 specific criteria for use in the diagnosis of myocardial infarction (MI)1 : (a) clinical symptoms typical for ischemic heart disease, (b) specific electrocardiogram changes, and (c) a typical change in serial measurements of cardiac enzymes (1). Later definitions have continued in the mold of listing specific criteria, and in the current definition of MI, a characteristic increase and/or decrease in a cardiac biomarker with at least 1 result >99 percentile of a healthy population and evidence of myocardial ischemia (either specific symptoms or electrocardiographic or ultrasound findings) are mandatory (2). During the last decade, troponin T or I molecules, which are found only in myocardial cells and released after cell necrosis, have been the preferred cardiac biomarkers because of their high sensitivity and specificity (3), although myocardial cell necrosis can be seen in conditions other than myocardial ischemia (renal failure, sepsis, treatment with cardiotoxic drugs, myocarditis, and so on). A common problem in clinical practice is how to diagnose an acute MI in a patient who already has increased troponin concentrations. The National Academy of Clinical Biochemistry has suggested that a 20% increase in troponin results can be used to diagnose an ischemic event. This recommendation is based on analytical variation for troponin analysis alone, without taking biological variation into account (4).