© 2004 BMJ Publishing Group Ltd & Association of Clinical Pathologists
EDITORIAL
EDITORIAL
Cardiac troponins
University Hospital Lewisham, Lewisham High Street. London SE13 6LH, UK
Correspondence to:
Correspondence to:
Dr S Sharma
Consultant Cardiologist, University Hospital Lewisham, Lewisham High Street, London SE13 6LH, UK; ssharma21@hotmail.com
Benefits and pitfalls for diagnosing myocardial infarction
Keywords: cardiac troponins; myocardial infarction; ischaemic heart disease; diagnosis
| The first 150 words of the full text of this article appear below. |
The diagnosis of myocardial infarction has conventionally relied on the presence of chest pain or typical ST segment and T wave abnormalities on the 12 lead electrocardiogram (ECG) and a rise in the serum concentrations of cardiac muscle enzymes. Whereas most patients with ST segment elevation also invariably have high serum cardiac muscle enzyme values, indicating myocardial damage, a considerable proportion of patients with less specific ST segment changes may not have increased cardiac muscle enzymes, and in the past have been diagnosed as having either stable angina or non-cardiac chest pain. Cardiac troponin T (cTnT) and troponin I (cTnI) are cardiac regulatory proteins that control the calcium mediated interaction between actin and myosin. The cardiac forms of these regulatory proteins are coded by specific genes and theoretically have the potential of being unique to the myocardium. Indeed, cTnI has not been identified outside the myocardium.1 Cardiac troponin T
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