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In recent years the use of troponin testing to monitor myocardial damage has become more pervasive and prominent, replacing the old style CK-MB measurement. Troponin elevation is a marker of cardiac injury and high risk, it is also raised in a minority of acute coronary syndrome patients. However, it is important for clinicians to realise that a single rise in troponin levels is of indeterminable significance. An appropriate series of tests over time, fitting in with the right clinical picture, is of most value.
The troponin complex in striated muscle fibres has three distinct subtypes and c-troponin-I is believed to be the one present only in cardiac muscle. Consequently, c-troponin-I is released when there is an assault to the myocardium and this is what laboratory testing picks up (some laboratories may measure the troponin-T subunit; this, however, has been found to be less specific and less sensitive). Interpretation of results can be confusing and there are several caveats to be aware of. A positive c-troponin-I level means that cardiac muscle contents have leaked out of cells. The primary reason why this occurs is in response to injury. There are multiple causes of cardiac muscle injury that includes acute coronary events, but there is also a whole spectrum of disorders that can cause a rise in troponin. The largest study of this subject1 showed that all of the following were associated with raised c-troponin-I levels. Pulmonary embolism,2 congestive cardiac failure, cardiomyopathy, myocarditis, rhabdomyolosis, chest contusions, sepsis, mural thrombi, prosthetic heart valves, neoplasms, radiation induced coronary stenosis, homocystinuria, systemic lupus erythematosus, and rheumatoid arthritis. Surprisingly, high troponin levels have also been found in cocaine abusers and marathon runners.
Some of these are obviously significant while others merely represent a normal response to a physiological event; c-troponin-I can therefore be distinctly raised in many “non-cardiac” disorders. The rise is evidence of cardiac damage per se and the relative importance of this should be determined by the state of the patient.
The troponin test is a valuable and sensitive one but always needs to be assessed in the cold light of the clinical scenario as its specificity to acute coronary syndromes can be questionable, especially on a one-off basis.3 Perhaps the advancement of this ultimate biochemical test leads us round in full circle when we attempt to clarify its rise. That is, to a thorough clinical history taking.