Cardiac troponin in the general adult critical care unit: solution or problem

Abstract

Cardiac troponin T (cTnT) and troponin I (cTnI) are the most sensitive and specific biochemical markers of myocardial injury available, but do not indicate the mechanism of such injury [1]. There are many problems with their interpretation in the critical care setting. A recent editorial has highlighted that frequent determination of troponin in the ICU patient can lead to 'troponinitis'! [2]. The editorial quotes various studies, including those showing association between elevated cTnI levels and mortality. After analysis of 346 samples measured over 22 months from our general adult ICU (annual admissions 850), we also found a statistical relationship between levels of elevated cTnI and both ICU and hospital mortality (Table ​(Table1)1) using chi-square testing. However, we have not found this to be clinically significant. A hospital mortality of 51.2% may be high, but not so high as to precipitate the withdrawal of intensive care treatment. Table 1 Due to the low specificity and positive predictive value of cTnI in mixed adult general critical care patients, it is difficult for us as intensivists to place elevated troponin levels in their clinical context. We also have difficulty in using elevated troponin levels to influence patient management in the absence of a classical history and ECG changes. Thrombolysis, ACE-inhibitors and β-blockers can be doubled-edged swords in the critically ill; echocardiography in the resting patient provides scant meaningful information; a pulmonary artery catheter is invasive – and all this before we consider the risks associated with coronary angiography. We therefore believe that cardiac troponins in a mixed adult ICU should only be requested when it could confirm an acute coronary syndrome. In the ICU setting, this would almost always entail obtaining new ECG changes before requesting a cTnI level.