in the present issue of critical care , king and colleagues have examined the role of troponin as an outcome predictor . the troponins , troponin t and troponin i , are part of the contractile apparatus of all striated muscles . voltage changes across the sarcolemmal membrane alter the intracellular calcium concentrations that act as the coupling mechanism to alter the conformation of the troponin  tropomyosin complex . this complex acts as a molecular switch to regulate muscle contraction and relaxation via activation or inhibition of the actinomyosin atpase . there are tissue - specific isoforms of both troponin t and troponin i in cardiac muscle : cardiac troponin t ( ctnt ) and cardiac troponin i ( ctni ) . this has produced a paradigm shift in the ability of the diagnostic laboratory to diagnose myocardial infarction . a series of landmark studies established that the measurement of ctnt and ctni was superior to the existing methods of biochemical detection of myocardial infarction , the measurement of creatine kinase and its mb isoenzyme ( creatine kinase - mb ) . initial studies showed that ctnt and ctni measurements identified a high - risk group in patients where creatine kinase - mb   or creatine kinase   measurement excluded myocardial infarction . subsequently , ctnt and ctni measurements on admission were shown to identify high - risk groups   even in patients with st - elevation myocardial infarction . the ability of ctnt and ctni measurements to diagnose myocardial infarction , to predict prognosis and to guide management in patients admitted with acute coronary syndromes ( acs ) is now well documented . measurement of ctnt and ctni is now included in the current guidelines for diagnosis   and management   of acs and myocardial infarction , and other biomarkers are no longer recommended . this is not the case . in situations where there is skeletal muscle damage , creatine kinase and creatine kinase - mb the sensitivity and specificity of ctnt and ctni measurements have demonstrated that elevations of both can be documented in a large range of non - acs populations , including patients in intensive care . in such cases , the mechanism of troponin elevation this has been demonstrated not to be the case , and it is recognised that non - acs troponin elevations are both true reflections of myocardial damage and associated with an adverse prognosis . non - acs elevations of cardiac troponin may occur on a background of ischaemic heart disease ( secondary ischaemic cardiac injury ) or as non - ischaemic cardiac injury , although both situations may coexist . it is possible that this might be previously unrecognised microinfarction . in cocaine - induced cardiac damage , magnetic resonance imaging demonstrates diffuse myocardial damage associated with troponin elevation but no specific coronary artery occlusion . it has also been suggested that under conditions of myocardial stress there may be ischaemia with intracellular degradation of troponin and release of troponin fragments . whatever the mechanism , the elevation of cardiac troponins in intensive care patients was described early ; this finding has been replicated subsequently , including by this study . all studies are consistent in acknowledging the fact that elevation of cardiac troponin carries prognostic significance . the disagreement within the literature concerns whether the troponin elevation is an independent risk predictor or whether it is an organ system failure marker . if the latter , it would be expected to be a dependant variable within an organ system failure score , and therefore a univariate predictor rather than a multivariate predictor . there are published data to support both arguments , as the authors point out . in a study of septic patients who had troponin measurements and ventricular function assessment by trans - oesophageal echocardiography , although mortality was predicted by ctnt and ctni elevation , multivariate analysis showed that the major predictor of troponin elevation was left ventricular dysfunction , consistent with previous reports . it is therefore probable that , for a given population , cardiac troponin as the dominant predictor will be dictated by whether or not ventricular dysfunction is the major contributor to mortality . given the different population mixes in different intensive care units , it will be expected that different conclusions will be drawn from different studies . the search for a single biomarker that will be the holy grail for prognosis on admission is seductive . differences in demographics and case mix across different intensive care units , as well as a lack of standardisation of ctni methods , make it probable that this particular search for a holy grail will be similarly inconclusive  occasional glimpses of the truth but no certainty . acs = acute coronary syndromes ; ctni = cardiac troponin i ; ctnt = cardiac troponin t.
the cardiac troponins are integral components of the myofibrillary apparatus and they regulate muscle contraction . the measurement of cardiac troponins has replaced other biomarkers for the specific detection of myocardial necrosis and for the diagnosis of myocardial infarction . 
 the tissue specificity plus sensitivity of the measurement technology has meant that cardiac damage can be detected in circumstances other than conventional acute coronary syndromes . 
 the ability to specifically detect cardiac damage as part of multiple organ failure in intensive care patients has been shown to provide prognostic information , but it is unclear whether this is a dependent or an independent marker of outcome .