oa Editorial [Hot topic: Myocardial Damage: Not the Only Cause of Cardiac Troponin Release? (Guest Editor: Rob Shave)]

Following their introduction in the late 1980's cardiac troponins (cTn) have become a “cornerstone” within the diagnosis and management of acute coronary syndrome (ACS) [1]. Since the initial introduction of cTn assays many manufacturers have improved the sensitivity of their assays, which in turn has lead to a reduction in the recognized clinical cut-offs for ACS. The ongoing development of high sensitive assays in an attempt to further improve the analytical performance provides significant challenge within the clinical/laboratory setting. The first paper in this special edition by Gaze [2] provides insight into some of the issues associated with the assessment and interpretation of cTn data in relation to both currently available assays, and also future potential developments. Although cTn release has become synonymous with cardiac damage it is important to note that not all release of cTn is related to acute myocardial infarction (AMI). Indeed, a number of other secondary-ischemic and non-ischemic conditions have been identified that also result in cTn release, all of which are associated with poor patient prognosis [2]. Exercise, and specifically prolonged exercise is presently the only known stimulus for cTn release that does not appear to be related to poor outcome. In order to demonstrate and to characterize the various exercise stimuli that result in cTn release Williams et al. [3] and Nie et al. [4] present original data from two very different exercise studies. These studies show that exercise cTn release is not only restricted to highly trained endurance athletes following ultra-endurance exercise, but can also occur in adolescents completing moderate duration exercise. These data build on previous work demonstrating cTn release following as little as 30 minutes of exercise [5]. The fact that relatively short duration activity elicits a post-exercise release of cTn, coupled with the manufacturers' drive to increase assay sensitivity means that there is increasing potential for a significant elevation in the false-positive diagnosis of ACS. The risk of falsepositives is increased further as it is well known that exercise is a potent trigger for ACS [6], accordingly a real threat exists for clinical confusion if hospital admission is preceded by strenuous exercise [7]. Using a case-study approach in the last paper of this special edition, Eijsvogels et al. [8] highlight a number of real-life situations that may result in clinical dilemma and offer practical advice on how patients presenting with elevations in cTn following a bout of exercise may be clinically managed.