THIS issue of the Journal contains an important clinical study that describes the significance of a cardiac troponin I release in severe trauma patients.1The incidence of troponin release was 12% and the authors identified three different patterns of troponin release: 1) a very transient (≤12 h) and limited (<2 μg/l) release that is likely related to the hyperadrenergic state observed in hemorrhagic shock2or severe head trauma,32) a transient (≤36 h) and significant (≥2 μg/l) release, and 3) a sustained (>36 h) and significant (≥2 μg/l) release that was associated with coronary artery injury in 41% of the cases. Diagnosis of the lesions of the heart related to blunt trauma is difficult, mainly because of confusion about the term used and the absence of recognized standards.4Several conclusions can be drawn from the study from Edouard et al. 1First, as previously noted,5troponin is probably not the key diagnostic method for myocardial contusion because a troponin release can be attributable to several other causes in severe trauma patients and because no detectable troponin release may occur in small myocardial contusion. Myocardial contusion is an elusive diagnosis that should be replaced by the term “blunt cardiac trauma” only in the presence of pump failure or malignant cardiac arrhythmias.6Numerous clinical evidences suggest that repeated electrocardiogram remain appropriate to detect blunt cardiac trauma with malignant cardiac arrhythmias and that echocardiography is appropriate to detect blunt cardiac trauma with pump failure or pericardial lesions.4The study from Edouard et al. 1demonstrates that serial troponin dosages are appropriate to identify blunt cardiac trauma with coronary traumatic lesions. Two important issues remain a matter of debate. First, because coronary angiography was not performed in patients with significant but transient release, one cannot make a conclusion regarding the need for further invasive examination in this subpopulation. It should be pointed that the incidence was low (2%), meaning that this concerns few patients, and that occult coronary traumatic lesions may explain some late death attributed to blunt cardiac trauma.7Therefore, I suggest that coronary angiography be discussed in these cases until further studies have been conducted. Second, the absence of any prognosis value of troponin release in the study from Edouard et al. 1should be cautiously analyzed. Indeed, the power of their study was relatively low because of the small number of patients with a sustained and significant release. Moreover, mixing patients with significant and nonsignificant release of troponin, which reflects different pathophysiological processes, may not be appropriate. The study from Edouard et al. 1has markedly clarified the role of troponin dosage in severe trauma patients and even provides some insights on the different pathophysiological mechanisms involved in troponin release.
For more than a decade, troponin has been known as a highly sensitive and specific marker of myocardial damage mainly resulting from myocardial ischemia. There are few biologic markers that could be considered as sensitive and as specific as troponin. Therefore, it is amazing that such an efficient marker took such a long time to be incorporated into guidelines for the diagnosis of myocardial infarction.8Moreover, it is interesting to note that several very recent studies have markedly improved our knowledge concerning troponin release in the postoperative period, cardiac surgery,9and now severe trauma.1Troponin is now also recognized as an important prognosis marker in cardiac surgery,9in critically ill patients, and in acute pulmonary embolism.10The troponin story illustrates the long way necessary to precisely assess the diagnostic and prognostic values and the clinical significance of a new biologic marker in different clinical situations.
We must think well about the troponin story because many new biologic markers, such as natriuretic peptides and procalcitonin, are now available.11A wave of new biologic markers exploring central nervous system ischemia, sepsis, and the cardiovascular system is under the scrutiny of bioengineering companies. It is likely that we will see a biologic revolution as we have seen an imaging technique revolution during recent years. Assessing these markers is complex and difficult and will need considerable efforts, but it is worth it in perioperative and critical care, and emergency medicine. Do not underestimate the task and remember the troponin story, a highly sensitive and specific marker that means so different things in so many different clinical situations such as chest pain and severe trauma. An improvement in the methodology used to assess the interest of these biologic markers is also mandatory. Although considerable progress has been made in the methodology and report of randomized trials in the past decade, we are behind the times concerning the assessment of diagnostic tests. It is important to handle the appropriate methodological tools to face this biologic marker revolution.12