In developing a critical pathway for emergency-department management of low-risk patients with chest pain to improve quality and efficiency of care, Nichol and colleagues [1] used a single normal creatine kinase-MB level (obtained at least 4 hours after the onset of pain) to complement clinical observations. Other markers for myocardial injury, such as troponin T and troponin I, were not used in the pathway because their role was considered unclear or because no controlled trials had shown the effects of their use on clinical outcomes.

Only a few days after this paper was published, a prospective study reported on how clinical decision making for patients with acute chest pain that had lasted less than 12 hours and no ST-segment elevation may be facilitated and improved [2]. In this study of 773 consecutive patients, troponin T and troponin I status (positive or negative) was determined at least twice (on arrival and 4 or more hours later so that one sample was taken at least 6 hours after the onset of pain) by sensitive, qualitative, rapid bedside tests based on the use of monoclonal antibodies. Troponin T and troponin I were strong, independent predictors of cardiac events. The risk for major cardiac events (nonfatal myocardial infarction or death) during the 30-day follow-up period was 1.1% in patients with negative troponin T results and 0.3% in those with negative troponin I results. The authors concluded that in addition to being highly sensitive for the early detection of myocardial-cell injury, negative bedside test results for such markers are associated with low risk and allow safe early discharge of patients with acute chest pain [2].

Serial measurements of creatine kinase and its MB isoenzyme have been shown to have limited prognostic power; many patients are unnecessarily hospitalized [3]. Measurements of the cardiac-specific troponins are superior to measurement of creatine kinase-MB for the detection of minor myocardial injury and are valid predictors of adverse events in patients with acute coronary syndromes, as revealed in studies reported after Nichol and associates' MEDLINE search period [4, 5]. I believe that Nichol and colleagues' study would have been notably improved by using single troponin T and troponin I results in their critical pathway; this would have led to more accurate reduced numbers of admissions and days of hospitalization than those suggested by using creatine kinase-MB only.