Is it time to do away with the 99th percentile for cardiac troponin in the diagnosis of acute coronary syndrome and the assessment of cardiac risk?

The concept and use of the 99th percentile for interpretation of cardiac troponin was introduced with the redefinition of myocardial infarction in 2000, a time when few assays could detect cardiac troponin at the 99th percentile and none could meet the criteria of an assayCVof 10% at this concentration. There have been many reports of the 99th percentile providing useful information toward defining a population at high risk of future myocardial injury (1 ). However, as we increase our knowledge regarding cardiac troponin, it is apparent that the 99th percentile has limitations. Cardiac troponin may be released in response to minor noncardiac illness, and this can cause confusion. Further, with the new high-sensitivity (hs)6 assays becoming available, it is apparent that most healthy persons have low concentrations of cardiac troponin present in their blood. Thus we have to come to terms with the concept that cardiac troponin may be released by physiological mechanisms as well as pathological ones. As assay quality has improved, the use of cardiac troponin in a clinical setting has become more complex and confusing. We list below some of the ways in which 99th percentile has problems and how we may be better served by other criteria when using cardiac troponin for the assessment of individual patients.