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We appreciated the comments by Porto et al. concerning the different prognostic impact of the increases in creatine kinase MB (CK-MB) and troponin I (cTnI) emerging from our study. They suspect that a methodological problem associated with the calculation of the cTnI ratio may have conditioned our results. In line with the Joint Ad Hoc Committee of the European Society of Cardiology and American College of Cardiology for the Redefinition of Myocardial Infarction,1 we defined CK-MB and cTnI elevations as any post-procedural level above the upper reference limit (or an increase of >50% over baseline when the baseline level was already high2), a definition that does not mention the CK-MB or cTnI ratio. However, we did use the CK-MB and cTnI ratios to explore the relationship between the degree of marker elevation and the risk of death. In accordance with the available literature, we graded peak CK-MB or cTnI elevation on the basis of the ratio between the observed post-procedural peak value of the marker and its upper reference limit (or the baseline value, when high). Although we agree that calculating the peak ratio in the case of high baseline levels is arbitrary and may lead to an underestimate of the degree of elevation, we consider it a reasonable attempt to separate the amount of myocardial damage due to the interventional procedure per se from that attributed to pre-procedural myocardial necrosis. How to make a qualitative and quantitative biochemical assessment of an ongoing ischaemic insult superimposed on a recently damaged myocardium is still a matter of debate,1,3 and all of the proposed methodologies have some limitations. In this regard, even the absolute increase in marker values suggested by Porto et al. is susceptible to criticism as it does not take into account the potential spontaneous post-procedural increase in the marker during the early post-myocardial infarction phase; this is particularly true in the case of a marker such as troponin, which has a slow wash-out and a delayed peak. To eliminate the potential effect of high pre-procedural cardiac marker levels on the results of our study, we also performed a separate analysis after excluding the patients whose baseline marker levels were above the upper reference limit and obtained similar results. We would finally like to point out that increasing the troponin cut-off value to considerably above the 99th percentile of the distribution of a reference control group would probably have shown an association between cTnI elevation and a worse outcome;4 in this case, however, the post-procedural increase in cTnI would have been easily associated with a simultaneous increase in CK-MB, thus leaving the issue of the prognostic significance of the minor post-procedural myocardial damage, revealed by an isolated cTnI elevation, unaddressed. Our data now suggest that isolated cTnI elevations do not influence long-term mortality.

Issue Section:
Letters to the Editor
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