This commentary refers to ‘Procedural myocardial injury, infarction and mortality in patients undergoing elective PCI: a pooled analysis of patient-level data’, by J. Silvain et al., https://doi.org/10.1093/eurheartj/ehaa885 and the discussion piece ‘Appropriate criteria for the definition of Type 4a MI’, by J. Silvain et al., https://doi.org/10.1093/eurheartj/ehab808.
We have read the paper from Silvain et al.,1 recently published in the European Heart Journal, with interest. We congratulate the authors in their success to further clarify the relation between cardiac troponin (cTn) release after elective percutaneous coronary intervention (PCI) and outcome. The authors observed that procedural myocardial injury independently predicted 1-year all-cause mortality with a prognostic threshold at cTn levels ≥3 × 99th percentile. This level is well above the commonly used cTn cut-off to define spontaneous myocardial infarction (MI)2 but below the ≥5 × 99th percentile cut-off incorporated in the definition of procedural MI, i.e. Type 4a MI.2,3
The data presented by Silvain et al. raise the question whether a cTn cut-off lower than ≥5 × 99th percentile might be equally prognostic in patients fulfilling non-cTn criteria for Type 4a MI, i.e. clinical or electrocardiographic signs of myocardial ischaemia, imaging evidence of loss of viable myocardium or procedural disruption of coronary blood flow. A spline chart similar to the Take home figure in the original publication1 would be helpful. We are aware that such an analysis may be hampered by smaller patient numbers with available clinical information in the dataset. However, extrapolating the data reported for procedural myocardial injury, at least 1000 patients would have been labelled Type 4a MI if using cTn ≥1 × 99th percentile as cut-off. Proof of prognostic significance of such smaller cTn release magnitudes will have important implications on the management of patients sustaining clinically relevant myocardial ischaemia during elective PCI.
Conflict of interest: none declared.
Contributor Information
Kai M Eggers, Department of Medical Sciences, Uppsala Clinical Research Center, Uppsala University, Uppsala 751 85, Sweden.
Stefan K James, Department of Medical Sciences, Uppsala Clinical Research Center, Uppsala University, Uppsala 751 85, Sweden.
Bertil Lindahl, Department of Medical Sciences, Uppsala Clinical Research Center, Uppsala University, Uppsala 751 85, Sweden.
References
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