Perspective:

The following are 10 points to remember about this article:

1. The prognostic value of cardiac troponin (cTn) post-percutaneous coronary intervention (PCI) is controversial. In patients with non–ST-segment elevation acute coronary syndrome (NSTE ACS), it is especially difficult to distinguish between cTn elevations due to PCI or index myocardial infarction (MI).

2. A graphic-based methodology to review biomarkers trends over time allows identification of patients with NSTE ACS in whom a rise in post-PCI cardiac biomarkers can be distinguished from a rise in cardiac biomarkers due to the presenting MI.

3. Because of cTn’s sensitivity to detect small areas of necrosis, thresholds associated with a clinically relevant risk of adverse events need to be identified and incorporated into definitions of MI.

4. We need to define ‘clinically relevant’ risk for death or change in risk from baseline MI. After that, the thresholds for both spontaneous and PCI-related MI using either cTn or creatine kinase-myocardial band (CK-MB) can be determined relative to that benchmark, and then standardized.

5. The revised universal definition of MI indicates an identical threshold (>5× upper limit of normal [ULN]) for the diagnosis of peri-PCI MI for cTn and CK-MB, in addition to clinical and angiographic complications.

6. Because of different sensitivities and, consequently, different hazards of death associated with increased values of cTn and CK-MB, the threshold for cTn should be higher than the threshold for CK-MB, if equivalence in risk-per-unit-increase in level is desired.

7. An elevation of cTn >60× ULN carries an adjusted estimated risk of death similar to a >3× ULN CK-MB elevation, and an elevation of cTn >100× ULN carries an adjusted estimated risk of death similar to a >5× ULN CK-MB. This suggests that increase of cTn and CK-MB at those thresholds may indicate similar degrees of myocardial necrosis.

8. It appears that peak post-PCI cTn is significantly associated with 1-year mortality and adds prognostic value to cTn elevation associated with a presenting MI, with implications for both incorporating a cTn post-PCI MI definition and preventing PCI-related myonecrosis.

9. These results support the use of cTn, along with CK-MB, for the diagnosis of PCI-related MI, but they also indicate that thresholds for cTn and CK-MB will be different for similar risks of mortality.

10. The selection of a threshold for cTn-based diagnosis of PCI-related MI should consider both the sensitivity of the assay (thus, the amount of myonecrosis per unit increase) and an estimate of what defines clinically relevant increases in the rates of complications associated with myonecrosis, whether defined by cTn or CK-MB.