The third global MI task force has modified the cTn threshold levels for the diagnosis of PCI-related MI. A cTn level elevation >5 x 99th percentile URL within 48 hours of PCI (in Selleckchem Enzalutamide patients with normal baseline values) is now used to classify Type 4a MI.2 Moreover, the 2012 task force has also specified an increase in cTn levels of >20% to characterize PCI-related MI in patients with elevated but stable or falling baseline levels. It has also been recognized Inhibitors,research,lifescience,medical that up to 6% of patients with stable CAD have elevated pre-PCI cTn levels.8 The new cTn cutoff was arbitrarily defined and should be associated with one of the following for an event to be labeled as a PCI-related MI: (A) symptoms of

myocardial ischemia; (B) new ECG changes of

ischemia; (C) new loss of viable Inhibitors,research,lifescience,medical myocardium or new regional wall motion abnormality detected by imaging; or (D) angiographic findings consistent with a procedural complication. Using the 2007 definition (>3 x 99th percentile URL), ≥15% of patients undergoing PCI would be defined as having a PCI-related MI.9 The adoption of higher biomarker thresholds and more stringent criteria for revascularization-related MI resulted in widespread implications in the interventional cardiology community, especially with the increased performance of complex and aggressive multivessel coronary interventions.2,10 MI associated with stent thrombosis remains an important subcategory (type 4b) in the current Inhibitors,research,lifescience,medical classification of MI.2 Restenosis after PCI and coronary stenting is an important shortcoming of percutaneous revascularization and may be associated with MI in up to 10% of patients.11, 12 The significance of in-stent restenosis is emphasized in the third universal definition of MI by the incorporation of PCI-related MI associated with restenosis (type 4c Inhibitors,research,lifescience,medical MI).2 The new type Inhibitors,research,lifescience,medical 4c MI is defined by a rise and/or fall of cTn values in patients with ≥50% stenosis at coronary angiography (or a complex lesion) in the absence of more obstructive CAD following initially

successful PCI.2 MI related to coronary artery bypass surgery (CABG) was redefined by the 2012 ALOX15 task force using an arbitrarily defined cutoff of an elevation of cardiac biomarker >10 x 99th percentile URL during the first 48 hours following CABG. CABG-related MI should also satisfy one of the following additional diagnostic criteria: (1) new pathological Q waves or LBBB, or (2) angiographically documented new graft or native coronary artery occlusion, or (3) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality (except perhaps a paradoxical septal motion, which is a common finding after cardiac surgery). The 2012 global MI task force emphasized that the aforementioned threshold is more robust for isolated on-pump CABG. Cardiac biomarker release is, however, considerably higher after valve replacement with CABG than with CABG alone, and with on- versus off-pump CABG.