Serum biomarker evidence of myocyte necrosis is frequently found after percutaneous coronary intervention (PCI). About 20% of patients develop elevated levels of creatine kinasemyocardial band (CK-MB) (1,2) and up to 48% of patients develop elevated troponin levels following PCI (2-9). Several mechanisms related to procedural complications such as side branch occlusion, dissection, and disruption of collateral flow have been proposed for these elevations. The concept of plaque embolization at the time of balloon inflation or stent deployment leading to myocardial necrosis and scar formation has been supported by observations with magnetic resonance imaging (MRI) and late gadolinium enhancement (LGE) "scar" imaging after PCI (10). These data show an association between post-PCI elevations of troponin I with MRIdetectable scar formation.
See page 950Following stenting, LGE may occur at the site of stent deployment and distally in the treated coronary artery (11). Intravascular ultrasound has shown a correlation between changes in plaque volume before and after PCI and the mass of distal hyperenhancement, but not with hyperenhancement at the site of stenting. Thus providing indirect evidence that plaque embolization has occurred. Furthermore, post-PCI elevation of troponin I levels have been shown to be related to abnormal tissue perfusion (12) independent of the presence of thrombus, epicardial flow, or characteristics of the coronary artery stenosis undergoing PCI. Elevated biomarker levels are also associated with higher atheromatous plaque burden (13).The universal definition of myocardial infarction (MI) designates biomarker increase (with troponin preferred) from a normal baseline to a level 3 times the 99th percentile as PCI-related MI (Type 4a) (14). The importance of the association between elevated biomarker levels after PCI and prognosis continues to be debated. Several studies have shown that the elevation of troponin levels after PCI is strongly associated with the composite of death and MI (2,5). However, the associations have usually been with early outcomes (hospital or 90 days) and not with later follow-up (4). A further important consideration is the level of the elevation with 1 study (6) showing that only troponin levels Ͼ5 times the upper limit of normal were prognostically important. In some studies (7), prognosis did not seem to be influenced if baseline pre-PCI levels were not elevated (15). A recent meta-analysis (9) of 15 studies showed that patients with normal baseline and any elevation of post-PCI troponin levels had increased risk of major adverse cardiac events (death, MI, repeat PCI, and coronary artery bypass graft [CABG]) when compared with those patients without troponin elevation at an average follow-up of 17.7 months. For patients fulfilling the universal definition of type 4a MI (14), there was a further increased risk: odds ratio: 2.5 (95% confidence interval 1.26 to 4.00). Patients with elevation of troponin Ͻ3 times the upper limit of normal did not have a worse prognosis dur...