Abstract
In the recently published original article, Nienhuis and coworkers have througly examined the prognostic importance of elevated cardiac enyzmes after elective percutaneous coronary intervention (PCI). In that prospective observational study, they found that increase of troponin T after elective PCI had stronger prognostic implication when compared to increased creatine kinase (CK) [1]. Variable degrees of myocardial injury can be observed during PCI, as reflected by rises in cardiac enzymes such as CK and troponins [2–5]. Cardiac troponins aremore sensitive and more specific than CK for diagnosing minor myocardial damage [6]. Several reports have demonstrated that an increase in troponin T can be encountered in a proportion of patients ranging from b10% to 50% [7]. The adverse prognostic significance of myocardial biomarkers of injury after PCI is well known [3,8–10]. But, the degree of cardiac injury is modest making it unlikely that prognosis is closely related to the extent of injury in most cases. Elevations in myocardial biomarkers of injury might reflect the extent of coronary artery disease , embolic events, stent expansion, or the lack of collateral blood flow to area at the risk in patients undergoing PCI [11]. However the baseline troponin levels as a covariant have usually not included in most PCI outcome trials even though it has been measured and included in the analysis of the data like as the current study. Miller and coworkers have assessed the timing and magnitude of post-PCI troponin T levels and their relationships to outcomes in patients with or without pre-PCI baseline troponin T elevations [11]. They showed that long-term prognosis was most often related to baseline pre-PCI troponin value and not the biomarker res-
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