Abstract
Minor myocardial injury (MMI) is relatively common after complicated percutaneous coronary interventions (PCI) and is associated with increased risk of future cardiac events. It is possible that MMI may be detected by elevation of cardiac markers (e.g. enzymes and cardiac troponins). However, the occurrence, mechanism and long term outcome of minor myocardial injury after uncomplicated successful elective PCI in patients with stable angina has not been assessed previously. Cardiac troponins have been shown to be more sensitive and specific than CKMB for the detection of MMI. Therefore, the first purpose of our work was to study the occurrence of MMI after uncomplicated successful elective PCI in patients with stable angina by measuring cardiac troponin levels in serum after the procedure and to compare these results with serum CKMB. Much recent evidence supports the inflammatory nature of atherosclerotic coronary artery disease. Several inflammation markers have been implicated in this process with their serum concentrations increased in a variety of atherosclerotic disease. With this rapidly developing field in mind, the second purpose of our work was to examine the association of the systemic inflammatory state, reflected by different inflammation markers, with the occurrence of MMI. Such an association has never been studied before in this selected group of patients. Since relating the occurrence of MMI after PCI to outcome has important implications for clinical practice of interventional cardiology, the third purpose of the study was to prospectively evaluate the long-term prognostic significance of MMI after elective uncomplicated successful PCI which has never been reported before in patients with stable angina. Serum cardiac troponin I (cTnl), cardiac troponin T (cTnT) and creatine kinase MB (CKMB) levels were measured before and after uncomplicated, successful elective PCI in patients with stable angina. The frequencies of elevated cTnl and cTnT levels were significantly higher than that of CKMB after coronary intervention (p =0.00016 and 0.015, respectively). Inflammatory markers including serum levels of high-sensitivity C-reactive protein (CRP), interleukin-6, tumor necrosis factor-α, and intercellular adhesion molecule-1 were measured before PCI and were related to the occurrence of MMI after the procedure, and subjects were followed-up for adverse cardiac events for 24 months. Serum CRP was the only inflammatory marker that related to the occurrence of MMI after the procedure. CRP levels were above the reference range in 41% of patient group; of these, 46% developed MMI after PCI compared to 18% of patients that had a serum CRP within the reference range (p= 0.008). Patients with and without presumed MMI, identified by elevated cTnl levels, did not differ significantly with respect to age, body mass index, conventional coronary risk factors, medications, or severity of pre-existing coronary artery disease. Over a follow-up period of 24 months there was no significant difference in the medication used between the MMI positive and negative groups. The incidence of recurrent angina, repeat PCI, coronary bypass surgery and cardiac death was 54, 46,4 and 4% respectively in the cTnl positive patients versus 27, 16, 4 and 0% in the cTnl negative patients. Kaplan-Meier survival analysis showed that cTnl elevation was significantly related to cardiac events (p =0.0198, by log rank analysis). In conclusion, MMI identified by elevated serum levels of cardiac markers is not uncommon after elective uncomplicated successful PCI in patients with stable angina. Serum cardiac troponins, especially cTnl, were more sensitive than serum CKMB in detecting MMI. Cardiac troponin I elevation after elective uncomplicated successful PCI in patients with stable angina might be a marker of adverse long-term outcome. Increased serum CRP is common in patients with stable angina and is a significant and independent determinant of MMI after elective uncomplicated PCI indicating involvement of the systemic inflammatory state in the etiology of this periprocedural myocardial injury.