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  • Title: [Myonecrosis and inflammatory response following percutaneous coronary angioplasty. A protective role for betablockers?].
    Author: Radulescu B, Morel O, Faure A, Jesel L, Roul G, Chauvin M, Ohlmann P, Bareiss P.
    Journal: Ann Cardiol Angeiol (Paris); 2009 Feb; 58(1):27-33. PubMed ID: 18656848.
    Abstract:
    INTRODUCTION: Percutaneous coronary intervention (PCI) is widely used actually for the treatment of coronary disease. Stent implantation in the vessel wall is associated with local healing processes and some myonecrosis. However, little is known about the relationships between systemic inflammatory response, myonecrosis and the patient's and procedural characteristics. OBJECTIVES: (i) To evaluate the level of C-Reactive Protein (hsCRP) and cardiac troponin I (cTnI) elevation after PCI; (ii) to determine the patient's and procedural factors associated with those elevations. METHOD: This is a prospective monocentric study carried out in patients hospitalised for elective PCI or for ACS without cTnI elevation. CRP and cTnI were assessed before, after and 24 hours after the procedure. RESULTS: Thirty-four patients (mean age 64+/-10.9 years; sex ratio 28 males/six females) were included. hsCRP increased in 26 patients (76.4%) and cTnI in 16 patients (47%) after PCI. cTnI elevation did not correlate with inflammatory response. Whereas none of the studied parameters were statistically linked with hsCRP increase, cTnI elevation was significantly associated with AHA-ACC B(2)/C type lesion, the number and the total length of stents implanted, the duration of procedure and treatment by betablockers. Multivariate analysis showed that the independent predictors of cTnI elevation were procedure duration (p=0.032 OR=14.2 CI 95% 7.69-100) and the absence of pretreatment with betablockers (p=0.036, OR=2,6 CI 95% 1.35-35). CONCLUSION: cTnI elevation following PCI is very frequent and related with the duration of the procedure. Our data suggest a protective role of betablockers in the occurrence of cTnI elevation after PCI. Confirmation of the protective role of betablockers in larger cohort is mandatory.
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