Atherosclerosis · 2006
Serum C-reactive protein response to percutaneous coronary intervention in patients with unstable or stable angina pectoris is associated with the risk of clinical restenosis.
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Saleh Nawsad, Tornvall Per
Аннотация
BACKGROUND: Inflammation plays a pivotal role in the pathogenesis of atherosclerosis. Previous reports have used vaccination as a model to stimulate inflammation. The aim of the present study was to investigate the role of C-reactive protein response to PCI in the risk of clinical restenosis or new coronary stenosis, considering PCI as a model to stimulate inflammation.
MATERIAL AND METHODS: Eight hundred and ninety-one patients with stable or unstable angina pectoris and with normal serum troponin T<or=0.03 microg/L before PCI were investigated. The survivors after a follow-up period of 2.6 years (850 patients) were included. Serum CRP and troponin T concentration were measured before and the day after PCI. Restenosis and new coronary stenosis, detected by coronary angiography due to symptomatic coronary heart disease, were determined.
RESULTS: CRP response to PCI, unstable angina pectoris, the number of vessels dilated and lack of stent implantation were associated with restenosis or new coronary stenosis. In multivariate analysis, patients in the highest tertile of CRP, induced by PCI, had an increased risk (risk ratio 1.7 [95% CI 1.1-2.9]) for restenosis or new coronary stenosis. Furthermore, patients with restenosis had an increased CRP response to PCI compared with those with new coronary stenosis.
CONCLUSION: The CRP response to PCI, as a model to stimulate inflammation, is associated with an increased risk of clinical restenosis. The results emphasize the role of CRP in the pathogenesis of coronary artery disease progression and in particular restenosis.
MATERIAL AND METHODS: Eight hundred and ninety-one patients with stable or unstable angina pectoris and with normal serum troponin T<or=0.03 microg/L before PCI were investigated. The survivors after a follow-up period of 2.6 years (850 patients) were included. Serum CRP and troponin T concentration were measured before and the day after PCI. Restenosis and new coronary stenosis, detected by coronary angiography due to symptomatic coronary heart disease, were determined.
RESULTS: CRP response to PCI, unstable angina pectoris, the number of vessels dilated and lack of stent implantation were associated with restenosis or new coronary stenosis. In multivariate analysis, patients in the highest tertile of CRP, induced by PCI, had an increased risk (risk ratio 1.7 [95% CI 1.1-2.9]) for restenosis or new coronary stenosis. Furthermore, patients with restenosis had an increased CRP response to PCI compared with those with new coronary stenosis.
CONCLUSION: The CRP response to PCI, as a model to stimulate inflammation, is associated with an increased risk of clinical restenosis. The results emphasize the role of CRP in the pathogenesis of coronary artery disease progression and in particular restenosis.