Association between percutaneous coronary intervention and long-term C-reactive protein levels in patients with acute coronary syndromes

被引:17
作者
Ray, Kausik K. [5 ]
Nazer, Babak [4 ]
Cairns, Richard [3 ]
Gibson, C. Michael [2 ]
Cannon, Christopher P. [1 ]
机构
[1] Brigham & Womens Hosp, Thrombolysis Myocardial Infarct TIMI Study Grp, Div Cardiovasc, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Beth Israel Deaconess Hosp, Div Cardiovasc, Boston, MA 02115 USA
[3] Worldwide Clin Trials, Nottingham, England
[4] Brigham & Womens Hosp, Dept Internal Med, Boston, MA 02115 USA
[5] Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge, England
关键词
Percutaneous coronary intervention; Inflammation; Acute coronary syndromes; C-reactive protein; STENT IMPLANTATION; TRIAL; ATORVASTATIN; ELEVATION; STATINS;
D O I
10.1007/s11239-010-0463-7
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
C-reactive protein (CRP) is an independent predictor of risk in ACS patients, and it has been previously shown that percutaneous coronary intervention (PCI) is associated with an early rise in CRP. To assess the long-term relationship between PCI and CRP, we compared CRP levels at baseline, 30 days, 4 months and 24 months among patients in the Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 trial who were treated with PCI and those who did not receive PCI. At study entry, CRP was significantly higher among patients who had undergone PCI (13.2 vs. 9.5 mg/l, P < 0.001). However, by day 30 CRP was significantly lower among patients who had undergone PCI for management of the index event (1.5 vs. 2.1 mg/l, P < 0.001) and remained lower at 4 months and by end of study (average 2 years after ACS). Using a multivariable model, we observed that PCI was associated with 8.6% lower CRP level at month 4 (P = 0.05) and 14.2% at approximately 2 years (P = 0.0028). These analyses suggest that although PCI may acutely increase inflammation, it may also serve a role in decreasing inflammation associated with atherosclerotic plaques via long-term mechanical stabilization.
引用
收藏
页码:10 / 13
页数:4
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