Abstract
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.
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Acknowledgments
PROVE IT-TIMI 22 was funded by Bristol-Myers Squibb and Sankyo. http://www.clinicaltrials.gov/ registration number NCT00382460. Dr. Ray is funded by a BHF Intermediate Fellowship. Dr. Nazer has nothing to disclose. Dr. Cannon reports having received research grant support from Accumetrics, AstraZeneca, Bristol-Myers Squibb/Sanofi Partnership, GlaxoSmithKline, Intekrin Therapeutics, Merck, Merck/Schering Plough Partnership, Novartis, and Takeda. He has served as a clinical advisor to and has equity in Automedics Medical Systems. Dr. Gibson reports research support from Eli Lilly, Daichi Sankyo, Bayer and Schering-Plough (now Merck).
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Ray, K.K., Nazer, B., Cairns, R. et al. Association between percutaneous coronary intervention and long-term C-reactive protein levels in patients with acute coronary syndromes. J Thromb Thrombolysis 30, 10–13 (2010). https://doi.org/10.1007/s11239-010-0463-7
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DOI: https://doi.org/10.1007/s11239-010-0463-7