Author + information
- Received August 27, 2004
- Revision received March 24, 2005
- Accepted April 14, 2005
- Published online July 19, 2005.
- Teruo Inoue, MD, FACC⁎,⁎ (, )
- Toru Kato, MD⁎,
- Toshihiko Uchida, MD†,
- Masashi Sakuma, MD†,
- Atsuko Nakajima, BSc‡,
- Mitsuei Shibazaki, BSc‡,
- Yoshitaka Imoto, BSc§,
- Masahiko Saito, MD∥,
- Shigemasa Hashimoto, MD⁎,
- Yutaka Hikichi, MD⁎ and
- Koichi Node, MD⁎
- ↵⁎Reprint requests and correspondence:
Dr. Teruo Inoue, Department of Cardiovascular and Renal Medicine, Saga University Faculty of Medicine, 5-1-1 Nabeshima, Saga 849-8501, Japan.
Objectives The purpose of this study was to assess local release of C-reactive protein (CRP) from atherosclerotic plaques or the vessel wall injured by stenting.
Background Recent research has focused on the local production of CRP, especially in inflammatory atherosclerotic plaques.
Methods The study consisted of two separate protocols. In protocol 1, we measured serum high-sensitivity-CRP (hs-CRP) levels in coronary arterial blood sampled just distal and proximal to the culprit lesions in 36 patients with stable angina and 13 patients with unstable angina. In protocol 2, we measured serial serum hs-CRP levels and activated Mac-1 on the surface of neutrophils in both coronary sinus and peripheral blood in 20 patients undergoing coronary stenting.
Results In protocol 1, CRP was higher in distal blood than proximal blood in both stable (p < 0.05) and unstable angina (p < 0.01). The translesional CRP gradient (distal CRP minus proximal CRP, p < 0.05) as well as the proximal CRP (p < 0.05) and distal CRP (p < 0.05) was higher in unstable angina than in stable angina. In protocol 2, the transcardiac CRP gradient (coronary sinus minus peripheral blood) and activated Mac-1 increased gradually after stenting, reaching a maximum at 48 h (p < 0.001 vs. baseline for both). There was a positive correlation between the transcardiac CRP gradient and activated Mac-1 at 48 h (r = 0.45, p < 0.01).
Conclusions C-reactive protein is an excellent marker for plaque instability or poststent inflammatory status, and its source might be the inflammation site of the plaque or the coronary arterial wall injured by stenting.
This study was supported in part by a grant from the Vehicle Racing Commemorative Foundation, Tokyo, Japan.
- Received August 27, 2004.
- Revision received March 24, 2005.
- Accepted April 14, 2005.
- American College of Cardiology Foundation