Local Release of C-Reactive Protein From Vulnerable Plaque or Coronary Arterial Wall Injured by Stenting
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*
* Department of Cardiovascular and Renal Medicine, Saga University Faculty of Medicine, Saga, Japan
Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Koshigaya, Japan
Department of Laboratory Medicine, Dokkyo University School of Medicine, Koshigaya, Japan
Yufu Itonaga Co. Ltd., Tokyo, Japan
|| Department of Cardiology, Cardiovascular Center, Ageo Central General Hospital, Ageo, Japan.

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Figure 1 Translesional measurement of C-reactive protein (CRP). The distal CRP was higher than the proximal CRP in the groups with stable and unstable angina. Thus, a translesional CRP gradient was present. Both the proximal and distal CRP levels in unstable angina were higher than in stable angina. The translesional CRP in unstable angina was also greater than in stable angina.
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Figure 2 Correlation between proximal C-reactive protein (CRP) and translesional CRP. In all patients, there was a significant correlation between the two measurements.
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Figure 3 Serial changes in plasma C-reactive protein (CRP) levels after percutaneous coronary intervention (PCI). C-reactive protein increased after coronary stenting in a time-dependent manner, reaching a maximum at 48 h in both coronary sinus and peripheral blood. These changes were also more striking in coronary sinus blood (left). The transcardiac gradient of CRP increased after PCI reaching a maximum at 48 h (right). Closed circles = coronary sinus blood (CS); open circles = peripheral blood (P); squares = transcardiac gradient. *p < 0.05 vs. pre; **p < 0.01 vs. pre; ***p < 0.001 vs. pre; p < 0.01 CS vs. P.
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Figure 4 Serial changes in the expression of Mac-1 activation neo-epitope (8B2 binding) on the surface of neutrophils after PCI. Antibody binding capacity (ABC) of 8B2 began to increase immediately after coronary stenting reaching a maximum at 48 h in both coronary sinus and peripheral blood. These changes were more striking in coronary sinus blood (left). The transcardiac gradient (coronary sinus blood minus peripheral blood) of 8B2 binding increased after PCI, reaching a maximum at 48 h (right). Closed circles = coronary sinus blood (CS); open circles = peripheral blood (P); squares = transcardiac gradient. *p < 0.05 vs. pre; **p < 0.01 vs. pre; ***p < 0.001 vs. pre; p < 0.01 CS vs. P. PCI = percutaneous coronary intervention.
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Figure 5 Correlation between the transcardiac gradients (CS-P) of CRP and 8B2 binding at each time point. There was no significant correlation before PCI (upper left). However, positive correlations at 15 min (upper right) and at 24 h (lower left) reached borderline significance. There was a significant positive correlation at 48 h (lower right). CS = coronary sinus blood; P = peripheral blood; PCI = percutaneous coronary intervention.
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Figure 6 Relationship between angiographic late lumen loss and 8B2 binding or CRP. Late lumen loss correlated with the transcardiac gradient of 8B2 binding at 48 h (left) and that of CRP (right). CRP = C-reactive protein.
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Copyright © 2005 by the American College of Cardiology Foundation.