Key result
Unstable angina shows higher translesional CRP gradients, and stenting further increases transcardiac CRP at 48 hours.
Why the study?
Recent research focused on local CRP production in inflammatory atherosclerotic plaques, motivating an assessment of local CRP release from atherosclerotic plaques or the vessel wall injured by stenting.
Does local C-reactive protein release occur across vulnerable coronary plaques in unstable angina and across the coronary vascular bed injured by stenting?
Cohort (n=69)
Does local C-reactive protein release occur across vulnerable coronary plaques in unstable angina and across the coronary vascular bed injured by stenting?
Demonstrates that hs-CRP is locally released from unstable coronary plaques and stent-injured coronary arterial walls, correlating with local neutrophil activation.
Local CRP gradients mark plaque instability and post-stent inflammation; leaves open whether they guide therapy or predict events.
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.
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Inoue et al. (2005) conducted a cohort in Stable angina, unstable angina, or patients undergoing coronary stenting (n=69). Unstable angina vs. stable angina (Protocol 1) and coronary stenting (Protocol 2) vs. Stable angina (Protocol 1) and baseline pre-stenting levels (Protocol 2) was evaluated on Translesional hs-CRP gradient (distal minus proximal coronary blood) and transcardiac hs-CRP gradient (coronary sinus minus peripheral blood) with neutrophil activated Mac-1 (p=<0.05 (translesional gradient in unstable vs stable angina); <0.001 (transcardiac gradient at 48 h vs baseline)). Unstable angina showed a higher translesional CRP gradient than stable angina (p<0.05), and coronary stenting increased the transcardiac CRP gradient at 48 hours (p<0.001).
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