Involvement of C-reactive protein obtained by directional coronary atherectomy in plaque instability and developing restenosis in patients with stable or unstable angina pectoris

Ishikawa, Tetsunori; Hatakeyama, Kinta; Imamura, Takuroh; Date, Hiroyuki; Shibata, Yoshisato; Hikichi, Yutaka; Asada, Yujiro; Eto, Tanenao

doi:10.1016/s0002-9149(02)03156-9

Cited by 109 publications

(69 citation statements)

References 26 publications

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“…Therefore, our findings are consistent with recent studies 6,7,12,18,19) and further support the finding that CRP, an index of inflammation, has a proatherosclerotic effect and promotes the atherosclerotic process. 4,10,16,[18][19][20] One of the important findings of this study was that the circulating level of hs-CRP rapidly and significantly declined on day 30 following the procedure. We suggest that such a dramatic decline in hs-CRP level is likely due to the combined effects of stenting and atorvastatin therapy.…”

Section: Discussionsupporting

confidence: 93%

“…5,8,10,17) Importantly, growing data shows that CRP directly participates in endothelial cell dysfunction, 4) atherosclerosis, 16) and plaque rupture. 6,[18][19][20] In this study, patients with unstable angina had significantly higher circulating levels of hs-CRP before the procedure than healthy con- trol subjects. Additionally, the study patients also had significantly higher white blood cell counts at admission than the healthy control subjects.…”

Section: Discussionmentioning

confidence: 54%

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Re-Elevation of High-Sensitivity C-Reactive Protein but not the von Willebrand Factor After Withdrawing Atorvastatin Therapy in Patients With Unstable Angina Undergoing Coronary Artery Stenting A Kinetic Study

et al. 2006

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SUMMARYStatins are known to reduce high-sensitivity C-reactive protein (hs-CRP) concentrations and improve endothelial function. However, whether statin withdrawal causes re-elevated concentrations of hs-CRP and von Willebrand Factor (vWF) (a marker of endothelial damage) remains unknown. We hypothesized that the concentrations of hs-CRP and vWF are substantially increased in patients with unstable angina pectoris (UAP) and noticeably decreased following coronary stenting along with atorvastatin therapy. However, re-elevations of these biomarker concentrations occurred once again after withdrawing atorvastatin therapy. We serially examined the plasma concentrations of hs-CRP and vWF in 51 patients with UAP before (day 0) and after (days 21, 90, 180, 270) performing coronary artery stenting. The concentrations of these 2 biomarkers were also measured in 30 healthy control subjects. Patients were treated with atorvastatin (40 mg/ day orally) for 180 days, after which the therapy was withdrawn. The hs-CRP and vWF concentrations were significantly higher in the patients than in the healthy control subjects before the procedure (both P values < 0.001). The hs-CRP concentration decreased significantly on day 21 (P < 0.001), and further to a substantially lower level on day 180 (P < 0.0001). However, the hs-CRP level significantly increased again on day 270, as compared with that on day 180 (P < 0.001). The vWF plasma concentration decreased gradually to a significantly lower level on day 180. The concentration of this biomarker did not differ between days 180 and 270. In conclusion, although hs-CRP concentrations decreased markedly following combined stenting and atorvastatin therapy, re-elevation after atorvastatin therapy was withdrawn in UAP patients undergoing coronary stenting was not observed. Conversely, restoration of endothelial function was slow and persistent in these patients. (Int Heart J 2006; 47: 501-509)

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 54%

Re-Elevation of High-Sensitivity C-Reactive Protein but not the von Willebrand Factor After Withdrawing Atorvastatin Therapy in Patients With Unstable Angina Undergoing Coronary Artery Stenting A Kinetic Study

et al. 2006

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“…Both CRP and PTX3 are found in human atherosclerotic plaques [16][17][18] . We previously demonstrated that CRP accumulation is enhanced in unstable coronary plaques, suggesting that CRP is associated with plaque instability 19) ; however, its relationship to PTX3 in coronary plaques has not yet been examined. Also, regarding the differences between PTX3 and CRP, there is little histological evidence of their effect on coronary atherosclerotic plaques.…”

Section: Morphometric Image Analysismentioning

confidence: 99%

“…Serial sections (4-μm thick) were immunohistochemically stained using the primary antibodies mentioned below 19) . In brief, after blocking endogenous peroxidase activity in 3% hydrogen peroxide in methanol for 20 minutes, the sections were incubated with primary monoclonal antibodies to PTX3 (clone PPZ 1228; Perseus Proteomics Inc., Tokyo, Japan), CRP (clone CRP-8; Sigma, St. Louis, MO, USA), macrophages (CD68: clone PGM-1; Dako, Glostrup, Denmark, and CD163: clone 10D6; Leica Biosystems, Newcastle, UK), smooth muscle cells (α-smooth muscle actin (SMA); Dako) and T lymphocyte (CD3: clone F7.2.38; Dako).…”

Section: Immunohistochemistrymentioning

confidence: 99%

Different Distribution of Pentraxin 3 and C-Reactive Protein in Coronary Atherosclerotic Plaques

Matsuura

Hatakeyama

Imamura

et al. 2012

JAT

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Aim:To understand the differences between histopathological characteristics related to PTX3 (pentraxin 3) and CRP (C-reactive protein) in coronary atherosclerotic plaques. Methods and Results:To assess the localization of PTX3 and CRP in coronary plaque, immunohistochemistry was performed using 157 coronary artery specimens from 45 autopsied cases. Overall, immunoreactivity to CRP was more intense than that to PTX3 in lipid rich plaque; however, PTX3 was notably abundant in areas of intraplaque hemorrhage, in which CRP was quite sparse. On quantitative analysis, complicated plaques showed more immunopositive area of PTX3 than fibroatheroma, but with CRP, this trend disappeared. In addition, we examined the phenotype of macrophages in PTX3-and CRP-rich areas using CD163 staining (M2 macrophages). Consequently, these areas were differently characterized by the accumulation of macrophages with high and low magnitude of CD163 positivity, respectively. Next, we immunohistochemically investigated relationships among PTX3, CRP, histological components and clinical presentation in 73 coronary atherectomy specimens obtained from 35 and 38 patients with unstable (UAP) and stable angina pectoris (SAP), respectively. Both PTX3 and CRP were more intense in culprit plaques from patients with UAP than with SAP, and they significantly correlated with CD68 (pan macrophage)-positive areas; however, there was no correlation between PTX3 and CRP. Conclusion: Although PTX3 and CRP were more enhanced in unstable than in stable coronary plaques, their distribution distinctly differed, suggesting that they play distinct biological roles in unstable plaques. J Atheroscler Thromb, 2012; 19:837-845.

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“…CRP is an inflammatory acute-phase reactant that has emerged as a powerful predictor of cardiovascular disease (Ridker, 2007). CRP is localized in atherosclerotic plaques and is more in thrombotic plaques than non-thrombotic ones (Ishikawa et al, 2003, Sun et al, 2005. The findings imply that CRP is implicated in atherothrombogenesis.…”

Section: Vascular Factors On Thrombus Growthmentioning

confidence: 99%

Pathology and Pathophysiology of Atherothrombosis: Virchow's Triad Revisited

Yamashita¹,

Asada²

2012

Traditional and Novel Risk Factors in Atherothrombosis

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Involvement of C-reactive protein obtained by directional coronary atherectomy in plaque instability and developing restenosis in patients with stable or unstable angina pectoris

Cited by 109 publications

References 26 publications

Re-Elevation of High-Sensitivity C-Reactive Protein but not the von Willebrand Factor After Withdrawing Atorvastatin Therapy in Patients With Unstable Angina Undergoing Coronary Artery Stenting A Kinetic Study

Re-Elevation of High-Sensitivity C-Reactive Protein but not the von Willebrand Factor After Withdrawing Atorvastatin Therapy in Patients With Unstable Angina Undergoing Coronary Artery Stenting A Kinetic Study

Different Distribution of Pentraxin 3 and C-Reactive Protein in Coronary Atherosclerotic Plaques

Pathology and Pathophysiology of Atherothrombosis: Virchow's Triad Revisited

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