Stable Coronary Plaques Research Articles

TCT-600 Distinct Vascular Response between Vulnerable and Stable Coronary Plaques after the Second Generation Drug-eluting Stents Implantation: One-year Angioscopic Comparison

The second generation drug-eluting stents (G2-DES) have been implanted safely at culprit lesions not only of stable angina pectoris but also of acute coronary syndrome. The aim of this study was to angioscopically characterize vascular response after implantation of various G2-DES and to compare

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

To understand the differences between histopathological characteristics related to PTX3 (pentraxin 3) and CRP (C-reactive protein) in coronary atherosclerotic plaques. 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. 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.

Biochemical Markers for Determining Vulnerable Atherosclerotic Plaque in Stenotic Patient: Biochemical Markers Study of Myeloperoxidase (MPO), Matrix Metallo-Proteinase-9 (MMP-9), Secretory Phospholipase A2 (SPLA2) and CD40 Ligand

BACKGROUND: Thrombus is a main cause of cardiac death. Therefore identifying which coronary artery plaque is vulnerable to rupture is a critical step for cardiac intervention to prevent future cardiac events. Systemic biochemical markers are used for predicting rupture of coronary plaque or identifying stenotic coronary artery plaque(s) vulnerable to rupture.METHODS: Blood samples of 2x24 locations (2x10 controls, 2x12 stable plaques and 2x2 unstable plaques) of 13 patients to undergo stent placement were taken from an artery which showed no stenosis (control), 70% or more stenosis of stable plaques and unstable plaques, respectively. The blood samples were taken by using microcatheter distally and proximally. Concentrations of MPO, MMP-9, SPLA2 and CD40L of each sample were assayed.RESULTS: Concentration of MMP-9 in unstable coronary artery plaque (94.7+14.4 ng/ml) significantly increased compared with that of stable coronary artery plaque (71.0+67.8 ng/ml, p=0.024). SPLA2 concentration significantly decreased in unstable coronary artery plaque (45.9+14.0 pg/ml) compared with that of stable coronary artery plaque (80.9+39.3 pg/ml, p=0.015). Nine of ten studied subjects showed an average of 14.5% (range: 0.0-28.8%) decrease of the SPLA2 concentration in stable plaques compared with that of the non-stenotic coronary artery.CONCLUSION: MMP-9 increased in unstable coronary artery plaque compared with that of stable coronary plaque. Unstable coronary artery plaques absorbed SPLA2 from the vasculars more than the stable plaques and control plaques. MMP-9 and SPLA2 may be used as markers of stability of a plaque in coronary artery in relation to its rupture potential.KEYWORDS: stable and unstable plaque, myeloperoxidase, matrix metalloproteinase-9, secretory phospholipase A2, CD40 Ligand

Pragmatic Treatment versus Elaborative but Incomplete Testing

Pragmatic Treatment <i>versus</i> Elaborative but Incomplete Testing

Diffuse and Active Inflammation Occurs in Both Vulnerable and Stable Plaques of the Entire Coronary Tree: A Histopathologic Study of Patients Dying of Acute Myocardial Infarction

This study was undertaken to define and compare geographic coronary artery inflammation in patients who were dying of acute myocardial infarction (AMI), chronic stable angina (SA), and noncardiac causes (CTRL).Biochemical markers and flow cytometry provide indirect evidence of diffuse coronary inflammation in patients dying of acute coronary syndromes. Yet no histopathologic studies have corroborated these findings. A key unanswered question is whether the inflammatory burden involves the entire coronary tree or is limited to a few plaques.We examined 544 coronary artery segments from 16 patients with AMI, 109 segments from 5 patients with SA, and 304 coronary segments from 9 patients with CTRL.An average of 6.8 +/- 0.5 vulnerable segments per patient were found in the AMI group (in addition to culprit lesions) compared with an average of 0.8 +/- 0.3 and 1.4 +/- 0.3 vulnerable lesions/patient in the SA and CTRL groups, respectively. The AMI group, independent of the type of plaque observed, showed significantly more inflammatory infiltrates compared with the SA and CTRL groups (121.6 +/- 12.4 cell x mm2 vs. 37.3 +/- 11.9 cell x mm2 vs. 26.6 +/- 6.8 cell x mm2, p = 0.0001). In AMI patients, active inflammation was not only evident within the culprit lesion and vulnerable plaques but also involved stable plaques. These showed a three- to four-fold higher inflammation than vulnerable and stable plaques from the SA and CTRL groups, respectively.This histopathologic study found that both vulnerable and stable coronary plaques of patients dying of AMI are diffusely infiltrated by inflammatory cells.