scholarly journals 3-Dimensional Optical Coherence Tomography Imaging in Early Coronary Stent Thrombosis

2011 ◽  
Vol 4 (2) ◽  
pp. 256-257 ◽  
Author(s):  
Koen Teeuwen ◽  
Bastiaan Zwart ◽  
Jochem W. van Werkum ◽  
Michael Joner ◽  
Jurriën M. ten Berg
2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Akihiro Nakajima ◽  
Yoshiyasu Minami ◽  
Makoto Araki ◽  
Osamu Kurihara ◽  
Tsunenari Soeda ◽  
...  

Background Specific plaque phenotypes that predict a favorable response to statin therapy have not been systematically studied. This study aimed to identify optical coherence tomography predictors for a favorable vascular response to statin therapy. Methods and Results Patients who had serial optical coherence tomography imaging at baseline and at 6 months were included. Thin‐cap area (defined as an area with fibrous cap thickness <200 μm) was measured using a 3‐dimensional computer‐aided algorithm, and changes in the thin‐cap area at 6 months were calculated. A favorable vascular response was defined as the highest tertile in the degree of reduction of the thin‐cap area. Macrophage index was defined as the product of the average macrophage arc and length of the lesion with macrophage infiltration. Layered plaque was defined as a plaque with 1 or more layers of different optical density. In 84 patients, 140 nonculprit lipid plaques were identified. In multivariable analysis, baseline thin‐cap area (odds ratio [OR] 1.442; 95% CI, 1.024–2.031, P =0.036), macrophage index (OR, 1.031; 95% CI, 1.002–1.061, P =0.036), and layered plaque (OR, 2.767; 95% CI, 1.024–7.479, P =0.045) were identified as the significant predictors for a favorable vascular response. Favorable vascular response was associated with a decrease in the macrophage index. Conclusions Three optical coherence tomography predictors for a favorable vascular response to statin therapy have been identified: large thin‐cap area, high macrophage index, and layered plaque. Favorable vascular response to statin was correlated with signs of decreased inflammation. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01110538.


Author(s):  
Hiroshi Iwata ◽  
Eric A. Osborn ◽  
Giovanni J. Ughi ◽  
Kentaro Murakami ◽  
Claudia Goettsch ◽  
...  

BACKGROUND New pharmacological approaches are needed to prevent stent restenosis. This study tested the hypothesis that pemafibrate, a novel clinical selective PPARα (peroxisome proliferator‐activated receptor α) agonist, suppresses coronary stent‐induced arterial inflammation and neointimal hyperplasia. METHODS AND RESULTS Yorkshire pigs randomly received either oral pemafibrate (30 mg/day; n=6) or control vehicle (n=7) for 7 days, followed by coronary arterial implantation of 3.5 × 12 mm bare metal stents (2–4 per animal; 44 stents total). On day 7, intracoronary molecular‐structural near‐infrared fluorescence and optical coherence tomography imaging was performed to assess the arterial inflammatory response, demonstrating that pemafibrate reduced stent‐induced inflammatory protease activity (near‐infrared fluorescence target‐to‐background ratio: pemafibrate, median [25th‐75th percentile]: 2.8 [2.5–3.3] versus control, 4.1 [3.3–4.3], P =0.02). At day 28, animals underwent repeat near‐infrared fluorescence–optical coherence tomography imaging and were euthanized, and coronary stent tissue molecular and histological analyses. Day 28 optical coherence tomography imaging showed that pemafibrate significantly reduced stent neointima volume (pemafibrate, 43.1 [33.7–54.1] mm 3 versus control, 54.2 [41.2–81.1] mm 3 ; P =0.03). In addition, pemafibrate suppressed day 28 stent‐induced cellular inflammation and neointima expression of the inflammatory mediators TNF‐α (tumor necrosis factor‐α) and MMP‐9 (matrix metalloproteinase 9) and enhanced the smooth muscle differentiation markers calponin and smoothelin. In vitro assays indicated that the STAT3 (signal transducer and activator of transcription 3)–myocardin axes mediated the inhibitory effects of pemafibrate on smooth muscle cell proliferation. CONCLUSIONS Pemafibrate reduces preclinical coronary stent inflammation and neointimal hyperplasia following bare metal stent deployment. These results motivate further trials evaluating pemafibrate as a new strategy to prevent clinical stent restenosis.


1998 ◽  
Vol 4 (7) ◽  
pp. 861-865 ◽  
Author(s):  
Stephan A. Boppart ◽  
Brett E. Bouma ◽  
Costas Pitris ◽  
James F. Southern ◽  
Mark E. Brezinski ◽  
...  

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