scholarly journals Optical Coherence Tomography For the Detection of the Vulnerable Plaque

2016 ◽  
Vol 11 (2) ◽  
pp. 90 ◽  
Author(s):  
Konstantinos Toutouzas ◽  
Antonios Karanasos ◽  
Dimitris Tousoulis ◽  
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◽  
...  
2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Kimura ◽  
K Hara ◽  
M Ohmori ◽  
R Tateishi ◽  
T Kaneda ◽  
...  

Abstract Background Many vulnerable plaques would progress without clinical events and might result in healed plaques (HPs). Histopathological or intracoronary image assessment of HPs has been reported. However, the morphological characteristics of HPs remain unclear yet. Purpose We sought to assess the healed vulnerable plaque components in patients with coronary artery lesions using optical coherence tomography (OCT) and coronary angioscopy (CAS). Methods We enrolled 47 patients with 50 native coronary artery lesions with angiographical severe stenosis (>90% diameter-stenosis) and without severe calcification (36 lesions with stable angina pectoris (SAP) and 14 acute coronary syndrome (ACS)) undergoing pre-intervention OCT and CAS. HPs was defined as layered phenotype on OCT. Lesion morphologies and plaque characteristics in lesions with HPs were assessed using OCT and CAS images. Results HPs were observed in 27 lesions (54.0%) and their prevalence were similar among each clinical status (SAP 52.8%, ACS 57.1%, p=1.00). Lesions with HPs had higher prevalence of OCT-macrophage (88.0% vs. 52.0%, p=0.01), CAS-red thrombus (88.8% vs. 52.2%, p=0.004) and CAS-low grade-yellow plaque (grade 1) (55.6% vs. 21.7%, p=0.02) than those without. SAP lesions with HPs had higher prevalence of CAS-yellow plaque (35.3% vs. 5.9%, p=0.09) and OCT-thin-cap fibroatheroma (42.1% vs. 5.9%, p=0.04) than SAP without HPs. ACS lesions with HPs had less CAS-red thrombus (0.0% vs. 50.0%, p=0.03) and OCT-plaque rupture (12.5% vs. 66.7%, p=0.04) than ACS without HPs. Multivariate logistic regression analysis revealed that OCT-macrophages (odds ratio (OR): 6.65, 95%-confidence intervals: 1.07–41.5, p=0.043), CAS-red thrombus (OR 8.77, 95% CI 1.33–57.8, p=0.02), and low grade-yellow plaque (OR 13.05, 95% CI 1.97–86.5, p=0.008) were independently related with the existence of HPs lesions. Combination of these 3 factors showed a high predictive value of OCT-HPs lesions (90.9%). Conclusions HPs lesions showed the lower lesion vulnerability than common ACS lesions but had more intraplaque inflammatory condition compared with common SAP lesions. Combined CAS and OCT examination might be useful to clarify the plaque components of HPs lesions in vivo, leading to help us understand the clinical significance of HPs. Funding Acknowledgement Type of funding source: None


2012 ◽  
Vol 53 (2) ◽  
pp. 450
Author(s):  
Jeong Hoon Yang ◽  
Kyeongmin Byeon ◽  
Hyeon-Cheol Gwon ◽  
Jeong Euy Park ◽  
Young Bin Song

2006 ◽  
Vol 67 (6) ◽  
pp. 915-923 ◽  
Author(s):  
Mehmet Cilingiroglu ◽  
Jung Hwan Oh ◽  
Binu Sugunan ◽  
Nate J. Kemp ◽  
Jeehyun Kim ◽  
...  

2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Rocco Antonio Montone ◽  
Massimiliano Camilli ◽  
Michele Russo ◽  
Giulia La Vecchia ◽  
Giulia Iannaccone ◽  
...  

Abstract Aims Air pollution is an emerging key player in determining the residual risk of coronary events. However, pathophysiological mechanisms linking air pollution and coronary events have been not adequately investigated. We aimed at assessing the relationship between exposure to air pollutants and mechanisms of coronary instability evaluated by optical coherence tomography (OCT) in patients with acute coronary syndrome (ACS). Methods and results ACS patients undergoing OCT imaging were retrospectively selected. Mechanism of culprit lesion instability was classified as plaque rupture (PR) or intact fibrous cap (IFC) by OCT, and the presence of macrophage infiltrates (MØI) and thin-cap fibroatheroma (TCFA) at the culprit site was also assessed. Based on each case’s home address, exposure to several pollutants was evaluated, including particulate matter 2.5 (PM2.5), particulate matter 10 (PM10), and carbon monoxide (CO). Only patients with >2 years of available data on air pollution exposure prior to ACS were enrolled. We included 126 patients [median age 67.0 years (55.5–76.0), 97 (77.0%) male]. Sixty-six patients (52.4%) had PR as mechanism of plaque instability. Patients with PR were exposed to significantly higher PM2.5 levels compared to IFC, and PM2.5 was independently associated with PR [odds ratio per unit = 1.194, 95% CI: (1.036–1.377), P = 0.015]. Moreover, exposure to higher levels of PM2.5 was independently associated with the presence of TCFA and of MØI at the culprit site. Interestingly, PM2.5, PM10, and CO levels were positively and significantly correlated with serum levels of C-reactive protein. ROC curves were constructed to assess the ability of PM2.5 to predict the presence of plaque rupture, TCFA or MØI. The AUC for PM2.5 to predict plaque rupture was 0.62 (95% CI: 0.52–0.71, P = 0.018), for TCFA was 0.71 (95% CI: 0.61–0.80, P <0.001) and for MØI was 0.80 (95% CI: 0.71–0.88, P <0.001). Using a PM2.5 cut-off value of 13.40 μg/m3, the sensitivity and specificity for MØI were 81% and 66%, respectively. Conclusions We provide novel insights into the missing link between air pollution and increased risk of coronary events. In particular, exposure to higher concentrations of air pollutants is a risk factor for vulnerable plaque features and for plaque rupture as mechanism of coronary instability mediated by systemic and local plaque inflammation. Of importance, the thresholds of air pollutants that predicted the presence of vulnerable plaque features are far lower than commonly accepted safety thresholds used to start preventive measures for public health, suggesting that further efforts are needed in order to reduce the adverse effects on the cardiovascular system.


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