scholarly journals Plaque Rupture is a Determinant of Vascular Events in Carotid Artery Atherosclerotic Disease: Involvement of Matrix Metalloproteinases 2 and 9

2011 ◽  
Vol 7 (2) ◽  
pp. 69 ◽  
Author(s):  
Sung Hyuk Heo ◽  
Chang-Hoon Cho ◽  
Hye Ok Kim ◽  
Yong Hwa Jo ◽  
Kyung-Sik Yoon ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Carotid Artery ◽  
Plaque Rupture ◽  
Atherosclerotic Disease ◽  
Vascular Events

Activated inflammatory cells are associated with plaque rupture in carotid artery stenosis

Surgery ◽  
1997 ◽  
Vol 122 (4) ◽  
pp. 757-764 ◽  
Author(s):  
Sandra C Carr ◽  
Andrew Farb ◽  
William H Pearce ◽  
Renu Virmani ◽  
James S.T Yao
Keyword(s):  
Carotid Artery ◽  
Carotid Artery Stenosis ◽  
Plaque Rupture ◽  
Inflammatory Cells ◽  
Artery Stenosis

scholarly journals Biomarkers of Carotid Stenosis

2021 ◽  
Vol 3 (1) ◽  
pp. 104-130
Author(s):  
Sergey G. Sсherbak ◽  
Tatyana A. Kamilova ◽  
Svetlana V. Lebedeva ◽  
Dmitry A. Vologzhanin ◽  
Alexander S. Golota ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Carotid Stenosis ◽  
Plaque Rupture ◽  
Early Recognition ◽  
Clinical Problem ◽  
Vascular Wall ◽  
Inflammatory Factors ◽  
Atherosclerotic Lesions ◽  
Important Clinical Problem ◽  
Definition Of

Early recognition of rupture-prone atherosclerotic lesions in patients with high-graded carotid stenosis is an important clinical problem for preventing ischemic stroke. Various pathophysiological mechanisms are responsible for the progression and instability of plaques, such as changes in lipid composition, infiltration by immunoinflammatory cells and degradation of the extracellular matrix of the vascular wall by matrix metalloproteinases, enhanced inflammatory response and plaque neovascularization. These features are the main cause of plaque rupture and, as a consequence, neurologic symptoms. Therefore, matrix metalloproteinases and inflammatory factors can serve as possible markers for patients with severe unstable stenosis of carotid arteries. Due to the heterogeneity of atherosclerotic lesions, only one biomarker is not enough to reliably predict the development of a stroke. The use of a combination of biomarkers is better correlated with clinical data and, therefore, exceeds the analysis of individual factors. To increase the overall sensitivity and specificity and more reliable diagnosis of stroke in patients with symptomatic and asymptomatic carotid stenosis, the biomarker panel should include independent biomarkers. Further preclinical experiments and clinical trials are needed to assess the significance and precise definition of the threshold levels of such biomarkers before they can be used in clinical practice.

scholarly journals Eagle syndrome as a rare cause of recurrent transient ischemic stroke in Senegal (West Africa)

2021 ◽  
Vol 7 (9) ◽  
pp. 1534
Author(s):  
Birame Loum ◽  
Cheikh Ahmedou Lame ◽  
Cheikhna B. Ndiaye ◽  
Kamadore Toure ◽  
Mouhamadou Mansour Ndiaye
Keyword(s):  
Risk Factors ◽  
Ischemic Stroke ◽  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Internal Carotid ◽  
Rare Condition ◽  
Styloid Process ◽  
Neurological Impairment ◽  
Vascular Events ◽  
Eagle Syndrome

<p>Eagle syndrome is a rare condition, often characterized by nonspecific symptoms. It is due to an abnormally long or compressive styloid process on surrounding structures. Exceptionally, it can cause neuro-vascular manifestations. We report an observation of Eagle syndrome discovered incidentally in presence of recurrent transient ischemic stroke. A 74-year-old man with no cardiovascular risk factors, was admitted to our department following 4 episodes of transient ischemic stroke with right hemiplegia and aphasia, always rapidly resolving. Head and neck CT scan showed 2 long styloid processes with a marked impingement of the left one against the ipsilateral internal carotid artery. Intraoral styloidectomy was performed. The patient recovered fully and remained free of symptoms without neurological impairment, at 6 months. Eagle syndrome is a rare condition which may lead, exceptionally, to repetitive transient ischemic stroke. Surgical styloidectomy must be considered to reduce the risk of new vascular events and prevent serious complications such as dissection of the internal carotid artery.</p>

scholarly journals The effect of carotid artery stenting on capillary transit time heterogeneity in patients with carotid artery stenosis

2018 ◽  
Vol 3 (3) ◽  
pp. 263-271 ◽  
Author(s):  
Ethem M Arsava ◽  
Mikkel B Hansen ◽  
Berkan Kaplan ◽  
Ahmet Peker ◽  
Rahsan Gocmen ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Transit Time ◽  
Carotid Artery Stenting ◽  
Cerebral Blood Volume ◽  
Mean Transit Time ◽  
Oxygen Extraction Fraction ◽  
Consecutive Series ◽  
Dynamic Susceptibility ◽  
Dynamic Susceptibility Contrast ◽  
Vascular Events

Introduction Carotid revascularisation improves haemodynamic compromise in cerebral circulation as an additional benefit to the primary goal of reducing future thromboembolic risk. We determined the effect of carotid artery stenting on cerebral perfusion and oxygenation using a perfusion-weighted MRI algorithm that is based on assessment of capillary transit-time heterogeneity together with other perfusion and metabolism-related metrics. Patients and methods A consecutive series of 33 patients were evaluated by dynamic susceptibility contrast perfusion-weighted MRI prior to and within 24 h of the endovascular procedure. The level of relative change induced by stenting, and relationship of these changes with respect to baseline stenosis degree were analysed. Results Stenting led to significant increase in cerebral blood flow ( p < 0.001), and decrease in cerebral blood volume ( p = 0.001) and mean transit time ( p < 0.001); this was accompanied by reduction in oxygen extraction fraction ( p < 0.001) and capillary transit-time heterogeneity ( p < 0.001), but an overall increase in relative capillary transit-time heterogeneity (RTH: CTH divided by MTT; p = 0.008). No significant change was observed with respect to cerebral metabolic rate of oxygen. The median volume of tissue with MTT > 2s decreased from 24 ml to 12 ml ( p = 0.009), with CTH > 2s from 29 ml to 19 ml ( p = 0.041), and with RTH < 0.9 from 61 ml to 39 ml ( p = 0.037) following stenting. These changes were correlated with the baseline degree of stenosis. Discussion: Stenting improved the moderate stage of haemodynamic compromise at baseline in our cohort. The decreased relative transit-time heterogeneity, which increases following stenting, is probably a reflection of decreased functional capillary density secondary to chronic hypoperfusion induced by the proximal stenosis. Conclusion: Carotid artery stenting, is not only important for prophylaxis of future vascular events, but also is critical for restoration of microvascular function in the cerebral tissue.

Abstract 162: Processes of Care that are Associated With Reduced Risk of Recurrent Vascular Events Among Patients With a Transient Ischemic Attack and Minor Stroke

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Dawn Bravata ◽  
Laura Myers ◽  
Mat Reeves ◽  
Eric Cheng ◽  
Fitsum Baye ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Carotid Artery ◽  
Recurrent Events ◽  
Vascular Event ◽  
Fiscal Year ◽  
Minor Stroke ◽  
Vascular Events ◽  
Processes Of Care ◽  
Free Care ◽  
Reduced Risk

Background: Interventions that emphasize early evaluation and management of patients with TIA and minor stroke have demonstrated reductions in recurrent vascular events. Objective: To identify processes of care that were associated with reduced risk of recurrent vascular events after TIA or minor stroke. Methods: We identified patients with a TIA or minor stroke cared for in a Department of Veterans Affairs (VA) Emergency Department or inpatient ward (fiscal year 2011). Recurrent vascular events included ischemic stroke, myocardial infarction, heart failure, arrhythmia or death within 90-days and 1-year of discharge. 32 processes of care were examined. Defect-free care was assessed for a set of 6 processes (brain imaging, carotid artery imaging, hypertension management, high or moderate potency statin, antithrombotics, and anticoagulation for atrial fibrillation); patients who received all processes for which they were eligible passed the defect-free measure. Multivariable logistic regression with a random facility effect was used to model recurrent events. Clinically important potential confounders were forced into all models; other significant covariates were identified by backward selection. Results: Among 8107 patients, 14.0% had a recurrent vascular event within 90-days; 26.5% within 1-year. Three processes were associated with lower 90-day events after adjustment for 24 covariates: carotid artery imaging (adjusted OR, 0.74 [95%CI, 0.65-0.85], lipid measurement (0.80 [0.68-0.94]), and anticoagulation quality for atrial fibrillation (0.56 [0.35-0.88]). Three processes were associated with reduced 1-year events: carotid artery imaging (0.80 [0.71-0.89]), lipid measurement (0.85 [0.75-0.97]), and timely carotid stenosis intervention (0.49 [0.26-0.94]). The defect-free care rate, observed in 17.4%, was also associated with a reduction in recurrent vascular event risk both within 90-days (0.78 [0.65-0.93]) and 1-year (0.82 [0.71-0.94]). Conclusions: The delivery of a comprehensive set of clinical processes was associated with clinically meaningful reductions in short and longer-term risk of recurrent vascular events. Widespread implementation of these processes should be strongly considered.

Abstract 13: Inhibition of Nudt6 Stabilizes Advanced Atherosclerotic Plaques

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Hong Jin ◽  
Yuhuang Li ◽  
Ekaterina Chernogubova ◽  
Alexandra Bäcklund ◽  
Stina Sellberg ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Atherosclerotic Plaque ◽  
Plaque Rupture ◽  
Survival Rates ◽  
Atherosclerotic Plaques ◽  
Protein Coding ◽  
Fibrous Cap ◽  
Asymptomatic Patients ◽  
Rupture Model

Natural antisense transcripts (NATs), a non-coding RNA subclass, being transcribed in antisense direction to protein coding genes, are an intriguing novel class of targetable modulators, exerting crucial effects on gene expression. Aim of the current study was to investigate the contribution of NATs to atherosclerotic plaque vulnerability. Using laser capture micro-dissection, we isolated fibrous caps tissue of carotid artery plaques from 20 symptomatic patients with ruptured lesions vs. 20 samples from asymptomatic patients with stable lesions. A human transcriptome array (HTA; GeneChip 2.0 ) was used to profile the expression of all currently annotated RNA transcripts. Nucleoside diphosphate-linked moiety X motif 6 (NUDT6) was identified as one of the most significantly up-regulated transcripts in fibrous caps of ruptured lesions. Interestingly, NUDT6 is an established antisense RNA targeting the fibroblast growth factor 2 (FGF2). Of importance, FGF2 was among the most significantly down-regulated transcripts in ruptured lesions, corresponding to elevated NUDT6 expression. In situ hybridization in both, human and mouse carotid atherosclerotic plaques, confirmed substantially higher expression levels of NUDT6 in ruptured lesions compared to stable. In addition, in situ hybridization revealed a distinct co-localization with smooth muscle cells (SMCs) in advanced plaques. Overexpression of NUDT6 in cultured human carotid artery SMCs effectively limited FGF2 on the mRNA as well as protein level. Furthermore, reduction of NUDT6 via siRNA stimulated proliferation and blocked apoptosis in SMCs. In an inducible atherosclerotic plaque rupture model using incomplete ligation and cuff placement on common carotid arteries of male apoE -/- mice, NUDT6 inhibition with gapmeRs was able to significantly improve SMC survival rates, leading to thicker fibrous caps, and to reduce the plaque rupture rate compared to scramble-gapmeR control-treated mice (22% vs . 63%, p = 0.03). The present study presents NUDT6 as a novel crucial antisense regulator of fibrous cap stability through steering SMC survival via targeting its sense RNA transcript FGF2.

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