Abstract 18972: Iron Quantification in Carotid Artery Atherosclerosis Predicts Downstream Injury by Magnetic Resonance Imaging

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Travis P Sharkey-Toppen ◽  
Tam Tran ◽  
Suzanne Smart ◽  
Beth McCarthy ◽  
Xuan Nguyen ◽  
...  
Keyword(s):  
Brain Injury ◽  
Carotid Artery ◽  
Carotid Plaque ◽  
Carotid Artery Disease ◽  
Brain Mri ◽  
Flip Angle ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Carotid Artery Atherosclerosis ◽  
Artery Disease

Introduction: Luminal stenosis is the primary imaging parameter used to guide management of patients with carotid artery atherosclerosis (CAA). However, neuroimaging identifies subclinical events in patients with CAA not meeting anatomic guidelines for intervention. Strategies to characterize atherosclerotic plaque beyond %stenosis may help reduce the downstream ischemic burden of atherosclerotic disease. Hypothesis: Using noncontrast MRI T2* tissue mapping that we have previously validated for plaque iron characterization, we tested the hypothesis that carotid plaque T2* better predicts ischemic injury by brain MRI than symptom history. Methods: We enrolled 26 individuals with carotid artery stenosis ≥50%. Each subject underwent MRI that included carotid plaque T2* mapping (TR=75ms, 5 TEs, 20° flip angle, 0.44x0.44x2mm resolution), brain diffusion weighted imaging (TR=4436ms, TE=93ms, 0.9x0.9x3mm resolution) and brain fluid attenuated inverse recovery imaging (TR=13970ms, TE=2500ms, 150° flip angle, and 0.9x0.9x3mm resolution). Plaque T2* quantification and brain MRI were independently assessed by experienced observers blinded to patient history and other results. Brain MRIs with Wahlund score ≥2 were classified as positive for ischemic damage. Results: Patients with brain imaging positive for ischemic damage had shorter intraplaque T2* compared to patients with negative brain MRI (17.2±2.9 vs. 20.3±3.2ms, p=.012, Figure). Conversely, presence/absence of brain injury did not correlate with symptoms (p=.352). Conclusions: Noncontrast atherosclerosis imaging using an MRI biomarker of intraplaque iron in patients with carotid artery disease can discriminate between patients with vs. those without ischemic brain injury. Prospective studies that couple plaque characterization with anatomic and clinical factors may better identify at-risk patients with carotid artery disease before significant ischemic brain injury has accrued.

Carotid Plaque Mast Cells Associate with Atherogenic Serum Lipids, High Grade Carotid Stenosis and Symptomatic Carotid Artery Disease

2005 ◽  
Vol 19 (5) ◽  
pp. 291-301 ◽  
Author(s):  
Erno M.P. Lehtonen-Smeds ◽  
Mikko Mäyränpää ◽  
Perttu J. Lindsberg ◽  
Lauri Soinne ◽  
Eija Saimanen ◽  
...  
Keyword(s):  
Mast Cells ◽  
Carotid Artery ◽  
Carotid Stenosis ◽  
Carotid Plaque ◽  
Serum Lipids ◽  
Carotid Artery Disease ◽  
High Grade ◽  
Symptomatic Carotid ◽  
Artery Disease

scholarly journals Linoleic Acid Status in Cell Membranes Inversely Relates to the Prevalence of Symptomatic Carotid Artery Disease

Stroke ◽  
2020 ◽  
Author(s):  
Iolanda Lázaro ◽  
Montserrat Cofán ◽  
Antonio J. Amor ◽  
Emilio Ortega ◽  
Tania-Marisa Freitas-Simoes ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Linoleic Acid ◽  
Carotid Artery ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Carotid Plaque ◽  
Carotid Artery Disease ◽  
Multivariate Logistic Regression Analysis ◽  
Symptomatic Carotid ◽  
Artery Disease

Background and Purpose: The red blood cell fatty acid composition objectively reflects the long-term dietary intake of several fatty acids. In patients undergoing carotid endarterectomy, we explored whether red blood cell status of selected fatty acids related to symptomatic carotid artery disease. Methods: We included patients with symptomatic (n=22) and asymptomatic (n=23) carotid artery disease. We determined all-C18:1 trans, linoleic acid (LA, C18:2n6), alpha-linolenic acid (C18:3n3), and the omega-3 index (sum of eicosapentaenoic [C20:5n3] and docosahexaenoic [C22:6n3] acids) in both red blood cells and carotid plaque phospholipids by gas-chromatography. Results: In a multivariate logistic regression analysis, we only observed a significant association for LA, whose red blood cell status was inversely related to symptomatic carotid artery disease (odds ratio, 0.116 [95% CI, 0.022–0.607], P =0.011, for each 1-SD increase). A similar result was observed for LA in carotid plaque phospholipids. Conclusions: Cell membrane enrichment in LA, which reflects its intake, was inversely related to symptomatic carotid disease. This increases evidence supporting a favorable role of dietary LA in vascular health.

Antithrombotic Therapy in Carotid Artery Disease

2020 ◽  
Vol 26 (23) ◽  
pp. 2725-2734 ◽  
Author(s):  
Paraskevi Papanikolaou ◽  
Alexios S. Antonopoulos ◽  
Irene Mastorakou ◽  
Andreas Angelopoulos ◽  
Efthalia Kostoula ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Carotid Artery Stenosis ◽  
Antithrombotic Therapy ◽  
Carotid Plaque ◽  
Carotid Artery Disease ◽  
Artery Stenosis ◽  
Non Invasive ◽  
Risk Of Rupture ◽  
Artery Disease

: The management of asymptomatic atherosclerotic carotid artery disease and the role of antithrombotic therapy is of increasing importance for stroke prevention. Non-invasive imaging of carotid plaques can identify high-risk plaque features that are associated with the risk of plaque rupture. Carotid plaque necrosis, hemorrhage, fibrous cap thinning, and the presence of foam cells have all been correlated with the risk of rupture and onset of neurological symptoms in patients with carotid stenosis. Antiplatelets are currently recommended for patients with a history of ischemic stroke and/or significant carotid artery stenosis, with aspirin and clopidogrel being the most widely used and studied agents. The role of dual antiplatelet therapy remains controversial. Moreover, there is scarce evidence on the role of newer anticoagulant agents in stable patients with carotid artery stenosis. In this review article, we discuss the pathophysiology of carotid atherosclerosis, the use of non-invasive imaging for detecting the vulnerable carotid plaque and summarize the existing clinical evidence on the use of antiplatelet and antithrombotic agents in carotid artery disease.

scholarly journals Systemic Hyperthermia Induces Ischemic Brain Injury in Neonatal Mice With Ligated Carotid Artery and Jugular Vein

2007 ◽  
Vol 62 (1) ◽  
pp. 65-70 ◽  
Author(s):  
Siarhei Slinko ◽  
Casper Caspersen ◽  
Veniamin Ratner ◽  
Jin-Ji Kim ◽  
Paul Alexandrov ◽  
...  
Keyword(s):  
Brain Injury ◽  
Carotid Artery ◽  
Jugular Vein ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Neonatal Mice

scholarly journals Possible Pharmacodynamic Interaction of Azelnidipine with Citicoline Against Ischemic Brain Injury: Behavioral, Biochemical and Histological Alterations

2020 ◽  
Vol 27 (1) ◽  
pp. 9-17
Author(s):  
Varun Gupta ◽  
Zein Eddin Bader ◽  
Aakriti ◽  
Anil Kumar
Keyword(s):  
Brain Injury ◽  
Carotid Artery ◽  
Wistar Rats ◽  
Neuronal Damage ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Bilateral Common Carotid Artery ◽  
Common Carotid Artery Occlusion

Background: Currently, no drug has been approved for the management of postischemic neuronal damage. Existing studies show that calcium channel blockers have neuroprotective properties, while citicoline is involved in maintaining neuronal integrity. Purpose: This study was envisaged to investigate the effect of azelnidipine (novel calcium channel blocker) alone and in combination with citicoline (phosphatidyl-choline analogue) against ischemic brain damage in Wistar rats. Methods: Previously standardized bilateral common carotid artery occlusion model was used to induce cerebral ischemic injury in Wistar rats. Pretreatment with azelnidipine (1.5 mg/Kg and 3 mg/Kg; p.o.) or citicoline (250 mg/Kg; i.p.) was done every 24 h starting 7 days before the bilateral common carotid artery occlusion surgery. Pharmacological assessments (behavioral, biochemical, mitochondrial, molecular, and histological) were done after 48 h of the reperfusion period. Results: Azelnidipine and citicoline were found to protect the brain from progressive neuronal damage as seen by improved sensorimotor behavior (locomotion, rota rod, and beam balance performance) and reduced oxidative stress (decreased malondialdehyde (MDA), nitrite, increased glutathione (GSH), superoxide dismutase (SOD)). Impairment of mitochondrial enzyme system and increase in the infarct area were found to be arrested by individual treatments with azelnidipine and citicoline. These effects were further potentiated synergistically as the combination of citicoline and azelnidipine was found to decrease glutamate levels, caspase-3 activity and histological alterations as compared to their individual effects. Conclusion: Azelnidipine and citicoline synergistically decrease excitotoxic and oxidative damage against ischemic brain injury in Wistar rats and, therefore, propose a clinically relevant combination for the prevention of postischemic neuronal damage.

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