322: Correlation between lipids, inflammatory markers, some parameters of hemeostasis and carotid arteries atherosclerotic lesions in patients with stroke

2008 ◽  
Vol 2 (5) ◽  
pp. S150-S151
Keyword(s):  
Inflammatory Markers ◽  
Carotid Arteries ◽  
Atherosclerotic Lesions

scholarly journals Carotid webs produce greater hemodynamic disturbances than atherosclerotic disease: a DSA time–density curve study

2021 ◽  
pp. neurintsurg-2021-017588
Author(s):  
Charlie C Park ◽  
Retta El Sayed ◽  
Benjamin B Risk ◽  
Diogo C Haussen ◽  
Raul G Nogueira ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Carotid Artery ◽  
Carotid Arteries ◽  
Region Of Interest ◽  
Hemodynamic Parameters ◽  
Density Curve ◽  
Atherosclerotic Lesions ◽  
Clinically Significant ◽  
Flow Stasis ◽  
Time Density

BackgroundCarotid webs (CaWs) are associated with ischemic strokes in younger patients without degrees of stenosis that are traditionally considered clinically significant.ObjectiveTo compare the hemodynamic parameters in the internal carotid artery (ICA) bulbar segment in patients with CaW with those in patients with atherosclerotic lesions using time–density curve (TDC) analysis of digital subtraction angiography (DSA) images.MethodsWe retrospectively assessed DSA images of 47 carotid arteries in 41 adult patients who underwent ICA catheter angiography for evaluation after ischemic stroke. Hemodynamic parameters, including full width at half maximum (FWHM) and area under the time–density curve (AUC) as proxies for increased flow stasis, were calculated using TDC analyses of a region of interest (ROI) in the ICA bulb immediately rostral to the web/atherosclerotic plaque, relative to a standardized ROI in the ipsilateral distal common carotid artery (eg, relative FWHM (rFWHM)). Hemodynamic parameters were compared using non-parametric Kruskal-Wallis tests. Logistic regression was used to predict CaW versus mild/moderate atherosclerosis for each hemodynamic parameter, adjusting for degree of stenosis.ResultsMean age of patients was 56.0±13 years, with 22 (53.7%) women. 17 CaWs, 22 atherosclerotic plaques (15 mild/moderate and 7 severe), and eight normal carotid arteries were assessed. Significant between-group differences were present in the relative total AUC (p<0.001), relative AUC at wash out (p=0.031), and relative FWHM (p=0.001). Logistic regression to predict CaW versus mild/moderate atherosclerosis showed that rAUC total had the highest predictive value (pAUC=0.96, 95% CI 0.90 to 1.00), followed by rFWHM (0.87, 95% CI 0.74 to 1.00), and rAUC WO (0.74, 95% CI (0.57 to 0.91).ConclusionCaW results in larger local hemodynamic disruption, characterized by flow stasis, than mild/moderate carotid atherosclerotic lesions, suggesting that CaWs may produce larger regions of thrombogenic flow stasis.

Abstract P259: Endothelial Acid Sphingomyelinase Gene Determines Inflammasome Activation and Atherosclerotic Lesions in Carotid Arteries During Hypercholesterolemia

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Min Xia ◽  
Krishna M Bioni ◽  
Yang Chen ◽  
Xiang Li ◽  
Ashley L Pitzer ◽  
...  
Keyword(s):  
Carotid Arteries ◽  
Acid Sphingomyelinase ◽  
Receptor Protein ◽  
Inflammasome Activation ◽  
Neointimal Formation ◽  
Atherosclerotic Lesions ◽  
Junction Protein ◽  
Nlrp3 Inflammasomes

Nucleotide oligomerization domain (NOD)-like receptor protein with pyrin domain containing 3 (Nlrp3) inflammasome has been reported to be activated by atherogenic factors, thereby triggering endothelial injury and consequent atherosclerotic lesions in the arterial wall. However, the mechanism activating and regulating Nlrp3 inflammasomes remains poorly understood. The present study tested whether membrane raft (MR) signaling platforms associated with acid sphingomyelinase (ASM) and its product ceramide (Ce) importantly contribute to the activation of Nlrp3 inflammasomes and atherosclerotic lesions during hypercholesterolemia (HC). By confocal microscopy and biochemical analyses, we demonstrated the formation and activation of Nlrp3 inflammasomes in the intima of the carotid arteries of Asm +/+ mice with HC (as shown by a 2-fold increase in caspase-1 activity and a 6-fold enhancement of IL-1β positive stain areas), but not in Asm -/- mice. In endothelium-specific ASM transgenic mice (EC-Asm trg ), this inflammasome formation and activation were enhanced. Correspondingly, HC-induced increases in IL-1β production, ASM expression, Ce level and MR-gp91 phox clustering in the carotid intima were abolished in Asm -/- mice, but enhanced in EC-Asm trg mice. Functionally, endothelium-dependent vasodilation (EDVD) in carotid arteries in vivo (by ultrasound flowmetry) and in vitro (in perfused artery) was impaired by HC in Asm +/+ mice by 33% and 54%, respectively. This endothelial dysfunction was not observed in Asm -/- mice. The endothelial tight junction protein, ZO-1 was reduced by HC in both Asm +/+ and EC-Asm trg mice, but not in Asm -/- mice. It was also found that HC-increased neointimal formation, T-cell infiltration, and fibrosis in 2-week partially ligated carotid arteries (PLCA) occurred in Asm +/+ mice, but not in Asm -/- mice with HC. EC-Asm trg mice even exhibited more severe inflammatory and atherosclerotic lesions. All these results suggest that Asm gene and related MR clustering are essential to endothelial inflammasome activation and dysfunction in carotid arteries, ultimately determining the extent of atherosclerotic lesions.

Abstract 2771: Incidence of High Risk Atherosclerotic Lesions in Intracranial and Extracranial Carotid Arteries in Patients with Acute Ischemic Stroke: A 3.0T Magnetic Resonance Imaging Study

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Xihai Zhao ◽  
Huilin Zhao ◽  
Feiyu Li ◽  
Jie Sun ◽  
Ye Cao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
High Risk ◽  
Carotid Artery ◽  
Acute Ischemic Stroke ◽  
Cerebral Artery ◽  
Carotid Arteries ◽  
Atherosclerotic Plaques ◽  
Slice Thickness ◽  
Atherosclerotic Lesions ◽  
Vascular Beds

Introduction Rupture of vulnerable atherosclerotic plaques in the intracranial and extracranial carotid arteries could trigger ischemic stroke. However, the incidence of high risk atherosclerotic lesions in these vascular beds is not well known. This study sought to investigate the incidence of high risk atherosclerotic lesions in intracranial and extracranial carotid arteries in stroke patients using magnetic resonance (MR) imaging. Methods Seventy-five patients (mean age 62.7 years, 56 males) with acute ischemic stroke underwent MR imaging for index carotid arteries, assigned as the same side as the brain lesions, with a Philips 3.0T MR scanner. Intracranial carotid MR angiography was performed using 3D TOF sequence with FOV of 23 × 23 cm 2 , matrix of 256 × 256, and a slice thickness of 1mm. The multi-contrast vessel wall images (3D TOF, T1W, T2W, and MP-RAGE) were acquired for extracranial carotid arteries with FOV of 14 × 14 cm 2 , matrix of 256 × 256, and slice thickness of 2 mm. The intracranial artery includes middle cerebral artery (MCA), anterior cerebral artery (ACA), and posterior cerebral artery (PCA). The extracranial carotid artery was divided into internal carotid artery (ICA), bulb, and common carotid artery (CCA). Luminal stenosis for each intracranial and extracranial carotid segment was measured and graded (normal or mild = 0-29%, moderate =30-69%, severe=70-99%). Normalized wall index (NWI = wall area/total vessel area × 100%), and presence/absence of calcification, lipid-rich necrotic core (LRNC), and intraplaque hemorrhage (IPH) and/or fibrous cap rupture in each extracranial carotid segment were determined. Results MCAs developed more severe stenotic lesions (24.6%), followed by extracranial carotids (16.5%), PCAs (5.4%), and ACAs (4.1%) in stroke patients ( Figure 1 A). For extracranial carotid arteries, ICAs showed the largest plaque burden as measured by NWI (44.3%±13.1%), followed by bulbs (39.4%±13%), and CCAs (37%±6.8%). Compared to CCAs, ICAs and bulb regions had more LRNCs (38.4% and 49.3% for ICA and bulb respectively) and IPH and/or rupture (11% and 9.6% for ICA and bulb respectively) ( Figure 1 B). Conclusions In patients with acute ischemic stroke, high risk atherosclerotic plaques can be found in both intracranial and extracranial carotid arteries, particularly in the MCA, ICA and bulb regions. Compared to extracranial carotid arteries, intracranial arteries develop more high risk lesions. The findings of this study suggest the necessity for early screening to detect high risk atherosclerotic lesions in these carotid vascular beds prior to cerebravascular events.

Early atherosclerotic lesions of the carotid arteries: detection with ultrasonography and111In-labeled polyclonal human IgG (HIG) scintigraphy

1994 ◽  
Vol 109 (1-2) ◽  
pp. 295
Author(s):  
H. Kritz ◽  
P. Schmid ◽  
M. Wenger ◽  
Ch. Pirich ◽  
M. Rodrigues ◽  
...  
Keyword(s):  
Carotid Arteries ◽  
Human Igg ◽  
Atherosclerotic Lesions

scholarly journals Hybrid technologies in surgical treatment of patients with concomitant atherosclerotic lesions of carotid and coronary arteries

2015 ◽  
Vol 17 (1) ◽  
pp. 45 ◽  
Author(s):  
A. M. Chernyavskiy ◽  
M. A. Chernyavskiy ◽  
T. Ye. Vinogradova ◽  
A. G. Yedemskiy
Keyword(s):  
Surgical Treatment ◽  
Coronary Arteries ◽  
Carotid Arteries ◽  
Rapid Development ◽  
Peripheral Arteries ◽  
Endovascular Techniques ◽  
Hybrid Procedures ◽  
Atherosclerotic Lesions ◽  
Hybrid Technologies ◽  
Revascularization Surgery

Cardiovascular diseases, which have their origins in atherosclerosis, are the "leaders" in morbidity and mortality among the population in many countries. Given the increase of elderly people in the population, it is important to choose the best strategy for surgical treatment of patients with combined atherosclerotic lesions of several arteries (coronary arteries, carotid arteries, peripheral arteries of the lower extremities, atherosclerosis visceral branches of the abdominal aorta). Currently, there is yet no common approach to the timing and sequence of revascularization surgery in this group of patients. The rapid development of endovascular techniques enables us to carry out the so-called hybrid procedures in patients with atherosclerotic lesions of several arteries. In this article we analyze different strategies that are used to manage patients with both coronary and carotid arteries atherosclerotic lesions.

scholarly journals Choline Treatment Activates NLRP3 Inflammasome Formation and Leads to Endothelial Dysfunction in Mice

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 44-44
Author(s):  
Saisudha Koka ◽  
Goverdhan Puchchakayala ◽  
Krishna Boini
Keyword(s):  
Endothelial Dysfunction ◽  
Tight Junction ◽  
Real Time ◽  
Nlrp3 Inflammasome ◽  
Real Time Pcr ◽  
Inflammatory Markers ◽  
Carotid Arteries ◽  
Pcr Analysis ◽  
Tight Junction Proteins ◽  
Junction Proteins

Abstract Objectives Choline and other trimethylamine-containing nutrients are metabolized by gut microbiota into Trimethylamine N-oxide (TMAO), which is involved in the pathogenesis of various cardiovascular diseases. The present study was designed to investigate the relation between dietary choline and endothelial dysfunction in mice. Methods Nlrp3 +/+ and Nlrp3 −/− mice were treated with 3% choline chloride in drinking water for 6 months. Plasma concentration of TMAO levels were measured after the treatment. Cardiac and endothelial dysfunction were monitored using echocardiography. Vascular permeability was measured by Evans blue dye perfusion. Confocal microscopy was used to detect the co-localization of Nlrp3 inflammasome components. Caspase-1 activity was measured by colorimetric assay and IL-1β production was measured using ELISA. Western blotting was used to measure tight-junction proteins. Real time PCR analysis was used to determine the TLR-4 and inflammatory markers (ICAM and VCAM) in the carotid arteries of the mice. Results Choline treatment significantly increased plasma TMAO levels in all the groups. Choline treated Nlrp3+/+ mice showed significant impairment in endothelial function and had increased vascular hyper-permeability, enhanced Nlrp3 activation and decreased expression of tight junction proteins like ZO2, VE-cadherin and occludin expression in carotid arteries compared to choline treated Nlrp3−/− mice. Caspase-1 activity and IL-1β production was significantly enhanced in choline treated Nlrp3+/+ mice but not in Nlrp3−/- mice. Real time PCR analysis showed that TLR-4 and inflammatory markers (ICAM & VCAM) were significantly increased in carotid arteries of choline treated Nlrp3+/+ mice compared to Nlrp3−/− mice. Conclusions Our results suggest that chronic choline treatment induced endothelial dysfunction via activation of Nlrp3 inflammasome and other inflammatory markers. Funding Sources NIH - NHLBI, AHA.

Effect of antiplatelet therapy on inflammatory markers in atherothrombotic patients

2010 ◽  
Vol 103 (01) ◽  
pp. 71-82 ◽  
Author(s):  
Joseph Muhlestein
Keyword(s):  
Antiplatelet Therapy ◽  
Inflammatory Markers ◽  
Thrombus Formation ◽  
Inflammatory Marker ◽  
Vascular Inflammation ◽  
Antiplatelet Agents ◽  
Cd40 Ligand ◽  
Reactive Protein ◽  
Atherosclerotic Lesions

SummaryInflammation is central to the pathogenesis and progression of atherosclerosis and thrombosis, the underlying cause of major cardiovascular disease. Platelets, in addition to their role in haemostasis, play a key role in both thrombus formation and inflammation following vascular injury, especially atherosclerotic lesions. An increasing body of evidence suggests that inhibition of platelet function can modulate inflammatory markers, particularly those associated with activated platelets, such as CD40 ligand, P-selectin, and C-reactive protein. The currently available antiplatelet agents aspirin, clopidogrel, prasugrel, abciximab, and eptifibatide have shown varying effects on inflammatory markers. These effects seem to be mostly indirect, i.e. mediated primarily through reduced platelet activation that results in reduced inflammatory marker expression. However, there is some evidence that suggests direct effects (i.e. those independent of platelets) may also play a role in modulating inflammatory markers. Evidence linking inflammation and thrombosis supports the hypothesis that agents with both anti-inflammatory and antiplatelet effects may reduce vascular inflammation and limit acute and long-term thrombotic events. An assessment of the involvement of inflammatory mediators in atherosclerosis may provide further insight into important predictive markers of cardiovascular outcomes that may also serve as potential therapeutic targets. This review examines the evidence for and potential clinical relevance of the effects of antiplatelet therapy on inflammatory markers.

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