Dataset Information

Microbleeds after Carotid Artery Stenting: Small Embolism May Induce Cerebral Microbleeds.

ABSTRACT:

Background

Since the advent of magnetic resonance imaging technology, cerebral microbleeds can be diagnosed in vivo. However, the underlying mechanism of cerebral microbleed formation is not fully understood.

Objectives

This study aimed to identify the factors associated with cerebral microbleeds after carotid artery stenting (CAS).

Method

We retrospectively examined 125 patients who underwent CAS for carotid stenosis. Cerebral microbleeds were investigated using T2*-weighted gradient-echo (GRE) imaging before and after CAS. We analyzed the possible association of new microbleeds with the following risk factors: the number of baseline microbleeds and ischemic cerebral lesions, the occurrence of cerebral hyperperfusion syndrome, and new ischemic cerebral lesions after CAS.

Results

Baseline cerebral microbleeds were detected in 53 patients (42.4%). New cerebral microbleeds after CAS were observed in 13 of 125 patients (10.4%) and were exclusively associated with new ischemic lesions but not with other risk factors. No patient showed a merged image of a new cerebral microbleed on GRE imaging or a new ischemic lesion on diffusion-weighted imaging. Lobar and deep microbleeds were noted in 12/13 (92.3%) and 1 patient (7.7%), respectively. Of 12 patients with new microbleeds, 10 (76.9%) and 2 (15.4%) had a new microbleed in the ipsilateral and contralateral hemispheres, respectively.

Conclusions

We found that new cerebral microbleeds developed after CAS and that these might be associated with new ischemic lesions, mostly in the territory of the treated carotid artery. We speculate that these microbleeds result from the deoxygenation of hemoglobin in the embolus or, alternatively, small hemorrhagic transformation of ischemic lesions.

SUBMITTER: Ogawa Ito A

PROVIDER: S-EPMC6600049 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Publications

Microbleeds after Carotid Artery Stenting: Small Embolism May Induce Cerebral Microbleeds.

Ogawa Ito Ai A Shindo Akihiro A Ii Yuichiro Y Matsuura Keita K Tabei Ken-Ichi KI Maeda Masayuki M Umino Maki M Suzuki Yume Y Shiba Masato M Toma Naoki N Suzuki Hidenori H Tomimoto Hidekazu H

Cerebrovascular diseases extra 20190614 2

<h4>Background</h4>Since the advent of magnetic resonance imaging technology, cerebral microbleeds can be diagnosed in vivo. However, the underlying mechanism of cerebral microbleed formation is not fully understood.<h4>Objectives</h4>This study aimed to identify the factors associated with cerebral microbleeds after carotid artery stenting (CAS).<h4>Method</h4>We retrospectively examined 125 patients who underwent CAS for carotid stenosis. Cerebral microbleeds were investigated using T2*-weight ...[more]

PMID: 31203282

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Project description:BackgroundFew studies have focused on cerebral hemodynamics in the early stage following carotid artery stenting (CAS). This retrospective cohort study aimed to investigate cerebral hemodynamic changes within 6 hours of unilateral CAS in patients with different degrees of carotid stenosis.MethodsA total of 104 patients who underwent CAS accompanied by transcranial color-code Doppler or transcranial Doppler were enrolled in the study. The participants were divided into the following 3 groups based on the degree of carotid stenosis: severe stenosis group, extreme stenosis group, and near occlusion group. Bilateral middle cerebral artery (MCA) peak systolic velocity (PSV) and pulsatility index (PI) were measured using transcranial color-code Doppler before and 1 and 3 hours following CAS. Blood pressure, MCA-PSV, and PI were compared among the 3 groups.ResultsAt 1 hour following CAS, ipsilateral MCA-PSV increased compared to the baseline in the severe stenosis group [84±21 vs. 93±27 cm/s; 8.1%; interquartile range (IQR), 1.4-20.1%; P<0.001]. A similar hemodynamic change, but of a larger magnitude, was observed in the extreme stenosis group (83±24 vs. 100±29 cm/s; 20.8%; IQR, 5.3-33.1%; P<0.001) and near occlusion group (73±24 vs. 109±29 cm/s, 45.8%; IQR, 24.3-73.1%; P<0.001). At 3 hours after CAS, the hemodynamic changes were the same as those at 1 hour. PI increased in all 3 groups following CAS. A subgroup analysis was performed according to symptoms, sex, smoking status, history of hypertension, and presence of hyperlipidemia or diabetes, and the increase in ipsilateral MCA-PSV was not significant. In terms of adverse events, only 4 patients in the near occlusion group experienced transient post-CAS hyperperfusion.ConclusionsThe ipsilateral MCA-PSV and PI in patients following unilateral CAS increased significantly in the initial hours. The increase in ipsilateral MCA-PSV was considerably higher in patients with a severe degree of stenosis. Near occlusion of the carotid artery was an independent risk factor for hyperperfusion after unilateral CAS.

Project description:BackgroundIn-stent restenosis is a crucial problem after carotid artery stenting, but the exact predictors of in-stent restenosis remain unclear. We aimed to evaluate the effect of cerebral collateral circulation on in-stent restenosis after carotid artery stenting and to establish a clinical prediction model for in-stent restenosis.MethodsThis retrospective case-control study enrolled 296 patients with severe carotid artery stenosis of C1 segment (≥70%) who underwent stent therapy from June 2015 to December 2018. Based on follow-up data, the patients were divided into the in-stent restenosis and no in-stent restenosis groups. The collateral circulation of the brain was graded according to the criteria of the American Society for Interventional and Therapy Neuroradiology/Society for Interventional Radiology (ASITN/SIR). Clinical data were collected, such as age, sex, traditional vascular risk factors, blood cell count, high-sensitivity C-reactive protein, uric acid, stenosis degree before stenting and residual stenosis rate, and medication after stenting. Binary logistic regression analysis was performed to identify potential predictors of in-stent restenosis, and a clinical prediction model for in-stent restenosis after carotid artery stenting was established.ResultsBinary logistic regression analysis showed that poor collateral circulation was an independent predictor of in-stent restenosis (P=0.003). We also found that a 1% increase in residual stenosis rate was associated with a 9% increase in the risk of in-stent restenosis (P=0.02). Ischemic stroke history (P=0.03), family history of ischemic stroke (P<0.001), in-stent restenosis history (P<0.001), and nonstandard medication after stenting (P=0.04) were predictors of in-stent restenosis. The risk of in-stent restenosis was lowest when the residual stenosis rate was 12.5% after carotid artery stenting. Furthermore, we used some significant parameters to construct a binary logistic regression prediction model for in-stent restenosis after carotid artery stenting in the form of a nomogram.ConclusionsCollateral circulation is an independent predictor of in-stent restenosis after successful carotid artery stenting, and the residual stenosis rate tends to be below 12.5% to reduce restenosis risk. The standard medication should be strictly carried out for patients after stenting to prevent in-stent restenosis.

Project description:BackgroundCarotid atherosclerosis is associated with subclinical ischemic cerebrovascular disease, but its role in hemorrhage-prone small vessel disease-represented by cerebral microbleed (CMB)-is unclear, although vascular risk factors underlie both conditions. We hypothesized that persons with carotid atherosclerosis would have higher risk of CMB, particularly in deep regions.Methods and resultsWe studied 1243 participants in the Framingham Offspring Study (aged 56.9±8.8 years; 53% women) with carotid ultrasound available on 2 occasions (1995-1998 and 2005-2008) prior to brain magnetic resonance imaging. Using multivariable logistic regression, we related baseline carotid stenosis, baseline intima-media thickness, and site-specific carotid intima-media thickness progression (at internal and common carotid locations) to the prevalence and location (lobar or deep plus mixed) of CMB. In addition, we assessed effect modification by lipid levels and use of statin and antithrombotic medications. Carotid stenosis ≥25% (a marker of cerebrovascular atherosclerosis) was associated with presence of CMB overall (Odds Ratio 2.20, 95% CI 1.10-4.40) and at deep and mixed locations (odds ratio 3.60, 95% CI 1.23-10.5). Baseline carotid intima-media thickness was not associated with CMB. Progression of common carotid artery intima-media thickness among persons on hypertension treatment was associated with lower risk of deep and mixed CMB (odds ratio per SD 0.41, 95% CI 0.18-0.96).ConclusionsCumulative vascular risk factor exposure may increase the risk of CMB, especially in deep regions. The apparent paradoxical association of carotid intima-media thickness progression with lower risk of CMB may reflect benefits of intensive vascular risk factor treatment among persons with higher cardiovascular risk and deserves further investigation. If replicated, the results may have potential implications for assessment of preventive and therapeutic interventions for subclinical cerebral hemorrhage.

Project description:ObjectiveTo decrease the procedural risk of carotid revascularisation it is crucial to understand the mechanisms of procedural stroke. This study analysed the features of procedural strokes associated with carotid artery stenting (CAS) and carotid endarterectomy (CEA) within the International Carotid Stenting Study (ICSS) to identify the underlying pathophysiological mechanism.Materials and methodsPatients with recently symptomatic carotid stenosis (1,713) were randomly allocated to CAS or CEA. Procedural strokes were classified by type (ischaemic or haemorrhagic), time of onset (intraprocedural or after the procedure), side (ipsilateral or contralateral), severity (disabling or non-disabling), and patency of the treated artery. Only patients in whom the allocated treatment was initiated were included. The most likely pathophysiological mechanism was determined using the following classification system: (1) carotid-embolic, (2) haemodynamic, (3) thrombosis or occlusion of the revascularised carotid artery, (4) hyperperfusion, (5) cardio-embolic, (6) multiple, and (7) undetermined.ResultsProcedural stroke occurred within 30 days of revascularisation in 85 patients (CAS 58 out of 791 and CEA 27 out of 819). Strokes were predominately ischaemic (77; 56 CAS and 21 CEA), after the procedure (57; 37 CAS and 20 CEA), ipsilateral to the treated artery (77; 52 CAS and 25 CEA), and non-disabling (47; 36 CAS and 11 CEA). Mechanisms of stroke were carotid-embolic (14; 10 CAS and 4 CEA), haemodynamic (20; 15 CAS and 5 CEA), thrombosis or occlusion of the carotid artery (15; 11 CAS and 4 CEA), hyperperfusion (9; 3 CAS and 6 CEA), cardio-embolic (5; 2 CAS and 3 CEA) and multiple causes (3; 3 CAS). In 19 patients (14 CAS and 5 CEA) the cause of stroke remained undetermined.ConclusionAlthough the mechanism of procedural stroke in both CAS and CEA is diverse, haemodynamic disturbance is an important mechanism. Careful attention to blood pressure control could lower the incidence of procedural stroke.

Dataset Information

Microbleeds after Carotid Artery Stenting: Small Embolism May Induce Cerebral Microbleeds.

Background

Objectives

Method

Results

Conclusions

Publications

Microbleeds after Carotid Artery Stenting: Small Embolism May Induce Cerebral Microbleeds.

Similar Datasets

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