Association between carotid artery perivascular fat density and cerebral small vessel disease.
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ABSTRACT:
SUBMITTER: Zhang DH
PROVIDER: S-EPMC8351687 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Background Studies have shown that pericoronary artery inflammation can be accurately detected via increased attenuation on computed tomography. Our purpose was to evaluate the association between pericarotid inflammation, measured by density of carotid perivascular fat on computed tomography angiography, with stroke and transient ischemic attack. Methods and Results We screened computed tomography angiography examinations for patients with unilateral internal carotid artery ( ICA ) stenosis ?50% to 99%. A blinded neuroradiologist placed regions-of-interest in the pericarotid fat on the slice showing maximal stenosis. Two-sample t tests were performed to assess between-subject differences in mean Hounsfield Units in carotid perivascular fat between symptomatic and asymptomatic patients. Paired t tests were used to assess within-subject differences in mean Hounsfield Units between stenotic versus nonstenotic ICA s in a given patient. We included 94 patients, including 42 symptomatic and 52 asymptomatic patients. In the between-subject analysis of stenotic ICA s, we found symptomatic patients had higher mean pericarotid fat density compared with asymptomatic patients (-66.2±19.2 versus -77.1±20.4, P=0.009). When comparing nonstenotic ICA s, there was no significant difference between pericarotid fat density in symptomatic compared with asymptomatic patients (-81.0±13.3 versus -85.3±18.0: P=0.198). Within-subject comparison showed statistically significant increased density in stenotic ICA versus nonstenotic ICA with mean Hounsfield Units difference of 11.1 ( P<0.0001). Conclusions We found increased density, a surrogate marker for perivascular inflammation, in the fat surrounding ICA s ipsilateral to stroke or transient ischemic attack compared with asymptomatic ICA s. Our findings suggest that inflammation associated with culprit carotid plaques extends beyond the vessel lumen and can be identified using simple methods on computed tomography angiography imaging.
| S-EPMC6405622 | biostudies-literature
Project description:ObjectivesThis study investigated the association between perivascular fat density (PFD) via preoperative computed tomographic angiography (CTA) and early in-stent restenosis (ISR) after carotid artery stenting (CAS).MethodsWe retrospectively evaluated 248 consecutive patients who had undergone initial CAS and received a preoperative cervical CTA examination between January 2019 and October 2020. The patients were categorized into two according to whether they sustained ISR during the 2 years postoperative follow-up period. Correlations between PFD and ISR were assessed, and multivariate regression for evaluating predictors of ISR was conducted. Receiver operating characteristic (ROC) curves were used to determine the cutoff value for the PFD.ResultsA total of 181 eligible patients (mean age 61.25 ± 10.35 years, 57 male) were enrolled. The ISR group had a higher proportion of closed-cell stents (48.8% versus 27.5%; p = 0.009) and a greater degree of residual stenosis (28[20,33] % versus 20[14.75,30] %; p < 0.001) than the non-ISR group. The ISR group had a higher mean HU value of PFD than the non-ISR group on the operated side (-42.26 ± 6.81 versus -59.66 ± 10.75; p < 0.001). The degree of residual stenosis (OR 1.146, 95%CI 1.071-1.226, p < 0.001) and PFD on the operated side (OR1.353, 95%CI 1.215-1.506, p < 0.001) were significantly associated with the ISR.ConclusionsThe occurrence of the early ISR after CAS is associated with a higher PFD on the operated side. The results indicate that PFD is a promising marker to predict the ISR after CAS.
| S-EPMC10279783 | biostudies-literature
Project description:Background Carotid artery stiffness is associated with cognitive impairment and dementia, but the underlying mechanisms remain unknown. We examined the associations of carotid artery stiffness with cerebral small-vessel disease markers, cognition, and dementia subtypes in a memory clinic cohort. Methods and Results A total of 272 participants underwent carotid ultrasonography, 3 Tesla brain magnetic resonance imaging, and neuropsychological assessment. Carotid ultrasonography was used to assess β-index, pressure-strain elastic modulus, and pulse-wave velocity-β. Brain magnetic resonance images were graded for cerebral small-vessel disease markers, including white matter hyperintensities, lacunes, and cerebral microbleeds. Participants were classified as having no cognitive impairment, cognitive impairment and no dementia, or dementia subtyped as Alzheimer disease and vascular dementia. Cognition was assessed using National Institute of Neurological Disorders and Stroke-Canadian Stroke Network harmonization battery. After adjusting for age, sex, cardiovascular risk factors, and diseases, multivariable models showed that β-index (β=0.69; P=0.002), elastic modulus (β=0.78; P<0.001), and pulse-wave velocity-β (β=0.80; P<0.001) were associated with white matter hyperintensities, and elastic modulus (odds ratio [OR], 1.39 [95% CI, 1.04-1.85]) and pulse-wave velocity-β (OR, 1.47 [95% CI, 1.10-1.98]) were independently associated with lacunes. Similarly, β-index (OR, 2.04 [95% CI, 1.14-4.13]), elastic modulus (OR, 2.22 [95% CI, 1.25-4.42]), and pulse-wave velocity-β (OR, 2.50 [95% CI, 1.36-5.18]) were independently associated with vascular dementia. Carotid stiffness measures were independently associated with worse performance in global cognition, visuomotor speed, visuospatial function, and executive function. These associations became largely nonsignificant after further adjusting for cerebral small-vessel disease markers. Conclusions In memory clinic patients, carotid artery stiffness was associated with white matter hyperintensities and lacunes, impairment in global and domain-specific cognition, and causative subtypes of dementia, particularly vascular. The effects of carotid stiffness on cognition were not independent of, and were partially mediated by, cerebral small-vessel disease.
| S-EPMC9851463 | biostudies-literature
Project description:Background and aimsEnlarged perivascular spaces (also known as Virchow-Robin spaces) on T2-weighted brain magnetic resonance imaging are common, but their etiology, and specificity to small vessel as opposed to general cerebrovascular disease or ageing, is unclear. We tested the association between enlarged perivascular spaces and ischemic stroke subtype, other markers of small vessel disease, and common vascular risk factors.MethodsWe prospectively recruited patients with acute stroke, diagnosed and subtyped by a stroke physician using clinical features and brain magnetic resonance imaging. A neuroradiologist rated basal ganglia and centrum semiovale enlarged perivascular spaces on a five-point scale, white matter lesions, recent and old infarcts, and cerebral atrophy. We assessed associations between basal ganglia-, centrum semiovale- and total (combined basal ganglia and centrum semiovale) enlarged perivascular spaces, stroke subtype, white matter lesions, atrophy, and vascular risk factors.ResultsAmong 298 patients (mean age 68 years), after adjusting for vascular risk factors and white matter lesions, basal ganglia-enlarged perivascular spaces were associated with increasing age (P = 0.001), centrum semiovale-enlarged perivascular spaces (P < 0.001), cerebral atrophy (P = 0.03), and lacunar stroke subtype (P = 0.04). Centrum semiovale-enlarged perivascular spaces were associated mainly with basal ganglia-enlarged perivascular spaces. Total enlarged perivascular spaces were associated with increasing age (P = 0.01), deep white matter lesions (P = 0.005), and previous stroke (P = 0.006).ConclusionsEnlarged perivascular spaces are associated with age, lacunar stroke subtype and white matter lesions and should be considered as another magnetic resonance imaging marker of cerebral small vessel disease. Further evaluation of enlarged perivascular spaces in studies of ageing, stroke, and dementia is needed to determine their pathophysiological importance.
| S-EPMC4463944 | biostudies-literature
Project description:BackgroundIncreased arterial resistance is a potential pathological mechanism of cerebral small vessel disease (cSVD).AimIn this study, we aimed to investigate the association between pulsatility index (PI) representing cerebral arterial resistance and subtypes of cSVD in patients with lacunar stroke.MethodsWe included consecutive lacunar stroke patients between 2010 and 2013. White matter hyperintensity (WMH) volume was rated using semi-automated quantitative methods. Additionally, the presence of old lacunar infarct (OLI), cerebral microbleed (CMB), or enlarged perivascular space (EPVS) was also evaluated. The relationship between PI, measured in each middle cerebral artery, and the subtype/burden of cSVD was analyzed in the relevant hemisphere.ResultsA total of 206 lacunar patients were included and 412 hemispheres were analyzed (mean age: 64 years, male: 68.4%). In multivariable analysis, PI was positively associated with the WMH volume [beta = 1.372, 95% confidence interval (CI) = 0.624 to 2.120, P < 0.001] after adjusting for confounders. PI was also related to the presence of OLI (adjusted odds ratio = 11.37, 95% CI = 2.55-48.56, P = 0.001); however, this relationship was not significant in CMB or EPVS. Regarding the cSVD burden, PI increased according to the WMH tertiles (P for trend < 0.001), the burden of OLI (P for trend < 0.001), and EPVS tertiles (P for trend < 0.001), showing a quantitative relationship.ConclusionsIpsilateral PI is closely associated with cSVD in patients with lacunar stroke. Furthermore, this association is different between subtypes of cSVD, which is suggestive of underlying pathophysiological differences.
| S-EPMC7365409 | biostudies-literature
Project description:BackgroundSerum alkaline phosphatase (ALP) is a marker of vascular calcification. A high serum ALP level is associated with an increase in cardiovascular events, and predicts poor functional outcome in patients with stroke. We investigated whether serum ALP was associated with cerebral small vessel disease (cSVD) and large cerebral artery stenosis (LCAS).MethodsWe evaluated vascular risk factors, brain magnetic resonance images (MRIs), and MR angiograms from 1,011 neurologically healthy participants. The presence of silent lacunar infarction (SLI) and moderate-to-severe cerebral white matter hyperintensities (MS-cWMH) were evaluated as indices of cSVD on brain MRIs. Findings of extracranial arterial stenosis (ECAS) or intracranial arterial stenosis (ICAS) were considered to be indices of LCAS on MR angiograms.ResultsSubjects with SLI (odds ratio [OR]: 2.09; 95% confidence interval [CI]: 1.27-3.42; p = 0.004) and MS-cWMH (OR: 1.48; 95% CI; 1.03-2.13, p = 0.036) were significantly more likely to have ALP levels in the third tertile (ALP ? 195 IU/L) than the first tertile (ALP ? 155 IU/L), after adjusting for cardiovascular risk factors. The mean serum ALP level was significantly higher in patients with SLI or MS-cWMH compared to patients without those findings. After adjustment for confounding factors, the multivariate model found that the statistical significance of serum ALP remained when the presence of SLI (OR: 1.05 per 10 IU/L increase in ALP; 95% CI: 1.02-1.08; p = 0.003) or MS-cWMH (OR: 1.03 per 10 IU/L increase in ALP; 95% CI: 1.00-1.06; p = 0.025) were added to the model. There were no differences in the proportions of patients with LCAS, ICAS, and ECAS across the serum ALP tertiles.ConclusionsOur study of neurologically healthy participants found a positive association between serum ALP level and indicators of cSVD, but no association between serum ALP level and the indicators of LCAS.
| S-EPMC4651565 | biostudies-literature
Project description:Perivascular space (PVS) burden is an emerging, poorly understood, magnetic resonance imaging marker of cerebral small vessel disease, a leading cause of stroke and dementia. Genome-wide association studies in up to 40,095 participants (18 population-based cohorts, 66.3 ± 8.6 yr, 96.9% European ancestry) revealed 24 genome-wide significant PVS risk loci, mainly in the white matter. These were associated with white matter PVS already in young adults (N = 1,748; 22.1 ± 2.3 yr) and were enriched in early-onset leukodystrophy genes and genes expressed in fetal brain endothelial cells, suggesting early-life mechanisms. In total, 53% of white matter PVS risk loci showed nominally significant associations (27% after multiple-testing correction) in a Japanese population-based cohort (N = 2,862; 68.3 ± 5.3 yr). Mendelian randomization supported causal associations of high blood pressure with basal ganglia and hippocampal PVS, and of basal ganglia PVS and hippocampal PVS with stroke, accounting for blood pressure. Our findings provide insight into the biology of PVS and cerebral small vessel disease, pointing to pathways involving extracellular matrix, membrane transport and developmental processes, and the potential for genetically informed prioritization of drug targets.
| S-EPMC10115645 | biostudies-literature
Project description:Frailty is a common syndrome in older individuals that is associated with poor cognitive outcome. The underlying brain correlates of frailty are unclear. The aim of this study was to investigate the association between frailty and MRI features of cerebral small vessel disease in a group of non-demented older individuals. We included 170 participants who were classified as frail (n = 30), pre-frail (n = 85) or non-frail (n = 55). The association of frailty and white matter hyperintensity volume and shape features, lacunar infarcts and cerebral perfusion was investigated by regression analyses adjusted for age and sex. Frail and pre-frail participants were older, more often female and showed higher white matter hyperintensity volume (0.69 [95%-CI 0.08 to 1.31], p = 0.03 respectively 0.43 [95%-CI: 0.04 to 0.82], p = 0.03) compared to non-frail participants. Frail participants showed a non-significant trend, and pre-frail participants showed a more complex shape of white matter hyperintensities (concavity index: 0.04 [95%-CI: 0.03 to 0.08], p = 0.03; fractal dimensions: 0.07 [95%-CI: 0.00 to 0.15], p = 0.05) compared to non-frail participants. No between group differences were found in gray matter perfusion or in the presence of lacunar infarcts. In conclusion, increased white matter hyperintensity volume and a more complex white matter hyperintensity shape may be structural brain correlates of the frailty phenotype.
| S-EPMC6683288 | biostudies-literature
Project description:Background: Perivascular adipose tissue (PVAT) imaging can be used in clinical practice as a surrogate marker of vascular disease. We aimed to analyze the association between the density of carotid artery PVAT and clinical features and outcomes in stroke patients treated with mechanical thrombectomy. Methods: A total of 183 consecutive patients treated with mechanical thrombectomy due to anterior circulation large vessel occlusion were retrospectively included from January 2016 to May 2021. The density of carotid artery PVAT was evaluated by preoperative computed tomography angiography. Successful arterial recanalization was defined as a modified Thrombolysis in Cerebral Infarction score of 2b-3 on the final angiographic examination. Poor functional outcome was defined as a modified Rankin Scale (mRS) score > 2 at 3 months after stroke. We assessed the independent effect of carotid artery PVAT density on revascularization, functional outcome, and mortality using logistic regression models adjusted for relevant confounders. Results: Patients with large artery atherosclerotic stroke have higher carotid artery PVAT density than patients with other stroke etiologies (-65.82 ± 12.96 vs. -75.77 ± 13.44, P < 0.001). Higher carotid artery PVAT density was associated with unsuccessful recanalization [adjusted odds ratio (AOR) (95% CI), 2.968 (1.292, 6.819), P = 0.010], and poor outcome [AOR (95% CI), 2.704 (1.610, 4.541), P < 0.001] and mortality [AOR (95% CI), 1.894 (1.040, 3.449), P = 0.037] at 3 months in stroke patients treated with thrombectomy. Conclusion: Higher carotid artery PVAT density before mechanical thrombectomy is an indicator of worse postprocedural arterial revascularization and a worse functional outcome in acute stroke patients.
| S-EPMC8652413 | biostudies-literature
Project description:BackgroundCerebral small vascular disease (CSVD) is one of the leading causes of death in the aged population and is closely related to abnormalities in low-density lipoprotein cholesterol (LDL-C). Our study aims to clarify the relationship between small and dense low-density lipoprotein cholesterol (sdLDL-C) (a subcomponent of LDL-C) and neuroimaging markers of CSVD.MethodsIn total, 1211 Chinese adults aged ≥45 years with cranial magnetic resonance imaging (MRI) were recruited in this retrospective study from January 2018 to May 2021. Serum lipids and other baseline characteristics were investigated in relation to the occurrence of CSVD. A logistic regression model was performed to analyze the relationships between LDL subtypes and CSVD risk, and the Pearson correlation coefficient was used to analyze the correlation between clinical characteristics and CSVD risk. ROC curves and AUCs were created and depicted to predict the best cutoff value of LDL-C subtypes for CSVD risk. Based on these data, we performed comprehensive analyses to investigate the risk factors for CSVD.ResultsUltimately, 623 eligible patients were included in the present study. Of the 623 eligible patients, 487 were included in the CSVD group, and 136 were included in the group without CSVD (control group). We adjusted for confounders in the multivariate logistic regression model, and LDL-C3 was still higher in the CSVD patients than in the group of those without CSVD (OR (95% CI), 1.22(1.08-1.38), P < 0.05). Pearson correlation showed that there was a positive correlation between the levels of LDL-C3, LDL-C4, LDL-C5, glucose, age, hypertension, previous ischemic stroke and CSVD risk (r > 0.15, P < 0.01). Moreover, the best cutoff value of LDL-C3 to predict CSVD was 9.5 mg/dL with 68.4% sensitivity and 72.8% specificity, and the best cutoff value of LDL-C4 to predict CSVD was 5.5 mg/dL with 50.5% sensitivity and 90.4% specificity.ConclusionThe results indicate that LDL-C3 is an independent risk factor for CSVD. A new prediction model based on LDL-C3 and LDL-C4 can help clinicians identify high-risk CSVD, even in people with normal LDL-C levels. The levels of sdLDL-C should be considered in the assessment and management of CSVD.
| S-EPMC8576978 | biostudies-literature