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Objective: To determine the association between the burden of cerebral small vessel disease (CSVD) due to hypertensive angiopathy (HA) and cerebral amyloid angiopathy (CAA) on MRI in patients with primary intracerebral hemorrhage (ICH). Methods: Patients with primary ICH admitted to our center from March 2012 to November 2021 were consecutively enrolled. We used multivariate binary and ordinal regression analyses to assess the association between HA-CSVD burden and CAA-CSVD burden. Lobar cerebral microbleeds (CMBs) were categorized into three level of severity: 0--1, 2--4, and ≥ 5 lobar CMBs. A high CAA-CSVD score was defined as a CAA-CSVD score of ≥3. Results: Overall, 222 participants (mean age 59.88 ± 13.56) were included into analysis. Age and ICH etiology differed among different lobar CMB severity and between the presence and absence of high CAA-CSVD score (all p < 0.05). Positive associations between HA-related markers and both lobar CMB severity and high CAA-CSVD score (p < 0.05 for the presence of lacune, deep CMBs ≥5, the presence of WMH, and HA-CSVD score) were observed in univariate analysis. These associations remained significant after adjusting for age, sex, ICH etiology, and potential vascular risk factors. The distribution of CAA-CSVD score was significantly different between patients with and without CMBs ≥5 (adjusted OR 2.351, 95% CI 1.242--4.455, p = 0.009) after correcting for age, sex, ICH etiology, and vascular risk factors. Conclusion: Our study provides evidence of an association between HA-CSVD and CAA-CSVD in patients with primary ICH, which needs to be verified in future studies. [ABSTRACT FROM AUTHOR]

Background and Purpose: Small vessel disease (SVD) imaging markers are related to ischemic and hemorrhage stroke and to cognitive dysfunction. This study aimed to clarify the relationship between SVD imaging markers and subcortical vascular dementia in severe SVD burden. Methods: A total of 57 subjects with multiple lobar cerebral microbleeds (CMBs) and four established SVD imaging markers were enrolled from the dementia and stroke registries of a single center. Visual rating scales that are used to semi-quantify SVD imaging changes were analyzed individually and compositely to make correlations with cognitive domains and subcortical vascular dementia. Results: Dementia group had higher subcortical and total white matter hyperintensities (WMHs) and SVD composite scores than non-dementia group. Individual imaging markers correlated differently with one another and had distinct cognitive correlations. After adjusting for demographic factors, multivariate logistic regression indicated associations of subcortical WMHs (odds ratio [OR] 2.03, CI 1.24–3.32), total WMHs (OR 1.43, CI 1.09–1.89), lacunes (OR 1.18, CI 1.02–1.35), cerebral amyloid angiopathy-SVD scores (OR 2.33, CI 1.01–5.40), C1 scores (imaging composite scores of CMB and WMH) (OR 1.41, CI 1.09–1.83), and C2 scores (imaging composite scores of CMB, WMH, perivascular space, and lacune) (OR 1.38, CI 1.08–1.76) with dementia. Conclusions: SVD imaging markers might have differing associations with cognitive domains and dementia. They may provide valuable complementary information in support of personalized treatment planning against cognitive impairment, particularly in patients with a heavy SVD load. [ABSTRACT FROM AUTHOR]

Background and Purpose: Small vessel disease (SVD) imaging markers are related to ischemic and hemorrhage stroke and to cognitive dysfunction. This study aimed to clarify the relationship between SVD imaging markers and subcortical vascular dementia in severe SVD burden.Methods: A total of 57 subjects with multiple lobar cerebral microbleeds (CMBs) and four established SVD imaging markers were enrolled from the dementia and stroke registries of a single center. Visual rating scales that are used to semi-quantify SVD imaging changes were analyzed individually and compositely to make correlations with cognitive domains and subcortical vascular dementia.Results: Dementia group had higher subcortical and total white matter hyperintensities (WMHs) and SVD composite scores than non-dementia group. Individual imaging markers correlated differently with one another and had distinct cognitive correlations. After adjusting for demographic factors, multivariate logistic regression indicated associations of subcortical WMHs (odds ratio [OR] 2.03, CI 1.24–3.32), total WMHs (OR 1.43, CI 1.09–1.89), lacunes (OR 1.18, CI 1.02–1.35), cerebral amyloid angiopathy-SVD scores (OR 2.33, CI 1.01–5.40), C1 scores (imaging composite scores of CMB and WMH) (OR 1.41, CI 1.09–1.83), and C2 scores (imaging composite scores of CMB, WMH, perivascular space, and lacune) (OR 1.38, CI 1.08–1.76) with dementia.Conclusions: SVD imaging markers might have differing associations with cognitive domains and dementia. They may provide valuable complementary information in support of personalized treatment planning against cognitive impairment, particularly in patients with a heavy SVD load.

Background: The key imaging features of cerebral amyloid angiopathy (CAA) are lobar, cortical, or cortico-subcortical microbleeds, macrohaemorrhages and cortical superficial siderosis (cSS). In contrast, hypertensive angiopathy is characterized by (micro) haemorrhages in the basal ganglia, thalami, periventricular white matter or the brain stem. Another distinct form of haemorrhagic microangiopathy is mixed cerebral microbleeds (mixed CMB) with features of both CAA and hypertensive angiopathy. The distinction between the two entities (CAA and mixed CMB) is clinically relevant because the risk of haemorrhage and stroke should be well balanced if oral anticoagulation is indicated in CAA patients. We aimed to comprehensively compare these two entities. Methods: Patients with probable CAA according to the modified Boston criteria and mixed CMB without macrohaemorrhage were retrospectively identified from our database. Comprehensive comparison regarding clinical and radiological parameters was performed between the two cohorts. Results: Patients with CAA were older (78 ± 8 vs. 74 ± 9 years, p = 0.036) and had a higher prevalence of cSS (19% vs. 4%, p = 0.027) but a lower prevalence of lacunes (73% vs. 50%, p = 0.018) and deep lacunes (23% vs. 51%, p = 0.0003) compared to patients with mixed CMB. Logistic regression revealed an association between the presence of deep lacunes and mixed CMB. The other collected parameters did not reveal a significant difference between the two groups. Conclusions: CAA and mixed CMB demonstrate radiological differences in the absence of macrohaemorrhages. However, more clinically available biomarkers are needed to elucidate the contribution of CAA and hypertensive angiopathy in mixed CMB patients. [ABSTRACT FROM AUTHOR]

WWP2 is a HECT‐type E3 ubiquitin ligase that regulates various physiological and pathological activities by binding to different substrates, but its function and regulatory mechanism in vascular smooth muscle cells (VSMCs) are still unknown. Here, we clarified the role of WWP2 in the regulation of SIRT1‐STAT3 and the impact of this regulatory process in VSMCs. We demonstrated that WWP2 expression was significantly increased in angiotensin II‐induced VSMCs model. Knockdown of WWP2 significantly inhibited angiotensin II‐induced VSMCs proliferation, migration and phenotypic transformation, whereas overexpression of WWP2 had opposite effects. In vivo experiments showed that vascular smooth muscle‐specific WWP2 knockout mice significantly relieved angiotensin II‐induced hypertensive angiopathy. Mechanistically, mass spectrometry and co‐immunoprecipitation assays identified that WWP2 is a novel interacting protein of SIRT1 and STAT3. Moreover, WWP2 formed a complex with SIRT1‐STAT3, inhibiting the interaction between SIRT1 and STAT3, then reducing the inhibitory effect of SIRT1 on STAT3, ensuing promoting STAT3‐K685 acetylation and STAT3‐Y705 phosphorylation in angiotensin II‐induced VSMCs and mice. In conclusion, WWP2 modulates hypertensive angiopathy by regulating SIRT1‐STAT3 and WWP2 suppression in VSMCs can alleviate hypertensive angiopathy vitro and vivo. These findings provide new insights into the treatment of hypertensive vascular diseases. [ABSTRACT FROM AUTHOR]

Vascular smooth muscle cells (VSMCs) proliferation and migration play a fundamental role during the process of hypertensive angiopathy. Angiotensin-II (Ang-II) is one of the robust phenotype-modulating agents, which changes VSMCs to efficiently proliferate and migrate. The mechanism of the proliferation and migration is not well understood yet. Septin4, as a member of GTP binding protein family, is widely expressed in the eukaryotic cells and considered to be an essential component of the cytoskeleton which is involved in many important physiological processes. We approved that Septin4 expression was upregulated in mouse aorta by continuous infusion of Ang-II and in cultured VSMCs treated with Ang-II. Overexpression of Septin4 led to lower level of autophagy and decreased capacity of proliferation and migration. In order to identify the mechanism by which Septin4 interacts with these processes, we blocked autophagy by chloroquine (CQ). After inhibiting the autophagy, the ability of proliferation and migration was further restrained in the Septin4 overexpression VSMCs. In conclusion, our results indicated that during the process of VSMCs proliferation and migration induced by Ang-II, Septin4 modulated autophagy and thus regulated the activity of proliferation and migration. • Septin4 was up-regulated in mice aortas in Ang-II induced vascular injury. • Septin4 inhibited the proliferation and migration of VSMCs stimulated by Ang-II. • Septin4 attenuated the promotion effect of Ang-II upon autophagic activity. • Septin-4 suppressed the proliferation and migration of VSMCs stimulated by Ang-II through modulating autophagy. [ABSTRACT FROM AUTHOR]

Objective: To determine the association between the burden of cerebral small vessel disease (CSVD) due to hypertensive angiopathy (HA) and cerebral amyloid angiopathy (CAA) on MRI in patients with primary intracerebral hemorrhage (ICH)., Methods: Patients with primary ICH admitted to our center from March 2012 to November 2021 were consecutively enrolled. We used multivariate binary and ordinal regression analyses to assess the association between HA-CSVD burden and CAA-CSVD burden. Lobar cerebral microbleeds (CMBs) were categorized into three level of severity: 0-1, 2-4, and ≥ 5 lobar CMBs. A high CAA-CSVD score was defined as a CAA-CSVD score of ≥3., Results: Overall, 222 participants (mean age 59.88 ± 13.56) were included into analysis. Age and ICH etiology differed among different lobar CMB severity and between the presence and absence of high CAA-CSVD score (all p  < 0.05). Positive associations between HA-related markers and both lobar CMB severity and high CAA-CSVD score ( p  < 0.05 for the presence of lacune, deep CMBs ≥5, the presence of WMH, and HA-CSVD score) were observed in univariate analysis. These associations remained significant after adjusting for age, sex, ICH etiology, and potential vascular risk factors. The distribution of CAA-CSVD score was significantly different between patients with and without CMBs ≥5 (adjusted OR 2.351, 95% CI 1.242-4.455, p  = 0.009) after correcting for age, sex, ICH etiology, and vascular risk factors., Conclusion: Our study provides evidence of an association between HA-CSVD and CAA-CSVD in patients with primary ICH, which needs to be verified in future studies., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision., (Copyright © 2023 Zhu, Liu, Zhong, Cheng, Zhang, Wu, Wang and Xu.)

Purpose: to evaluate the diagnostic capability of automated retinal vessels (RV) caliber estimation for hypertensive angiopathy.Methods: this study included 146 patients (292 eyes) with arterial hypertension. All the subjects underwent fundus photography and RV caliber estimation. the latter was performed using newly developed computer-based method for automated vessel detection and central retinal arteriolar and venular equivalents determination (CRAE & CRVE). Sensitivity, specificity, and reproducibility of the method were estimated.Results: the method of RV caliber assessment showed good reproducibility. the overall specificity and sensitivity were 74% and 80.77%, respectively. Computer-based method of retinal vascular caliber assessment revealed higher predictive value comparing with ophthalmoscopic assessment (AUC = 0.903 and 0.85, respectively). Retinal arteriolar and venular caliber and AVR tend to decrease with age. Higher blood pressure is associated with narrower retinal arterioles.Conclusion: Novel method of RV caliber estimation demonstrated high information value. these findings are in good agreementwith data from major population-based studies.

PURPOSE: To investigate, through an immunohistochemical method, whether there is deposition of plasma proteins in the wall of lenticulostriate, cortical and leptomeningeal arteries of hypertensive patients, with and without lipohyalinosis. METHOD: Forty patients with essential hypertension were selected at random, 20 with lipohyalinosis in the lenticulostriate arteries (HH group) and 20 without lipohyalinosis (H group), matched with 20 normotensive controls (C group). RESULTS: Plasma protein deposits were identified in eight patients (40%) in the C group, in 15 patients (75%) in the H group, and in all 20 patients (100%) in the HH group, the difference being significant for the H group and highly significant for the HH group, as compared with the C group. In all groups, the distribution of plasma protein deposits, subendothelial in normal arteries, and diffuse, irregular in the wall of arteries with lipohyalinosis, was more frequent in the lenticulostriate arteries of the putamen. CONCLUSION: Deposition of plasma proteins in the lenticulostriate arteries seems to be relatively frequent in normotensive individuals, starting in middle age. Such process appears to be intensified by hypertension, especially in individuals with lipohyalinosis.PROPÓSITO: Investigar, por meio de método imuno-histoquímico, a deposição de proteínas plasmáticas na parede das artérias lentículo-estriadas, corticais e leptomeníngeas em pacientes com hipertensão arterial, com e sem lipo-hialinose. MÉTODO: Quarenta pacientes com hipertensão arterial foram selecionados aleatoriamente, sendo 20 com lipo-hialinose nas artérias lentículo-estriadas (grupo HH) e 20 sem lipo-hialinose (grupo H), pareados com 20 controles normotensos (grupo C). RESULTADOS: Depósitos de proteínas plasmáticas foram identificados em oito pacientes (40%) do grupo C, em 15 pacientes (75%) do grupo H e em todos os 20 pacientes (100%) do grupo HH, a diferença sendo significativa para o grupo H e altamente significativa para o grupo HH, quando comparada com o grupo C. Em todos os grupos, a distribuição dos depósitos de proteínas plasmáticas, subendotelial em artérias normais e difusa, irregular, na parede das artérias com lipo-hialinose, foi mais freqüente nas artérias lentículo-estriadas do putâmen. CONCLUSÃO: A deposição de proteínas plasmáticas nas artérias lentículo-estriadas parece ser um fenômeno relativamente freqüente em indivíduos normotensos, a partir da meia-idade. Tal processo parece ser intensificado pela hipertensão arterial, particularmente naqueles pacientes com lipo-hialinose.

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Abstract: This article reviews the epidemiology, pathophysiology and management of primary intracerebral hemorrhage. In North American and European populations, 15% of strokes are due to intracerebral hemorrhage. Pathologically in hypertension, early arteriolar proliferation of smooth muscle is followed later by smooth muscle cell death and collagen deposition. This eventually leads to occlusion or ectasia of arterioles. The latter leads to Charcôt-Bouchard aneurysm formation and possible intracerebral hemorrhage. Amyloid deposition in the tunica media causes similar brittle arterioles. Fibrin globes in concentric spheres attempt to seal off the site of bleeding. But vasculopathy (either amyloid or hypertensive) inhibits the contractile capability of arterioles. The size of the final sphere of blood at cessation of bleeding determines the clinical spectrum, from asymptomatic to fatal. Since arteriolar bleeding is slower than arterial bleeding, several hours exist where intervention may be useful. While medical intervention is controversial, guidelines for blood pressure, intracranial pressure, glucose and seizure management exist. Surgical trials have tended to show no benefit. Recombinant factor VIIa is undergoing investigation as hemostatic therapy for intracerebral hemorrhage, to limit clot expansion and possibly also as a hemostatic adjunct to surgery. [Copyright &y& Elsevier]

Brain microbleeds are defined as small, circular hypointense changes in T2-sequensec of brain MRI, well demarcated from the surrounding tissue. They represent the phagocytized products of blood distribution extravasated from pathologically altered vessels. The echo-T2-dependent gradient (GRE) and magnetic susceptibility testing (SWI) sequences are usually used to visualize them. The pathogenesis of microbleeds very complex but angiopathy associated with arterial hypertension and cerebral amyloid angiopathy play a special role. Atherosclerotic lesions and inflammatory processes are also important. Microbleeds can be found in healthy people as well as in many disorders such as hypertension, Alzheimer's disease or other types of dementia. Their prevalence increases with age. Microbleeds may have a multidimensional effect on the surrounding brain tissue. It is suggested that they disrupt both the brain structure and the electrical function of neurons. In this review article we present current knowledge on the cerebral microbleeds.