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Background: Breakthrough neurotechnologies have allowed for new understanding of some brain disorders; however, identification and differential diagnosis of intracranial stenotic and occlusive lesions remains challenging. Magnetic resonance imaging (MRI) with dynamic contrast enhancement (DCE) is a tool that could be used for the quantitative assessment of endothelial permeability and microvascular volume in atherosclerotic plaques (AP). Aim: To assess quantitative parameters of vascular wall abnormalities in AP area and in obviously unchanged wall of intracranial arteries with MRI DCE and high spatial resolution Т1-weighed images before and after contrast injection, with calculation of the wall enhancement index (WEI) by mathematical modelling. Methods: This was a pilot cross-sectional uncontrolled study with consecutive recruitment of 29 patients with atherosclerotic abnormalities of brachiocephalic arteries, including intracranial. The patients’ median age was 66 [57; 72] years; they were mostly men (75.9%, n = 22). For the assessment of any brain abnormalities, MRI (magnetic induction 3 Tesla, Magnetom Prisma, Siemens) was performed in patients with standard sequence (Т2, T2-FLAIR), as well as MRI DCE for the assessment of intracranial arteries, before and after intravenous contrast injection, with high spatial resolution T1-weighed imaging and suppression of the signal from bloodstream and fat, with the calculation of WEI. Results: There were significant differences in WEI in AP and in unchanged wall (0.962 [0.686; 1.387] vs. 0.111 [0.014; 0.206], p 0.001). No significant differences were found between WEI values in internal carotid arteries APs (0.722 [0.573; 1.580]), middle cerebral arteries (0.921 [0.725; 1.183]), and basilar artery (1.343 [1.002; 1.419]) (p = 0.381). We also found significant difference (p = 0.034) in the extravascular extracellular fraction volumes ve (Tofts) in AP located in the basilar artery (0.171 [0.146; 0.325]), internal carotid arteries (0.579 [0.358; 1.000]), and middle cerebral arteries (0.134 [0.101; 0.269]). Conclusion: This is the first description of quantitative parameters characterizing vascular wall abnormalities in intracranial atherosclerosis. Despite its obviously intact state, vascular walls outside the intracranial AP was shown to be abnormal as well.

Fibrosis is usually the final pathological state of many chronic inflammatory diseases and may lead to organ malfunction. Excessive deposition of extracellular matrix (ECM) molecules is a characteristic of most fibrotic tissues. The blood vessel wall contains three layers of membrane structure, including the intima, which is composed of endothelial cells; the media, which is composed of smooth muscle cells; and the adventitia, which is formed by the interaction of connective tissue and fibroblasts. The occurrence and progression of vascular remodeling are closely associated with cardiovascular diseases, and vascular remodeling can alter the original structure and function of the blood vessel. Dysregulation of the composition of the extracellular matrix in blood vessels leads to the continuous advancement of vascular stiffening and fibrosis. Vascular fibrosis reaction leads to excessive deposition of the extracellular matrix in the vascular adventitia, reduces vessel compliance, and ultimately alters key aspects of vascular biomechanics. The pathogenesis of fibrosis in the vasculature and strategies for its reversal have become interesting and important challenges. Ion channels are widely expressed in the cardiovascular system; they regulate blood pressure, maintain cardiovascular function homeostasis, and play important roles in ion transport, cell differentiation, proliferation. In blood vessels, different types of ion channels in fibroblasts, smooth muscle cells and endothelial cells may be relevant mediators of the development of fibrosis in organs or tissues. This review discusses the known roles of ion channels in vascular fibrosis remodeling and discusses potential therapeutic targets for regulating remodeling and repair after vascular injury.

IntroductionTransplant vasculopathy (TV) is a major complication after solid organ transplantation, distinguished by an arterial intimal thickening that obstructs the vascular lumen and leads to organ rejection. To date, TV remains largely untreatable, mainly because the processes involved in its development remain unclear. Aortic transplantation in mice, used to mimic TV, relies on highly variable experimental protocols, particularly regarding the type of anastomosis used to connect the donor aorta to the recipient. While the amount of trauma undergone by a vessel can dramatically affect the resulting pathology, the impact of the type of anastomosis on TV in mice has not been investigated in detail.MethodsIn this study, we compare the cellular composition of aortic grafts from BALB/C donor mice transplanted into C57BL/6J recipient mice using two different anastomosis strategies: sleeve and cuff.ResultsWhile both models recapitulated some aspects of human TV, there were striking differences in the cellular composition of the grafts. Indeed, aortic grafts from the cuff group displayed a larger coverage of the neointimal area by vascular smooth muscle cells compared to the sleeve group. Aortic grafts from the sleeve group contained higher amounts of T cells, while the cuff group displayed larger B-cell infiltrates.DiscussionTogether, these data indicate that a seemingly minor technical difference in transplant surgery protocols can largely impact the cellular composition of the graft, and thus the mechanisms underlying TV after aortic transplantation in mice.

Background: The displacements and strains in the cylindrical coordinate system provide information easier to correlate to the pathologic feature of the tubular blood vessel than those in the Cartesian coordinate system. However, distortions and speckle decorrelation have obstructed accurate vascular strain measurement. Objective: This study is to introduce an improved optical coherence elastography (OCE) method based on digital volume correlation (DVC) and correction of distortions to measure the full-field vascular deformation. Methods: Refractive index normalization together with refractive distortion correction based on the Fermat's principle was proposed to recover the actual shape of the vascular wall imaged by optical coherence tomography (OCT). Meanwhile, the displacement fields calculated by DVC were also corrected. The cylindrical coordinate system was created with the origin at the central line of the vascular phantom or sample. Then the full-field 3D displacements in cylindrical coordinates were obtained through coordinate transformation and strains were calculated. Results: A vascular phantom and a porcine artery inflated from 80 mmHg to 85 mmHg were measured. 3D intramural displacements and strains were obtained. The absolute difference between the measured and theoretically calculated strains of the phantom is less than 0.2%. The standard deviation is less than 0.2% as well. A stripe is shown on the radial strain image, which is consistent with the feature of the layered structure. Conclusions: To the best of our knowledge, this is the first experimental study of the 3D intramural vascular deformation under inflation. The proposed DVC-OCE method based on distortion correction and coordinate transformation has the potential to be further developed as an effective full-field nondestructive measurement method of vascular mechanics. [ABSTRACT FROM AUTHOR]

Background: Determination of predictors that can affect development of atherosclerosis progression in the postoperative period is an urgent problem in vascular surgery. Objectives: Integrated assessment of markers of apoptosis and cell proliferation in atherosclerotic lesions and their progression after surgery in patients with peripheral arterial diseases. Methods: The investigation included 30 patients with stage IIB-III peripheral arterial disease. All patients have undergone open surgical interventions on the arteries of the aorto-iliac and femoral-popliteal segments. During these interventions, intraoperative specimens were obtained from the vascular wall with atherosclerotic lesions. The following values were evaluated: VEGF A165, PDGF BB, and sFas. Samples of normal vascular wall were obtained from post-mortem donors and used as a control group. Results: The levels of Bax and p53 were increased (p<0.001) in samples from arterial wall with atherosclerotic plaque, while sFas values were reduced (p<0.001), compared to their levels in control samples. Values of PDGF BB and VEGF A165 were 1.9 and 1.7 times higher in atherosclerotic lesion samples (p=0.001), in comparison with the control group. The levels of p53 and Bax were increased against a background of reduced sFas levels in samples with progression of atherosclerosis compared to their baseline values in samples with atherosclerotic plaque (p<0.05). Conclusions: Initially increased values of the Bax marker against a background of reduced sFas values in vascular wall samples from patients with peripheral arterial disease is associated with risk of atherosclerosis progression in the postoperative period. [ABSTRACT FROM AUTHOR]

Nowadays, cardiovascular diseases (CVDs) occupy a leading position in population mortality. Since it is known that the development of cardiovascular pathologies is determined mainly by the human genetic burden, an urgent task of primary prevention of CVDs is to assess the contribution of gene polymorphism to the formation of cardiovascular risk. The material for the study was the blood of volunteers aged 21 to 102 years. Polymorphisms were determined by real–time PCR. Multichannel volumetric sphygmography was performed to analyze the functional state of the vascular wall. The study revealed that the rs5742904 polymorphism of the ApoB gene was found to be absent in the studied groups of long-livers and descendants of long-livers. Results indicated that the carriage of the heterozygous variant of the MMP9 polymorphism is associated with a favorable prognosis for cardiovascular system functioning. A tendency towards an increase in the rate of biological age acceleration among subgroups with AA and GG genotypes of the MMP9 gene and a negative value of biological age acceleration among heterozygous carriers of this polymorphism allele were found. The conducted studies make it possible to identify new associations of the studied polymorphisms with the functional state of the cardiovascular system, which is of great clinical importance and requires further study. [ABSTRACT FROM AUTHOR]

Abstract Background Determination of predictors that can affect development of atherosclerosis progression in the postoperative period is an urgent problem in vascular surgery. Objectives Integrated assessment of markers of apoptosis and cell proliferation in atherosclerotic lesions and their progression after surgery in patients with peripheral arterial diseases. Methods The investigation included 30 patients with stage IIB-III peripheral arterial disease. All patients have undergone open surgical interventions on the arteries of the aorto-iliac and femoral-popliteal segments. During these interventions, intraoperative specimens were obtained from the vascular wall with atherosclerotic lesions. The following values were evaluated: VEGF А165, PDGF BB, and sFas. Samples of normal vascular wall were obtained from post-mortem donors and used as a control group. Results The levels of Bax and p53 were increased (p

Vascular wall resident stem cells (VW-SCs) play a key role in vascular formation and remodeling under both physiological and pathological situations. They not only serve as a reservoir to supply all types of vascular cells needed, but also regulate vascular homeostasis by paracrine effects. Venous malformations (VMs) are common congenital vascular malformations which are just characterized by the deficient quantity and abnormal function of vascular cells. However, the existence and role of VW-SCs in VMs is still unclear at present. In this study, the level and distribution of VW-SCs in 22 specimens of VMs were measured by immunochemistry, double-labeling immunofluorescence, and qPCR, followed by the Spearman rank correlation test. We found that both the protein and mRNA expression levels of CD34, vWF, VEGFR2, CD44, CD90, and CD105 were significantly downregulated in VMs compared with that in normal venules. VW-SCs were sporadically distributed or even absent within and outside the endothelium of VMs. The expression of the VW-SC-related markers was positively correlated with the density of both endothelial cells and perivascular cells. All those results and established evidence indicated that VW-SCs were more sporadically distributed with fewer amounts in VMs, which possibly contributing to the deficiency of vascular cells in VMs. [ABSTRACT FROM AUTHOR]

Aim: To create a device for PWPV evaluation which would be cheap and could be easily used not only at the inpatient but also at the restorative outpatient and health-resort stages of rehabilitation. materials and methods: The clinical examination included 90 people who were randomized into the group of observation (n=75) with patients of AH various degrees. 15 practically healthy persons were involved into the control group. PWPV was measured using a specially designed device according to the generally accepted carotid-femoral technique. Results: Our results showed that the PWPV of healthy persons measured using original device failed to differ statistically from the literature reference values and indicated the correspondence of the measurements we obtained with the data received using traditional apparatus. Out data of original PWPV measurement obtained from examined and treated patients do not differ from the results obtained in wide range of patients aged from 40 to 70 years with the 1st -2nd stages of AH. Conclusions: We described an efficacy of PWPV determination using an original device. The use of the proposed device does not contradict with the generally accepted method of vascular stiffness measuring and studying. The results obtained on it are comparable with the data of the most used stationary device SphygmoCor for these purposes. The prospects of the device using are without the limitations in patients with vascular diseases at the stage of rehabilitation. [ABSTRACT FROM AUTHOR]

• Morphology of cerebral blood vessels is provided by label-free in vivo SHG imaging. • Type III collagen in vascular wall is dominant signal source to SHG imaging. • Early and subtle dynamics in vascular wall can be identified by in vivo SHG imaging after local ischemia. Second harmonic generation (SHG) imaging is label-free and non-invasive, and it has been extensively applied in multiple biological and medical studies, but not in the brain in vivo. In this study, we modified classical two photon excited fluorescence (TPEF) system to perform in vivo simultaneous TPEF and SHG imaging in the local ischemia mouse model. In cerebral vascular walls, we found strong SHG signal, which co-localized with collagen. In the continuous 2 days' in vivo imaging, this SHG signal remained stable in the local ischemic blood vessel in the initial 4 h, then its signal abruptly increased and got spatially thickened 5 h after thrombosis, and this tendency continued in the following 48 h. This study provides direct and precise timeline of rapid collagen change in cerebral vascular walls in vivo , and reveals the subtle but significant temporal-spatial dynamics of this structural signal during local ischemia. Thus, this cerebral in vivo SHG imaging provides a powerful tool to identify the early and subtle pathological change of collagen around clinical key therapeutic time window. [ABSTRACT FROM AUTHOR]

The aim. To analyze the frequency of atherosclerotic lesions of the carotid arteries and association with the lipid metabolism and inflammatory markers in hypertensive patients with gout. Materials and methods. 122 patients with hypertension aged 30 to 65 years were examined (mean age (56.0 (47.0; 62.0)), inclu­ding 104 men (85.2 %) and 18 women (14.8 %). Group 1 included 72 hypertensive patients with gout; group 2 – 50 hypertensive patients without gout; group 3 – 20 gout patients without hypertension. Serum levels of high sensitivity C-reactive protein were detected by enzyme-linked immunosorbent assay. Serum ferritin levels were measured using electrochemiluminescent detection. The patients underwent carotid artery ultrasound according to standard methods. Results. The duration of gout exacerbation and the pain intensity evaluated with the visual analog scale (VAS) (P < 0.01) were significantly higher in group 1, than those in group 3 (P < 0.01). Serum ferritin levels were 2.6 (P < 0.01) times higher in group 1 than those in group 2. In patients with gout, the levels of ferritin were significantly 2.1 times higher, than in group 2 (P < 0.01). The levels of hsСRP in patients of group 1 were 3.1 times higher than those in group 2 (P < 0.01). The proportion of patients with intima-media complex (IMC) thickness ≥0.9 mm was higher in group 1 than in groups 2 (χ2 = 4.58, P < 0.05) and 3 (χ2 = 24.96, P < 0.01). In the structure of plaques, isoechoic were significantly more often seen among group 1 patients as compared to group 3 (χ2 = 6.56, P < 0.01), and hyperechoic – as compared to group 2 (χ2 = 4.63, P < 0.05). Hypoechoic plaques were detected in groups 1 and 2 with similar frequency (P > 0.05). This type of plaque was associated with a high risk of cerebrovascular events. In the patients with arterial hypertension and gout, a significant moderate positive correlation was found between the IMC thickness and the serum uric acid level (rs = 0.46, P < 0.01), hsCRP (rs = 0.33, P < 0.01), age (rs = 0.33; P < 0.01), duration of gout (rs = 0.27, P < 0.05) and VAS (rs = 0.39, P < 0.01); the level of hsCRP was correlated with the presence of atherosclerotic plaques (τ = +0.64, P < 0.05). Conclusions. The combination of hypertension with gout in patients was associated with a high incidence of IMC thickness ≥0.9 mm and atherosclerotic plaques, more severe disorders of purine and lipid metabolism, increased inflammatory markers (ferritin and hsCRP), that should be considered not only in the aspect of chronic inflammation, but also as a part of the disease.

Assesment of arterial stiffness the substantional prognostic factor for evaluating complications of cardiovascular diseases (CVD) in patients with atherosclerosis, hypertension and type 2 diabetes, may be performed using different parameters, including cardio-ankle vascular index (CAVI). The main purpose of this review is to analyze data from studies where CAVI is used to test the arterial wall stiffness in magistral vessels. CAVI measurement is non-invasive and performed by portable devices which makes it comfortable for ambulatory use in patients who come for a check-up and also in those who already are hospitalized. It does not require any special knowledge from investigator and the test lasts a couple of minutes long. CAVI does not depend on blood pressure changes and is more specific in structural changes of arterial wall assessment than brachial-ankle pulse wave velocity (baPWV). CAVI shows considerable correlation with markers of CVD like atherosclerotic plaques in vessels, diastolic disfunction of left ventricle and angina pectoris. CAVI may be used for early monitoring and assessing the lesions of target organs in patients with atherosclerosis, chronic hypertension and type 2 diabetes. Establishing CAVI as a standart parameter in assessing patients who are at risk of CVD can help to improve complications prevention, reduce mortality and prolong their lifespan.

Fibrosis is usually the final pathological state of many chronic inflammatory diseases and may lead to organ malfunction. Excessive deposition of extracellular matrix (ECM) molecules is a characteristic of most fibrotic tissues. The blood vessel wall contains three layers of membrane structure, including the intima, which is composed of endothelial cells; the media, which is composed of smooth muscle cells; and the adventitia, which is formed by the interaction of connective tissue and fibroblasts. The occurrence and progression of vascular remodeling are closely associated with cardiovascular diseases, and vascular remodeling can alter the original structure and function of the blood vessel. Dysregulation of the composition of the extracellular matrix in blood vessels leads to the continuous advancement of vascular stiffening and fibrosis. Vascular fibrosis reaction leads to excessive deposition of the extracellular matrix in the vascular adventitia, reduces vessel compliance, and ultimately alters key aspects of vascular biomechanics. The pathogenesis of fibrosis in the vasculature and strategies for its reversal have become interesting and important challenges. Ion channels are widely expressed in the cardiovascular system; they regulate blood pressure, maintain cardiovascular function homeostasis, and play important roles in ion transport, cell differentiation, proliferation. In blood vessels, different types of ion channels in fibroblasts, smooth muscle cells and endothelial cells may be relevant mediators of the development of fibrosis in organs or tissues. This review discusses the known roles of ion channels in vascular fibrosis remodeling and discusses potential therapeutic targets for regulating remodeling and repair after vascular injury.

Background: Determination of predictors that can affect development of atherosclerosis progression in the postoperative period is an urgent problem in vascular surgery. Objectives: Integrated assessment of markers of apoptosis and cell proliferation in atherosclerotic lesions and their progression after surgery in patients with peripheral arterial diseases. Methods: The investigation included 30 patients with stage IIB-III peripheral arterial disease. All patients have undergone open surgical interventions on the arteries of the aorto-iliac and femoral-popliteal segments. During these interventions, intraoperative specimens were obtained from the vascular wall with atherosclerotic lesions. The following values were evaluated: VEGF A165, PDGF BB, and sFas. Samples of normal vascular wall were obtained from post-mortem donors and used as a control group. Results: The levels of Bax and p53 were increased (p<0.001) in samples from arterial wall with atherosclerotic plaque, while sFas values were reduced (p<0.001), compared to their levels in control samples. Values of PDGF BB and VEGF A165 were 1.9 and 1.7 times higher in atherosclerotic lesion samples (p=0.001), in comparison with the control group. The levels of p53 and Bax were increased against a background of reduced sFas levels in samples with progression of atherosclerosis compared to their baseline values in samples with atherosclerotic plaque (p<0.05). Conclusions: Initially increased values of the Bax marker against a background of reduced sFas values in vascular wall samples from patients with peripheral arterial disease is associated with risk of atherosclerosis progression in the postoperative period. [ABSTRACT FROM AUTHOR]

Aim. To study the relationship between telomerase activity and parameters of carbohydrate metabolism and vascular wall depending on the type 2 diabetes (T2D).Material and methods. The study included 50 patients with T2D and 139 healthy volunteers. All subjects were assessed for carbohydrate metabolism, chronic inflammation (C-reactive protein (CRP), fibrinogen), endothelial dysfunction, carotid intima-media thickness and number of atherosclerotic plaques by duplex scanning, carotid-femoral pulse wave velocity, lymphocyte telomere length and telomerase activity.Results. In T2D patients, telomerase activity was lower (p=0,039), telomeres were shorter (p=0,031) and CRP level was higher (p=0,031) than in patients without T2D. All patients were divided by telomerase activity. T2D patients with low telomerase activity had higher values of CRP (р=0,016), pulse wave velocity (р=0,010), carotid intima-media thickness (р

Objective . The widespread adoption of Photoplethysmography (PPG) as a non-invasive method for detecting blood volume variations and deriving vital physiological parameters reflecting health status has surged, primarily due to its accessibility, cost-effectiveness, and non-intrusive nature. This has led to extensive research around this technique in both daily life and clinical applications. Interestingly, despite the existence of contradictory explanations of the underlying mechanism of PPG signals across various applications, a systematic investigation into this crucial matter has not been conducted thus far. This gap in understanding hinders the full exploitation of PPG technology and undermines its accuracy and reliability in numerous applications. Approach . Building upon a comprehensive review of the fundamental principles and technological advancements in PPG, this paper initially attributes the origin of PPG signals to a combination of physical and physiological transmission processes. Furthermore, three distinct models outlining the concerned physiological transmission processes are synthesized, with each model undergoing critical examination based on theoretical underpinnings, empirical evidence, and constraints. Significance . The ultimate objective is to form a fundamental framework for a better understanding of physiological transmission processes in PPG signal generation and to facilitate the development of more reliable technologies for detecting physiological signals., (© 2024 Institute of Physics and Engineering in Medicine. All rights, including for text and data mining, AI training, and similar technologies, are reserved.)

Aim. To develope and justify the use of the abbreviated protocol of ultrasound duplex scanning (DS) of the carotid arteries (CA) to detect atherosclerotic changes in the carotid system in various groups of cardiovascular risk and to reduce the time of DS, based on solving a “narrow” task — identifying an atheroma.Material and methods. Ultrasound CA examination was carried out in the department of ultrasound studying methods in National Medical Research Center of Cardiology. Forty three patients aged 32 to 81 years (mean 56±13 years) who are hospitalized in A. L. Myasnikov Institute of Clinical Cardiology Institute of Clinical Cardiology were examined. DS was performed with the use of the ultrasonic system “IU 22” (Philips) with a linear sensor with 3-9 MHz. Three types of DS protocol were used — standard protocol (with automatic measurement of intima-media thickness (IMT) of common carotid artery (CCA)), abbreviated protocol 2 (atheroma and IMT of CCA), abbreviated protocol 1 (atheroma).Results. The work showed a decrease in DS time when conducting a abbreviated protocol 2 by 32,1% or 1,5 times, a shortened protocol 1 — by 72,1% or approximately 3,5 times compared with the standard DS protocol, while the efficiency of atheroma detecting has not decreased. A decision-making algorithm has been developed on the basis of conducting an ultrasound SA examination using abbreviated protocols.Conclusion. The introduction of a abbreviated protocol of ultrasound DS will significantly reduce the time and increase the cost-effectiveness of early diagnosis of atherosclerosis.

Introduction: Transplant vasculopathy (TV) is a major complication after solid organ transplantation, distinguished by an arterial intimal thickening that obstructs the vascular lumen and leads to organ rejection. To date, TV remains largely untreatable, mainly because the processes involved in its development remain unclear. Aortic transplantation in mice, used to mimic TV, relies on highly variable experimental protocols, particularly regarding the type of anastomosis used to connect the donor aorta to the recipient. While the amount of trauma undergone by a vessel can dramatically affect the resulting pathology, the impact of the type of anastomosis on TV in mice has not been investigated in detail., Methods: In this study, we compare the cellular composition of aortic grafts from BALB/C donor mice transplanted into C57BL/6J recipient mice using two different anastomosis strategies: sleeve and cuff., Results: While both models recapitulated some aspects of human TV, there were striking differences in the cellular composition of the grafts. Indeed, aortic grafts from the cuff group displayed a larger coverage of the neointimal area by vascular smooth muscle cells compared to the sleeve group. Aortic grafts from the sleeve group contained higher amounts of T cells, while the cuff group displayed larger B-cell infiltrates., Discussion: Together, these data indicate that a seemingly minor technical difference in transplant surgery protocols can largely impact the cellular composition of the graft, and thus the mechanisms underlying TV after aortic transplantation in mice., 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. Authors NS and ADB 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., (© 2024 Mickiewicz, Zahreddine, Cormier, Peries, Del Bello, Laffargue and Smirnova.)

Cell-based therapies using adult stem cells are promising options for the treatment of a number of diseases including autoimmune and cardiovascular disorders. Among these, vascular wall-derived mesenchymal stem cells (VW-MSCs) might be particularly well suited for the protection and curative treatment of vascular damage because of their tissue-specific action. Here we report a novel method for the direct conversion of human skin fibroblasts towards MSCs using a VW-MSC-specific gene code (HOXB7, HOXC6 and HOXC8) that directs cell fate conversion bypassing pluripotency. This direct programming approach using either a self-inactivating (SIN) lentiviral vector expressing the VW-MSC-specific HOX-code or a tetracycline-controlled Tet-On system for doxycycline-inducible gene expressions of HOXB7, HOXC6 and HOXC8 successfully mediated the generation of VW-typical MSCs with classical MSC characteristics in vitro and in vivo. The induced VW-MSCs (iVW-MSCs) fulfilled all criteria of MSCs as defined by the International Society for Cellular Therapy (ISCT). In terms of multipotency and clonogenicity, which are important specific properties to discriminate MSCs from fibroblasts, iVW-MSCs behaved like primary ex vivo isolated VW-MSCs and shared similar molecular and DNA methylation signatures. With respect to their therapeutic potential, these cells suppressed lymphocyte proliferation in vitro, and protected mice against vascular damage in a mouse model of radiation-induced pneumopathy in vivo, as well as ex vivo cultured human lung tissue. The feasibility to obtain patient-specific VW-MSCs from fibroblasts in large amounts by a direct conversion into induced VW-MSCs could potentially open avenues towards novel, MSC-based therapies. [ABSTRACT FROM AUTHOR]

The organ-on-a-chip model mimics the structural and functional features of human tissues or organs and has great importance in translational research. For vessel-on-a-chip model, conventional fabrication techniques are unable to efficiently imitate the intimal-medial unit of the vessel wall. Bioprinting technology, which can precisely control the organization of cells, biomolecules, and the extracellular matrix, has the potential to fabricate three-dimensional (3D) tissue constructs with spatial heterogeneity. In this study, we applied the gelatin-methacryloyl-based bioprinting technology to print 3D construct containing endothelial cells (ECs) and smooth muscle cells (SMCs) on a microfluidic chip. Compared with traditional culture system, EC-SMC coculturing chip model upregulated αSMA and SM22 protein expression of the SMC to a greater degree and maintains the contractile phenotype of the SMC, which mimics the natural vascular microenvironment. This strategy enabled us to establish an in vitro vascular model for studies of the physiologic and pathologic process in vascular wall. [ABSTRACT FROM AUTHOR]

Success haemocirculation largely determines the overall physiological and biological status of newborn calves and is very largely due to the peculiarities of platelet aggregation and blood neutrophils and severity of control over it by the vascular wall. The goal - to establish the severity of antiaggregation opportunities vascular effects on platelets and neutrophils in newborn calves during the phase. The study was performed on 32 calves black-motley and Simmental breeds made in research on the 1-2 days of life. The examination was performed during the neonatal phase fivefold - 1-2, 3-4, 5-6, 7-8 and 9-10 days of life with hematologic and statistical methods. Throughout the newborn calves marked by low platelet aggregation at the uptrend their sensitivity to disaggregate effects of the vascular wall. Indistinct aggregation of neutrophils in colostric power calves effectively constrained by severe vascular antiplatelet activity. Thus, for the newborn calves characterized physiologically justified balance of platelet aggregation and blood neutrophils and disaggregating control over it from the vascular wall.

Background: Contrast enhancement of intracranial aneurysm wall during MRI with targeted visualization of vascular wall correlates with previous aneurysm rupture and, according to some data, may be a predictor of further rupture of unruptured aneurysms., Objective: To analyze possible causes of aneurysm contrast enhancement considering morphological data of aneurysm walls., Material and Methods: The study included 44 patients with intracranial aneurysms who underwent preoperative MRI between November 2020 and September 2022. Each aneurysm was assessed regarding contrast enhancement pattern. Microsurgical treatment of aneurysm was accompanied by resection of its wall for subsequent histological and immunohistochemical analysis regarding thrombosis, inflammation and neovascularization. Specimens were subjected to histological and immunochemical analysis. Immunohistochemical analysis was valuable to estimate inflammatory markers CD68 and CD3, as well as neurovascularization marker SD31., Results: Aneurysms with contrast-enhanced walls were characterized by higher number of CD3+, CD68+, CD31+ cells and parietal clots. Intensity of contrast enhancement correlated with aneurysm wall abnormalities., Conclusion: Contrast enhancement of aneurysm wall can characterize various morphological abnormalities.

Background: Electrospun fibers have attracted a lot of attention from researchers due to their several characteristics, such as a very thin diameter, three-dimensional topography, large surface area, flexible surface, good mechanical characteristics, suitable for widespread applications. Indeed, electro-spinning offers many benefits, such as great surface-to-volume ratio, adjustable porosity, and the ability of imitating the tissue extra-cellular matrix. Methods: we processed Poly ε-caprolactone (PCL) via electrospinning for the production of bilayered tubular scaffolds for vascular tissue engineering application. Endothelial cells and fibroblasts were seeded into the two side of the scaffolds: endothelial cells onto the inner side composed of PCL/Gelatin fibers able to mimic the inner surface of the vessels, and fibroblasts onto the outer side only exposing PCL fibers. Extracellular matrix production and organization has been performed by means of classical immunofluorescence against collagen type I fibers, Scanning Electron-Microscopy (SEM) has been performed in order to evaluated ultrastructural morphology, gene expression by means gene expression has been performed to evaluate the phenotype of endothelial cells and fibroblasts. Results and conclusion: results confirmed that both cells population are able to conserve their phenotype colonizing the surface supporting the hypothesis that PCL scaffolds based on electrospun fibers should be a good candidate for vascular surgery.

Clinical trials and animal experimental studies have demonstrated an association of arterial baroreflex impairment with the prognosis and mortality of cardiovascular diseases and diabetes. As a primary part of the arterial baroreflex arc, the pressure sensitivity of arterial baroreceptors is blunted and involved in arterial baroreflex dysfunction in cardiovascular diseases and diabetes. Changes in the arterial vascular walls, mechanosensitive ion channels, and voltage-gated ion channels contribute to the attenuation of arterial baroreceptor sensitivity. Some endogenous substances (such as angiotensin II and superoxide anion) can modulate these morphological and functional alterations through intracellular signaling pathways in impaired arterial baroreceptors. Arterial baroreceptors can be considered as a potential therapeutic target to improve the prognosis of patients with cardiovascular diseases and diabetes. [ABSTRACT FROM AUTHOR]

Arterial wall stiffness is an early marker of cardiovascular diseases. The gold standard for assessment of the stiffness of large vessels is presently pulse wave velocity (PWV). Work is in progress on the study of the reference values of PWV in people of different genders and ages. 24-hour blood pressure (BP) monitoring is not only a procedure that can estimate diurnal BP variability, but also monitor the indicators of vascular wall stiffness in a number of cases over a 24-hour period. The given review highlights the pathophysiology of arterial stiffness, methods for its assessment, and the aspects of use in therapeutic practice.

State control of the vascular wall on haemostasis in adulthood significantly defines many functions of fauna throughout ontogeny, laying the foundations for his longevity. In spite of a high scientific and practical significance of Hemostatic activity of the vascular wall in adult rats, its features were investigated inadequately, dictating the need to plan and carry out the study. In a survey of 35 healthy male rats showed low content in their blood the number of product peroxide oxidation of high activity antioxidant capacity of plasma. For healthy male is characterized by a low level of endotheliazitemia, combined with a high level synthesis in the vascular wall substances with antiaggregatory activity antitrombin III and tissue plasminogen activators.

Treatment of socially significant diseases is an important task, acutely facing medicine today. In the work evaluated the possibility of a complex correction, including lisinopril, pioglitazone and non-pharmacological treatments, in terms of its impact on the antiaggregatory activity of the vascular wall in patients with arterial hypertension of 1-2 degrees in the metabolic syndrome. Against the backdrop of the surveyed contingent of this complex treatment after 4 months the full normalization of antiaggregatory activity of the vascular wall. The results are stored within a year of treatment, even if lax adherence to non-pharmacological component correction after 16 weeks of therapy.

Coronary artery disease (CAD) is the leading cause of mortality worldwide and poses a considerable public health burden. Recent genome-wide association studies (GWAS) have revealed >100 genetic loci associated with CAD susceptibility in humans. While a number of these loci harbor gene targets of currently approved therapies, such as statins and PCSK9 inhibitors, the majority of the annotated genes at these loci encode for proteins involved in vessel wall function with no known drugs available. Importantly many of the associated genes linked to vascular (smooth muscle, endothelial, and macrophage) cell processes are now organized into distinct functional pathways, e.g., vasodilation, growth factor responses, extracellular matrix and plaque remodeling, and inflammation. In this mini-review, we highlight the most recently identified loci that have predicted roles in the vessel wall and provide genetic context for pre-existing therapies as well as new drug targets informed from GWAS. With the development of new modalities to target these pathways, (e.g., antisense oligonucleotides, CRISPR/Cas9, and RNA interference) as well as the computational frameworks to prioritize or reposition therapeutics, there is great opportunity to close the gap from initial genetic discovery to clinical translation for many patients affected by this common disease.

The article presents the results of study of arterial stiffness, ankle-brachial index and pulse pressure in adult population of Tomsk in the framework of the project ESSAY RF (Epidemiology of Cardiovascular diseases in the Regions of the Russian Federation). 1379 men and women of 24-64 y.o. were studied by using volumetric sphygmography (VaSera VS-1500, Fukuda Denshi, Japan).The optimal values of CAVI (cardio-ankle vascular index), as a marker of arterial stiffness, were considered in group of relatively healthy persons in russian population. CAVI values in whole studied population were analyzed in comparison with data of other researchers and in association with CVD and CVD risk factors.

Summary Pulmonary hypertension is a devastating disease characterized by excessive vascular muscularization. We previously demonstrated primed platelet-derived growth factor receptor β + (PDGFR-β + )/smooth muscle cell (SMC) marker + progenitors at the muscular-unmuscular arteriole border in the normal lung, and in hypoxia-induced pulmonary hypertension, a single primed cell migrates distally and expands clonally, giving rise to most of the pathological smooth muscle coating of small arterioles. Little is known regarding the molecular mechanisms underlying this process. Herein, we show that primed cell expression of Kruppel-like factor 4 and hypoxia-inducible factor 1-α (HIF1-α) are required, respectively, for distal migration and smooth muscle expansion in a sequential manner. In addition, the HIF1-α/PDGF-B axis in endothelial cells non-cell autonomously regulates primed cell induction, proliferation, and differentiation. Finally, myeloid cells transdifferentiate into or fuse with distal arteriole SMCs during hypoxia, and Pdgfb deletion in myeloid cells attenuates pathological muscularization. Thus, primed cell autonomous and non-cell autonomous pathways are attractive therapeutic targets for pulmonary hypertension. [ABSTRACT FROM AUTHOR]

Aim — cross-sectional study of changes in various segments of the vascular bed in arterial hypertension (AH), defining the role of inducers and inhibitors of angiogenesis in these processes.Materials and methods. The study included 99 patients with arterial hypertension of I–II degree, average age of 63.2 ± 2.6 years, diseaseduration 9.2 ± 7.2 years.Results. It was found that patients with arterial hypertension have disorders in all segments of vascular bed: endothelial dysfunction (highvWF), microcirculatory disorders, and increased pulse wave velocity (PWV) of elastic-type vessels. The level of angioginesis factors doesnot depend on such parameters as gender, age, body mass index. Smoking and duration of hypertension influence on vascular endothelialgrowth factor raise and endostatin levels are higher in patients with family history of cardiovascular diseases. Duration of disease is directlycorrelated with microcirculatory disorders and the PWV, correlation between microcirculatory disorders and pulse wave velocity indicatetheir common processes.

Abstract. Specific autoantibodies against acetylated, maleylated and malonic dialdehyde-(MDA)-modified lipoproteins are detectable in human plasma. Immunization of rabbits with autologous, correspondingly modified low-density lipoproteins (LDLs) did induce autoantibodies against acetylated, maleylated and MDA-modified lipoproteins. In atherosclerotic lesions from hyman aorta, the epitopes have been detected that were recognized by the antibodies to acetylated, maleylated, and MDA-modified LDLs. Such antigens were detected at all atherogenesis stages, beginning with the earliest lesions (lipid spots), and their deposition pattern was quite variable.Rabbit and human autoantibodies against acetylated, maleylated and MDA-modified lipoproteins recognized antigens in human atherosclerotic aorta. Modified proteins were localized both intra- and extracellular in tectum, superficial and deep layers of the atherosclerotic lesions. The most typical mode of depositions for all modified proteins si represented by extracellular deposits in the cap of lipid streaks and fibrous plaques, especially in transitional “shoulder” area.The intimal deposits of modified proteins shared similar features with distribution of apo-B-containing lipoproteins, like as of lipids detectable by Oil Red staining. The areas where modified proteins and apo-B-containing lipoproteins were revealed did often coincide with foci of IgG deposits. Modified proteins were not detectable in the non-affected segments of aortic intima.

In contrast to the empirical therapy, 18month antihypertensive therapy based on administration of adrenoblockers to the patients with the sympathetic division activity (cholerics and sanguinics), and the angiotensinconverting enzyme activity in the patients with renninangiotensinaldosterone system due parasimpatikotonii (phlegmatics and melancholics) combined with the alignment of values of the studied parameters with those in healthy individuals of the same temperament.

Purpose of Review: This review aims to summarize recent findings regarding the plasticity and fate switching among somatic and progenitor cells residing in the vascular wall of blood vessels in health and disease. Recent Findings: Cell lineage tracing methods have identified multiple origins of stem cells, macrophages, and matrix-producing cells that become mobilized after acute or chronic injury of cardiovascular tissues. These studies also revealed that in the disease environment, resident somatic cells become plastic, thereby changing their stereotypical identities to adopt proinflammatory and profibrotic phenotypes. Summary: Currently, the functional significance of this heterogeneity among reparative cells is unknown. Furthermore, mechanisms that control cellular plasticity and fate decisions in the disease environment are poorly understood. Cardiovascular diseases are responsible for the majority of deaths worldwide. From a therapeutic perspective, these novel discoveries may identify new targets to improve the repair and regeneration of the cardiovascular system. [ABSTRACT FROM AUTHOR]

We investigated the effect of a new indole derivative Sbt-828 with antiaggregant properties on prostacyclin-generating activity of the vascular wall and thromboxane A level in platelets of intact rats. The substance under study did not affect prostacyclin production by the vascular wall and significantly reduced thromboxane A level, being superior to the reference drug acetylsalicylic acid by 1.6 times, as seen from reduced malonic dialdehyde level in the thrombin-induced rat platelets. [ABSTRACT FROM AUTHOR]

Premenopausal women have a decreased incidence of cardiovascular disease and a decreased rate of progression of renal disease. With the onset of menopause, however, decreased synthesis of 17β-estradiol (estradiol) is accompanied by an increased incidence of cardiovascular disorders and accelerated progression of renal diseases. The glomerulus and the vascular wall are not static, and components of these structures dynamically increase, decrease, or reorganize in response to physiological and pathological stimuli. Although multiple cellular and biochemical processes are involved in glomerular and vascular remodelling, glomerular mesangial cells (GMCs) in the kidney and smooth muscle cells (VSMC) and endothelial cells in the vasculature are the final common pathway for dynamic changes in glomerular and vascular wall structure. Estradiol may induce protective effects on the renal and cardiovascular system by altering VSMC, GMC, or endothelial cell biology so as to prevent glomerular and vascular remodelling. The purpose of this review is to provide an overview of the participating mechanisms in this regard, as well as the mechanism of estradiol signalling in cardiomyocytes, with an emphasis on mechanisms that might be important in cardioprotection. [ABSTRACT FROM AUTHOR]

Ultrasound imaging plays an essential role in the diagnosis of vascular lesions. Accurate segmentation of the vascular wall is important for preventing, diagnosing, and treating vascular diseases. However, existing methods have inaccurate localization of the vascular wall boundary. Segmentation errors occur in discontinuous vascular wall boundaries and dark boundaries. To overcome these problems, we propose a new boundary-delineation network (BDNet). First, we design the feature extraction module to prevent the feature information loss of low-quality images by multi-scale information fusion and multi-receptive field feature fusion. Secondly, we generate the initial coarse prediction results based on the extracted features. Based on the coarse prediction results, we use the boundary refinement module to obtain the boundary point locations and re-delineate the boundary points to prevent the boundary points from the offset. Finally, we use region mutual information loss and our designed global pixel relationship loss to model the relationship between pixels from global and neighbourhood aspects using the structural features of the vessel wall to help the model extract important structured information. To facilitate clinical applications, we design the model to be lightweight. Experimental results show that our model achieves the best segmentation results and significantly reduces memory consumption compared to existing models. [Display omitted] • Propose the boundary-delineation network (BDNet) for vascular wall segmentation. • Using a boundary refinement module to locate the boundary points precisely. • Design feature extraction module to extract low-quality image features. • Propose global pixel relationship loss function. • To facilitate clinical applications, the BDNet is designed to be lightweight. [ABSTRACT FROM AUTHOR]

Objective: set the activity limits the impact of vascular walls by aggregation ability of neutrophils in patients arterial hypertension with dyslipidemia patients. Material and methods. Under supervision were 34 sick arterial hypertension of 1-2 degrees with dyslipidemia II b type, risk 4, middle age. The control group was made by 26 healthy people of similar age. For the purpose of correction dyslipidemia all patients received a preparation simvastatin 10 mg for the night against appointment enalapril 10 mg two times a day. Results. In the conditions of an arterial hypertension with dyslipidemia decrease in control of a vascular wall over aggregative ability of neutrophils in many respects owing to infringements in lipidic an exchange, activation lipid peroxidation of plasma, easing of generation NO and formation prostacyclin is revealed. As a result of application simvastatin at sick the arterial hypertension with dyslipidemia notes improvement lipidic structure and processes lipid peroxidation in plasma and neutrophils, being accompanied by positive dynamics aggregative abilities of the last at the expense of optimization glycoprotein structure of their receptors. Conclusion. Use simvastatin hypertensive patients with dyslipidemia within 104 weeks can improve control of the vascular wall of platelet activity of neutrophils.

The activity of vascular-platelet hemostasis is determined by the functional state of its components. Hemostatic possible blood vessel walls is their ability to synthesize prostacyclin, antithrombin and potent activators of fibrinolysis. The participation of platelets in hemostasis is based on their angiotroficheskoy vazaspasticheskoy and functions, their ability to adhesion and aggregation, participation in blood coagulation and fibrinolysis in effect. Only the equilibrium interaction of platelet function and blood vessels can ensure the adequacy of the process of hemostasis in the body as a whole, in many respects to optimal fluid properties of blood under any circumstances.

The study was aimed at the evaluation of complex therapy (diltiazem, pioglitazone, and non-pharmaceutical measures) in the correction of anticoagulant, fibrinolytic, and anti-aggregant vascular wall activity among patients with arterial hypertension, metabolic syndrome, and recent ocular vessel occlusion. It was demonstrated that after 4 months of the above-mentioned complex therapy, the anticoagulant, fibrinolytic, and anti-aggregant vascular wall activity was improved, but not normalised. At the same time, the investigated parameters significantly deteriorated if the non-pharmaceutical therapy compliance was low.

The study was aimed at investigating the potential of complex therapy (irbesartan, pioglitazone, and non-pharmaceutical treatment) in the correction of anticoagulant, fibrinolytic, and anti-aggregant activity of vascular wall among patients with arterial hypertension, metabolic syndrome, and oculo-vascular occlusion in anamnesis. The four-month complex therapy improved anticoagulant, fibrinolytic, and anti-aggregant vascular wall activity, with the evaluated parameters reaching the lower level of control range, but not being normalized. These results were relatively stable and persisted up to the end of the follow-up period, even with non-strict compliance to non-pharmaceutical therapy.

Aim. To study atorvastatin (10 and 20 mg/d) effects on lipid, C-reactive protein, and fibrinogen levels, vascular wall structure and function in patients with coronary heart disease (CHD) and primary hyperlipidemia (PHL). Material and methods. In total, 50 CHD and PHL patients were randomized into two stable-dose atorvastatin groups (10 or 20 mg/d) for 24 weeks. Atorvastatin effects on lipid levels, endothelial function, vascular wall distensibility and stiffness, as well as treatment tolerability, were examined. Results. Twenty-four-week atorvastatin therapy (10 or 20 mg/d) reduced low-density lipoprotein cholesterol (LDL-CH) level by 34,9% and 43,9%, respectively (p

Background: The wall-to-lumen ratio (WLR) is an important parameter in vascular medicine because it indicates the character of vascular wall as well as the degree of stenosis. Despite the advances in medical imaging technologies, it is still difficult to measure the thin-walled normal intracranial arteries, and the reports on the WLR of normal intracranial artery are limited. It might be possible to calculate the WLR using the indocyanine green (ICG) angiography, which is used to observe intracranial vessels during microsurgery. Purpose: To evaluate the WLR of normal intracranial arteries using ICG angiography. Materials and Methods: From the three cases in which ICG angiography was recorded with a ruler during microsurgery, 20 measurement points were chosen for the analysis. The ICG was injected intravenously with a dose of 0.2 mg/kg, and the vessels were inspected at high magnification using an operating microscope equipped with near-infrared illumination system. The vessel outer diameter and the luminal diameter were measured using the images before and after the ICG arrival based on the pixel ratio method using a ruler as reference, respectively. The WLR was calculated as 0.5 × (vessel outer diameter - vessel luminal diameter). Results: The WLR (mean ± standard deviation) of normal intracranial arteries was 0.086 ± 0.022. The WLR tended to be high in small arteries. Conclusion: The WLR of normal intracranial arteries calculated using ICG angiography was consistent with the WLR reported in the previous reports based on human autopsy. [ABSTRACT FROM AUTHOR]

Animal models of atherosclerosis often present limitations of transferability, since important hallmarks of human disease are not completely reproduced in other species. Rabbits have been used in several approaches: 1) inbred strains: Watanabe hereditary hyperlipidemic animals which express a defect in the LDL receptor, 2) transgenic rabbits, which overexpress human lipoproteins, and first knock-out rabbits. 3) native New Zealand white rabbits (NZW) fed with cholesterol-rich diet for at least 8 weeks represent the quickest way to establish arteriosclerosis. Rabbits are arguably the most sensitive animal species to cholesterol overload. Interventions in native or arteriosclerotic arteries are used to induce local thrombus formation, e.g. endothelial denudation or photochemical injury. In contrast to smaller animals, catheterisation of coronary arteries is feasible, whose external ligation serves to induce myocardial infarction. As biological endpoints, arterial vasoreactivity/endothelial dysfunction can be studied in analogy to measurements of brachial artery vasomotion in humans in response to increasing doses of acetylcholine or volume challenges. Tissue fixation allows studying vascular morphology, plaque sizes and thrombi after local interventions. Macrophage and T lymphocyte invasion can be investigated histologically. Positron emission tomography (PET/MRI) offers to measure plaques and content in vivo serially in the same animals. Local virally mediated gene transfer to atherosclerotic rabbit arteries has been established as a rapid and reproducible method to test interesting transgenes. Histological plaque features correspond well to alterations in patients (inflammation and lipid load). Thus, effects of any proteins can be studied directly in the arteriosclerotic disease background – much quicker than after germline transgenesis and cross-breeding. [ABSTRACT FROM AUTHOR]

In this contribution we propose an engineering based approach to incorporate eigenstress distributions in arteries. Eigenstresses are known for a variety of biological tissues. In the case of arterial walls the so called opening angle experiment is frequently used to characterize the residual strains/stresses. Assuming that the transmural stress distribution of suitable stress measures should be smooth, a residual stress tensor is directly estimated from the Cauchy stresses. These stress measures are constructed in such a way that the basic biophysiological characteristics, like the fiber orientations which are taken into account by suitable structural tensors, are adequately respected. In order to achieve reasonable eigenstress distributions in the arteries the local stress measures should approach spatial-sector averaged values. These ideas are imbedded in an algorithm to update the residual stress tensor incrementally. An ideal tube and degenerated patient-specific arteries from medical imaging are used to demonstrate the performance of the proposed procedure and to estimate the opening angle. [ABSTRACT FROM AUTHOR]

Vasa vasorum supply both the tunica adventitia and the tunica media of major arteries with nutrients and oxygen. We estimated the density of von Willebrand factor-positive profiles of vasa vasorum visible in transversal histological sections of 123 tissue samples collected from five anatomical positions in the porcine aortae of growing pigs ( n = 25). The animals ranged in age from 0 to 230 days. The tunica media of the thoracic aorta had a greater vasa vasorum density, with microvessels penetrating deeper towards the lumen than in the abdominal aorta. The density of vasa vasorum gradually decreased with age in both the media and the adventitia. The relative depth into which the vasa vasorum penetrated and where they branched remained constant during the ageing and growth of the media. The ratio of the tunica media and tunica adventitia thicknesses did not change in the single aortic segments during ageing. The media of older animals received fewer but equally distributed vasa vasorum. A greater density of vasa vasorum in the media was correlated with greater media thickness and a greater elastin fraction (data on elastin taken from another study on the same samples). Immunohistochemical quantification revealed deeper penetration of vasa vasorum towards the adluminal layers of the tunica media that were hitherto reported to be avascular. The complete primary morphometric data, in the form of continuous variables, have been made available as a supplement. Mapping of the vasa vasorum profile density and position has promising illustrative potential for studies on atherosclerotic and inflammatory neovascularization, aortic aneurysms, and drug distribution from arterial stents in experimental porcine models. [ABSTRACT FROM AUTHOR]

Macrophages express a number of proteins involved in sterol efflux pathways, including apolipoprotein E (apoE) and scavenger receptor class B type I (SR-BI). We have investigated a potential interaction between these two sterol efflux pathways in modulating overall macrophage sterol flux. We utilized an experimental system in which we increased expression of each of these proteins to a high physiologic range in order to perform our evaluation. We show that in apoE-expressing cells, a 4-fold increase in SR-BI expression leads to reduction of sterol and phospholipid efflux. SR-BI-mediated reduction in sterol efflux was only observed in cells that expressed endogenous apoE. In J774 cells that did not express apoE, a similar increase in SR-BI level led to increased sterol efflux. The divergent response of sterol efflux after increased SR-BI was maintained in the presence of a number of structurally diverse extracellular sterol acceptors. Increased SR-BI expression also enhanced sterol efflux to exogenously added apoE. Investigation of a potential mechanism for reduced efflux in apoE-expressing cells indicated that SR-BI expression reduced macrophage apoE by accelerating the degradation of newly synthesized apoE. This led to decreased secretion of apoE and reduced the fraction of apoE sequestered on the cell surface. Thus, enhanced SR-BI expression in macrophages can reduce the cellular level and secretion of apoE by accelerating degradation of the newly synthesized protein. This reduction of endogenous apoE is accompanied by reduced sterol efflux from macrophages. —Huang, Z. H., and T. Mazzone. ApoE-dependent sterol efflux from macrophages is modulated by scavenger receptor class B type I expression.

Remnants of triglyceride-rich lipoproteins (TRL) have been implicated in the early development of atherosclerosis. We tested this hypothesis by quantifying the plasma concentration of remnant-like particle cholesterol (RLP-C) in a cohort of healthy 50-year-old men in whom the common carotid artery intima-media thickness (CCA-IMT) was assessed by B-mode ultrasound as a surrogate marker for atherosclerosis. The subjects were given a fat-rich meal to study the generation of RLP-C during postprandial lipemia. Fasting plasma RLP-C and other major fasting plasma lipids and lipoproteins were determined twice, and the mean RLP-C concentration was strongly correlated with CCA-IMT (r = 0.32, P = 0.002). In addition, low density lipoprotein (LDL) cholesterol (r = 0.25, P = 0.01) and plasma triglycerides (r = 0.20, P = 0.05) were significantly related to CCA-IMT. Multivariate analyses showed a triglyceride-independent contribution of RLP-C to CCA-IMT. After fat intake, the median plasma RLP-C concentration was doubled after 3 h. The increase was strongly related to the postprandial generation of TRL apolipoprotein (apo)B-48, and large (Sf 60–400) TRL apoB-100. The association with CCA-IMT was somewhat stronger for the 3-h RLP-C level than for the fasting RLP-C concentration [r = 0.27, P < 0.01 (3 h) compared with r = 0.22, P < 0.05 (0 h)]. We conclude that the plasma concentration of RLP-C is related to CCA-IMT, independent of plasma triglycerides and LDL cholesterol, in a healthy middle-aged male population.—Karpe, F., S. Boquist, R. Tang, G. M. Bond, U. de Faire, and A. Hamsten. Remnant lipoproteins are related to intima-media thickness of the carotid artery independently of LDL cholesterol and plasma triglycerides. J. Lipid Res. 2001. 42: 17–21.

Background: Determination of predictors that can affect development of atherosclerosis progression in the postoperative period is an urgent problem in vascular surgery., Objectives: Integrated assessment of markers of apoptosis and cell proliferation in atherosclerotic lesions and their progression after surgery in patients with peripheral arterial diseases., Methods: The investigation included 30 patients with stage IIB-III peripheral arterial disease. All patients have undergone open surgical interventions on the arteries of the aorto-iliac and femoral-popliteal segments. During these interventions, intraoperative specimens were obtained from the vascular wall with atherosclerotic lesions. The following values were evaluated: VEGF А165, PDGF BB, and sFas. Samples of normal vascular wall were obtained from post-mortem donors and used as a control group., Results: The levels of Bax and p53 were increased (p<0.001) in samples from arterial wall with atherosclerotic plaque, while sFas values were reduced (p<0.001), compared to their levels in control samples. Values of PDGF BB and VEGF A165 were 1.9 and 1.7 times higher in atherosclerotic lesion samples (p=0.001), in comparison with the control group. The levels of p53 and Bax were increased against a background of reduced sFas levels in samples with progression of atherosclerosis compared to their baseline values in samples with atherosclerotic plaque (p<0.05)., Conclusions: Initially increased values of the Bax marker against a background of reduced sFas values in vascular wall samples from patients with peripheral arterial disease is associated with risk of atherosclerosis progression in the postoperative period., Competing Interests: Conflicts of interest: No conflicts of interest declared concerning the publication of this article., (Copyright© 2023 The authors.)

Background: Hemorrhage from intracranial aneurysms is associated with high risk of adverse outcomes. In this regard, surgical treatment of unruptured asymptomatic aneurysms has been actively developed in recent decades. One of the objectives is searching for predictors of aneurysm rupture to clarify the indications for surgery. Non-invasive analysis of vascular wall is actively discussed in last years., Objective: To evaluate the possibilities of MRI of ruptured and unruptured intracranial aneurysm walls and determine clinical significance of certain morphological patterns., Material and Methods: The study included 111 patients with 158 ruptured and unruptured saccular aneurysms who underwent MRI according to a special protocol between November 2020 and September 2023. We analyzed each aneurysm regarding features of contrast enhancement and changes in SWAN images. After that, we compared these data with ruptures., Results: Wall of ruptured and unruptured aneurysms can accumulate contrast agent. We found 5 types of contrast enhancement. Thick-layer contrast enhancement was accompanied by 9.6-fold higher risk of aneurysm rupture compared to aneurysms without contrast enhancement. Dark MR signal from intracranial aneurysm wall in SWAN imaging is a significant sign of rupture., Conclusion: MRI of the vascular wall is valuable to verify ruptured aneurysms. Unruptured aneurysms can accumulate contrast agent inside the wall, and pattern of accumulation differs from ruptured aneurysms. Morphological analysis is needed to confirm contrast enhancement as a marker of aneurysm rupture.