Gaorui Liu, J. Clarke, D. Oomens, M. Vicaretti, T. Daly, Tae Hyun Cho, I. Mohan
The assessment of the saphenofemoral junction (SFJ) is important in the diagnosis and treatment of venous reflux of the great saphenous vein (GSV). In the clinical practice of venous medicine, the SFJ is used to represent the region at which the saphenous arch connects with the common femoral vein (CFV). A number of notable variations of the SFJ have been documented, and rare variable courses of the GSV have been described recently. Our case study reports two unusual GSV terminations. In both cases, the SFJ was located below the confluence of the profunda femoris vein (PFV) with the femoral vein (FV). Case 1 showed the SFJ was formed by the GSV and FV; whereas case 2 showed the PFV was joined by the GSV after a transposition with the FV. Anatomical variations of the SFJ are rare; however, they are increasingly diagnosed with the use of duplex ultrasound. The identification of SFJ variants warrants a safe endovenous procedure and prevents surgical complications.
{"title":"Termination of the great saphenous vein at variable levels","authors":"Gaorui Liu, J. Clarke, D. Oomens, M. Vicaretti, T. Daly, Tae Hyun Cho, I. Mohan","doi":"10.4081/vl.2022.10786","DOIUrl":"https://doi.org/10.4081/vl.2022.10786","url":null,"abstract":"The assessment of the saphenofemoral junction (SFJ) is important in the diagnosis and treatment of venous reflux of the great saphenous vein (GSV). In the clinical practice of venous medicine, the SFJ is used to represent the region at which the saphenous arch connects with the common femoral vein (CFV). A number of notable variations of the SFJ have been documented, and rare variable courses of the GSV have been described recently. Our case study reports two unusual GSV terminations. In both cases, the SFJ was located below the confluence of the profunda femoris vein (PFV) with the femoral vein (FV). Case 1 showed the SFJ was formed by the GSV and FV; whereas case 2 showed the PFV was joined by the GSV after a transposition with the FV. Anatomical variations of the SFJ are rare; however, they are increasingly diagnosed with the use of duplex ultrasound. The identification of SFJ variants warrants a safe endovenous procedure and prevents surgical complications.","PeriodicalId":421508,"journal":{"name":"Veins and Lymphatics","volume":"562 ","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133356165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The gold standard vascular access for hemodialysis is the arteriovenous fistula (AVF). Venous hypertension (VH) is an unusual complication of AVF, which can be misdiagnosed as cellulitis due to the similarities in clinical presentation. Here we present a case of venous hypertension in a 40-years-old gentleman, who presented with progressive pain and swelling of three lateral fingers of his left hand without other inflammatory signs after a year of AVF creation. Further evaluation with a duplex scan supported the clinical diagnosis of VH. He had undergone a surgical ligation of AVF and completely recovered from the symptoms.
{"title":"An unusual cause of venous hypertension","authors":"Vinojan Satchithanantham, Dhadchayini Rajahram","doi":"10.4081/vl.2022.10753","DOIUrl":"https://doi.org/10.4081/vl.2022.10753","url":null,"abstract":"The gold standard vascular access for hemodialysis is the arteriovenous fistula (AVF). Venous hypertension (VH) is an unusual complication of AVF, which can be misdiagnosed as cellulitis due to the similarities in clinical presentation. Here we present a case of venous hypertension in a 40-years-old gentleman, who presented with progressive pain and swelling of three lateral fingers of his left hand without other inflammatory signs after a year of AVF creation. Further evaluation with a duplex scan supported the clinical diagnosis of VH. He had undergone a surgical ligation of AVF and completely recovered from the symptoms.","PeriodicalId":421508,"journal":{"name":"Veins and Lymphatics","volume":"53 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115201281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Randa S. Eshaq, Minsup Lee, Wendy Leskova, N. Harris, J. Alexander
Background: Hypertension (HT) promotes structural and functional changes in the cerebral microcirculation that can provoke irreversible cerebrovascular injury, leading to neuronal loss and brain atrophy,1 cognitive impairment, vascular dementia,2 and Alzheimer’s disease.3 Currently, the mechanisms and consequences of such remodeling are not fully understood. Transforming growth factor (TGF) is a morphogen that regulates cellular differentiation, induces endothelial-to-mesenchymal transition (EndoMT), and works as a contractile-to-synthetic switch in vascular smooth muscle cells (VSMC) phenotype.4 Plasma levels of TGF are increased in HT patients, and in spontaneously hypertensive rats (SHR) that exhibit vascular fibrosis.5 Although coincidental, causal roles through which elevated TGF may drive cerebrovascular remodeling in the HT brain are suspected, but unproven. We hypothesize that HT-induced TGF drives cerebrovascular remodeling, which decreases blood-brain barrier and impairs cerebrovascular autoregulation. Methods: Brain cortices and penetrating cerebral microvessels (BMVs) were isolated from male and female SHR and Wistar-Kyoto rats (WKY, control), and subjected to western blotting and immunofluorescence labeling for endothelial cell (EC) and VSMC differentiation markers, TGF canonical pathway markers SMAD2, 3 and 4, as well as basement membrane protein expression, and glial fibrillary acidic protein (GFAP) as a marker of astrocyte inflammation. Additionally, TGF-treated rat retinal microvascular endothelial cells (RRMECs), and human brain microvascular endothelial cells (hCMEC/D3) ± the TGF inhibitor vactosertib, were also subjected to western blotting and immunofluorescence labeling to assess endothelial cell (EC) and VSMC differentiation markers, as well as basement membrane protein expression. Results: TGF was significantly increased in SHR BMVs. Moreover, GFAP levels were significantly increased in the SHR cortex. The EC junctional proteins platelet endothelial cell adhesion molecule-1 (PECAM-1) and vascular endothelial-cadherin (VE-cadherin), were significantly decreased in SHR. In contrast, CRBP-1, a marker for synthetic VSMC, and collagen IV and fibronectin levels significantly increased in SHR. Interestingly, female SHR rats had significantly increased levels of SMAD2/3, which was not evident in male SHRs, indicating a possible role for the non-canonical TGF pathway in male SHRs. Additionally, TGF significantly increased -smooth muscle actin (-SMA) and decreased VE-cadherin expression in RRMECs and D3 cells, consistent with EndoMT. TGF inhibition with vactosertib reversed these effects and significantly suppressed -SMA, and maintained VE-Cadherin similar to control RRMECs and D3s. Conclusions: We now have strong evidence for HT-induced cerebrovascular remodeling, where TGF mediates loss of both smooth muscle and endothelial differentiated phenotypes. The reversal of these effects using TGF blockers suggests that
{"title":"The role of transforming growth factor- in hypertension-induced cerebrovascular remodeling","authors":"Randa S. Eshaq, Minsup Lee, Wendy Leskova, N. Harris, J. Alexander","doi":"10.4081/vl.2022.10964","DOIUrl":"https://doi.org/10.4081/vl.2022.10964","url":null,"abstract":"Background: Hypertension (HT) promotes structural and functional changes in the cerebral microcirculation that can provoke irreversible cerebrovascular injury, leading to neuronal loss and brain atrophy,1 cognitive impairment, vascular dementia,2 and Alzheimer’s disease.3 Currently, the mechanisms and consequences of such remodeling are not fully understood. Transforming growth factor (TGF) is a morphogen that regulates cellular differentiation, induces endothelial-to-mesenchymal transition (EndoMT), and works as a contractile-to-synthetic switch in vascular smooth muscle cells (VSMC) phenotype.4 Plasma levels of TGF are increased in HT patients, and in spontaneously hypertensive rats (SHR) that exhibit vascular fibrosis.5 Although coincidental, causal roles through which elevated TGF may drive cerebrovascular remodeling in the HT brain are suspected, but unproven. We hypothesize that HT-induced TGF drives cerebrovascular remodeling, which decreases blood-brain barrier and impairs cerebrovascular autoregulation. \u0000Methods: Brain cortices and penetrating cerebral microvessels (BMVs) were isolated from male and female SHR and Wistar-Kyoto rats (WKY, control), and subjected to western blotting and immunofluorescence labeling for endothelial cell (EC) and VSMC differentiation markers, TGF canonical pathway markers SMAD2, 3 and 4, as well as basement membrane protein expression, and glial fibrillary acidic protein (GFAP) as a marker of astrocyte inflammation. Additionally, TGF-treated rat retinal microvascular endothelial cells (RRMECs), and human brain microvascular endothelial cells (hCMEC/D3) ± the TGF inhibitor vactosertib, were also subjected to western blotting and immunofluorescence labeling to assess endothelial cell (EC) and VSMC differentiation markers, as well as basement membrane protein expression. \u0000Results: TGF was significantly increased in SHR BMVs. Moreover, GFAP levels were significantly increased in the SHR cortex. The EC junctional proteins platelet endothelial cell adhesion molecule-1 (PECAM-1) and vascular endothelial-cadherin (VE-cadherin), were significantly decreased in SHR. In contrast, CRBP-1, a marker for synthetic VSMC, and collagen IV and fibronectin levels significantly increased in SHR. Interestingly, female SHR rats had significantly increased levels of SMAD2/3, which was not evident in male SHRs, indicating a possible role for the non-canonical TGF pathway in male SHRs. Additionally, TGF significantly increased -smooth muscle actin (-SMA) and decreased VE-cadherin expression in RRMECs and D3 cells, consistent with EndoMT. TGF inhibition with vactosertib reversed these effects and significantly suppressed -SMA, and maintained VE-Cadherin similar to control RRMECs and D3s. \u0000Conclusions: We now have strong evidence for HT-induced cerebrovascular remodeling, where TGF mediates loss of both smooth muscle and endothelial differentiated phenotypes. The reversal of these effects using TGF blockers suggests that","PeriodicalId":421508,"journal":{"name":"Veins and Lymphatics","volume":"223 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122886891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
G. Mantovani, P. De Bonis, M. Cavallo, Paolo Zamboni, A. Scerrati
Cerebral venous drainage impairment is related to a wide spectrum of pathologies, both acute or chronic. Among the most intriguing and less explained there are those caused by a long-lasting compression on internal jugular vein (IJV), mono or bilaterally. Recently, a jugular variant of the Eagle syndrome has been described,1,2 in which an elongated styloid process, coming from the mastoid tip down through the neck, compresses the IJV (more frequently J3) in its passage on the C1 anterior arch. Interestingly, those patients often complaint of typical symptoms of intracranial hypertension, such as headache (not frequent in classic Eagle syndrome), tinnitus, dizziness. They also seem to have an increased risk of perimesencephalic hemorrhages. Conceptually, it is not the styloid process length in itself to determine the compression, but rather its spatial orientation. We could therefore expect to find patients suffering from Eagle jugular syndrome who present normal or short styloid process, but in close proximity to C1. To test this hypothesis, we are developing a novel software to analyze 3-D spatial orientation of styloid process in patient with a previously diagnosed Eagle jugular syndrome compared to healthy controls. Methods We collected cervical computed tomography angiography (CTA) images from 8 patients with EJS confirmed by venous angiography at our institution, and a control group of 7 random patients, homogenous for sex and age. A blind operator created with a dedicated pre-existing software3, an editable 3-D model (.stl file) of the 3 main region of interest (ROI), namely: right styloid, left styloid, C1 anterior arch. Starting from this dataset, our software, written using the open-source package management system Anaconda4 ver. 2-2.4.0, compares all the possible couples of points between each styloid process and the C1 arch, detecting the minimum and maximum distance. Then, it provides the mean spatial orientation of the process respect the CT-axis: x-axis (from left to right), y-axis (from occiput to nose) and z-axis (cranio-caudal). Results By now we included 15 patients (8 cases, 7 controls), homogeneous for sex and age. Preliminary data (Table 1), although not statistically significant yet, seems to indicate that Eagle jugular patients effectively have a more vertical styloid process, meaning an angle between styloid and y-axis greater than controls, rather than a longer one. Conclusions Our preliminary results could confirm that spatial orientation is more important in Eagle jugular patients than styloid process length. This study is currently ongoing and we planned to enroll at least 20 subjects for each arm. At the same time, we are collecting data from patients with carotic variant of Eagle syndrome, to better characterize morphometric structure of styloid in various subset of this pathology.
{"title":"Eagle jugular syndrome: a morphometric computed study on styloid process orientation","authors":"G. Mantovani, P. De Bonis, M. Cavallo, Paolo Zamboni, A. Scerrati","doi":"10.4081/vl.2022.10955","DOIUrl":"https://doi.org/10.4081/vl.2022.10955","url":null,"abstract":"Cerebral venous drainage impairment is related to a wide spectrum of pathologies, both acute or chronic. Among the most intriguing and less explained there are those caused by a long-lasting compression on internal jugular vein (IJV), mono or bilaterally. Recently, a jugular variant of the Eagle syndrome has been described,1,2 in which an elongated styloid process, coming from the mastoid tip down through the neck, compresses the IJV (more frequently J3) in its passage on the C1 anterior arch. Interestingly, those patients often complaint of typical symptoms of intracranial hypertension, such as headache (not frequent in classic Eagle syndrome), tinnitus, dizziness. They also seem to have an increased risk of perimesencephalic hemorrhages. Conceptually, it is not the styloid process length in itself to determine the compression, but rather its spatial orientation. We could therefore expect to find patients suffering from Eagle jugular syndrome who present normal or short styloid process, but in close proximity to C1. To test this hypothesis, we are developing a novel software to analyze 3-D spatial orientation of styloid process in patient with a previously diagnosed Eagle jugular syndrome compared to healthy controls. Methods We collected cervical computed tomography angiography (CTA) images from 8 patients with EJS confirmed by venous angiography at our institution, and a control group of 7 random patients, homogenous for sex and age. A blind operator created with a dedicated pre-existing software3, an editable 3-D model (.stl file) of the 3 main region of interest (ROI), namely: right styloid, left styloid, C1 anterior arch. Starting from this dataset, our software, written using the open-source package management system Anaconda4 ver. 2-2.4.0, compares all the possible couples of points between each styloid process and the C1 arch, detecting the minimum and maximum distance. Then, it provides the mean spatial orientation of the process respect the CT-axis: x-axis (from left to right), y-axis (from occiput to nose) and z-axis (cranio-caudal). Results By now we included 15 patients (8 cases, 7 controls), homogeneous for sex and age. Preliminary data (Table 1), although not statistically significant yet, seems to indicate that Eagle jugular patients effectively have a more vertical styloid process, meaning an angle between styloid and y-axis greater than controls, rather than a longer one. Conclusions Our preliminary results could confirm that spatial orientation is more important in Eagle jugular patients than styloid process length. This study is currently ongoing and we planned to enroll at least 20 subjects for each arm. At the same time, we are collecting data from patients with carotic variant of Eagle syndrome, to better characterize morphometric structure of styloid in various subset of this pathology.","PeriodicalId":421508,"journal":{"name":"Veins and Lymphatics","volume":"11 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131764581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Simka, S. A. Iqrar, A. Rashid, Aiman Rashid, M. Nowak
Background. Currently, pathological jugular valves are thought to be the main cause of altered hemodynamics in the internal jugular veins, the so-called chronic cerebrospinal venous insufficiency. The alternative interpretation of flow disturbances in these veins is that the main source of abnormal outflow are nozzle-like strictures in their upper parts, at the level or just below the jugular foramen, for example, caused by an enlarged transverse process of the atlas and/or styloid process of the temporal bone.1 These in silico studies were aimed at validation of this hypothesis. Methods. With the use of computational fluid mechanics software: the Flowsquare+ and the COMSOL multiphysics, we simulated blood flow in the models of internal jugular veins that exhibited different morphologies (Figure 1). With the Flowsquare+ software, we performed 3-dimensional simulations for the assessment of relevance of the strictures at the level of jugular foramen, while the COMSOL multiphysics software, which was used in 2-dimensional mode, gave us more detailed insight into the behavior of the jugular valve. Results. There was a normal unidirectional flow, with the centrally positioned centerline velocity and no flow separation in modeled veins, which were not narrowed or presented with gradual narrowings. On the contrary, in a majority of models with nozzle-like strictures located at the beginning of the studied veins, abnormal flow patterns were revealed, with significant flow separation and regions with reversed flow. The most severe flow abnormalities were not seen in the models with nozzles of a small cross-sectional area, but rather in those positioned asymmetrically. Abnormal valves (with reversed or asymmetric leaflets) further impaired the flow in models with symmetrically positioned nozzles, but had no significant impact on the flow in a case of an already altered flow evoked by the asymmetric nozzles.1 Importantly, simulations performed with the COMSOL multiphysics revealed that flow disturbances evoked by significant stenosis in the upper part of the internal jugular vein distort leaflets of the jugular valve. This was not seen as a case of a minor stenosis. Conclusions. We demonstrated that our working hypothesis is credible and that impaired outflow from the brain through the internal jugular veins is likely to be primarily caused by pathological strictures in the upper parts of these veins, instead of pathological jugular valves that, as of yet, were the main target of clinical research. In addition, pathology of the jugular valves may be secondary to the strictures in the upper segments of the internal jugular veins.
{"title":"Abnormal jugular valves are not the sole explanation of an impaired outflow from the cranial cavity through the internal jugular veins: results of in silico studies","authors":"M. Simka, S. A. Iqrar, A. Rashid, Aiman Rashid, M. Nowak","doi":"10.4081/vl.2022.10957","DOIUrl":"https://doi.org/10.4081/vl.2022.10957","url":null,"abstract":"Background. Currently, pathological jugular valves are thought to be the main cause of altered hemodynamics in the internal jugular veins, the so-called chronic cerebrospinal venous insufficiency. The alternative interpretation of flow disturbances in these veins is that the main source of abnormal outflow are nozzle-like strictures in their upper parts, at the level or just below the jugular foramen, for example, caused by an enlarged transverse process of the atlas and/or styloid process of the temporal bone.1 These in silico studies were aimed at validation of this hypothesis. \u0000Methods. With the use of computational fluid mechanics software: the Flowsquare+ and the COMSOL multiphysics, we simulated blood flow in the models of internal jugular veins that exhibited different morphologies (Figure 1). With the Flowsquare+ software, we performed 3-dimensional simulations for the assessment of relevance of the strictures at the level of jugular foramen, while the COMSOL multiphysics software, which was used in 2-dimensional mode, gave us more detailed insight into the behavior of the jugular valve. Results. There was a normal unidirectional flow, with the centrally positioned centerline velocity and no flow separation in modeled veins, which were not narrowed or presented with gradual narrowings. On the contrary, in a majority of models with nozzle-like strictures located at the beginning of the studied veins, abnormal flow patterns were revealed, with significant flow separation and regions with reversed flow. The most severe flow abnormalities were not seen in the models with nozzles of a small cross-sectional area, but rather in those positioned asymmetrically. Abnormal valves (with reversed or asymmetric leaflets) further impaired the flow in models with symmetrically positioned nozzles, but had no significant impact on the flow in a case of an already altered flow evoked by the asymmetric nozzles.1 Importantly, simulations performed with the COMSOL multiphysics revealed that flow disturbances evoked by significant stenosis in the upper part of the internal jugular vein distort leaflets of the jugular valve. This was not seen as a case of a minor stenosis. \u0000Conclusions. We demonstrated that our working hypothesis is credible and that impaired outflow from the brain through the internal jugular veins is likely to be primarily caused by pathological strictures in the upper parts of these veins, instead of pathological jugular valves that, as of yet, were the main target of clinical research. In addition, pathology of the jugular valves may be secondary to the strictures in the upper segments of the internal jugular veins.","PeriodicalId":421508,"journal":{"name":"Veins and Lymphatics","volume":"3 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128528886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jiani Hu, Yimin Shen, Lara M. Fahmy, S. Krishnamurthy, Jie Li, L. Zhang, Yongsheng Chen, M. Haacke, Q. Jiang
Background: Impaired cerebral waste clearance (CWC) has been associated with a broad range of both physiological and pathophysiological neurologic conditions.1,2 Because of the unique anatomy of the brain parenchyma, theoretically, in the brain parenchyma, biochemically inert waste such as magnetic resonance imaging (MRI) contrast agents can only be removed through two possible pathways: cerebrospinal fluid (CSF) pathway, and/or vascular pathway. Despite the controversy, there seems to be a solid consensus on the participation of the CSF pathway in CWC.3 In contrast to the CSF system, the current consensus is that the parenchymal vascular system does not participate in CWC. Considering there is a big difference in flow rate between the blood (2 mL/min) and the CSF (3.7 µL/min) and the brain is the most bioactive, energy-consuming organ (20% nutrition for about 5% of body weight) in the body, it is illogical that the brain would rely on the slow CSF circulation for CWC while less bioactive tissues outside the brain require both the fast vascular and slow lymphatic systems to remove waste in a timely manner.4,5 Methods: Superparamagnetic iron oxide–enhanced susceptibility-weighted imaging (SPIO-SWI) and quantitative susceptibility mapping (QSM) methods were used to simultaneously study 7 T MRI signal changes in parenchymal veins, arteries, and their corresponding para-vascular spaces in 26 rats, following intra-cisterna magna (ICM) infusion of different CSF tracers (FeREX, ferumoxytol, Fe-Dextran) to determine the amount of tracer in the artery and vein quantitatively. Results: The parenchymal venous system participated in CSF tracer clearance following ICM infusion of different MRI tracers with different concentrations of iron. Parenchymal venous participation was more obvious when 75 μg iron was injected. In the parenchymal veins, the relative mean (±SE) value of the susceptibility increased by 13.5±1.0% at 15 min post-tracer infusion (p<0.01), and 33.6±6.7% at 45 min post-tracer infusion (p=0.01), compared to baseline. In contrast to the parenchymal veins, a negligible amount of CSF tracer entered the parenchymal arteries: 1.3±2.6% at 15 min post-tracer infusion (p=0.6), and 12±19% at 45 min post-tracer infusion (p=0.5), compared to baseline. Conclusions: MRI tracers can enter the parenchymal vascular system and more MRI tracers were observed in the cerebral venous than arterial vessels, suggesting the direct participation of parenchymal vascular system in CWC.
{"title":"Quantitative results for the direct participation of the parenchymal vascular system in cerebral waste removal","authors":"Jiani Hu, Yimin Shen, Lara M. Fahmy, S. Krishnamurthy, Jie Li, L. Zhang, Yongsheng Chen, M. Haacke, Q. Jiang","doi":"10.4081/vl.2022.10950","DOIUrl":"https://doi.org/10.4081/vl.2022.10950","url":null,"abstract":"Background: Impaired cerebral waste clearance (CWC) has been associated with a broad range of both physiological and pathophysiological neurologic conditions.1,2 Because of the unique anatomy of the brain parenchyma, theoretically, in the brain parenchyma, biochemically inert waste such as magnetic resonance imaging (MRI) contrast agents can only be removed through two possible pathways: cerebrospinal fluid (CSF) pathway, and/or vascular pathway. Despite the controversy, there seems to be a solid consensus on the participation of the CSF pathway in CWC.3 In contrast to the CSF system, the current consensus is that the parenchymal vascular system does not participate in CWC. Considering there is a big difference in flow rate between the blood (2 mL/min) and the CSF (3.7 µL/min) and the brain is the most bioactive, energy-consuming organ (20% nutrition for about 5% of body weight) in the body, it is illogical that the brain would rely on the slow CSF circulation for CWC while less bioactive tissues outside the brain require both the fast vascular and slow lymphatic systems to remove waste in a timely manner.4,5 \u0000Methods: Superparamagnetic iron oxide–enhanced susceptibility-weighted imaging (SPIO-SWI) and quantitative susceptibility mapping (QSM) methods were used to simultaneously study 7 T MRI signal changes in parenchymal veins, arteries, and their corresponding para-vascular spaces in 26 rats, following intra-cisterna magna (ICM) infusion of different CSF tracers (FeREX, ferumoxytol, Fe-Dextran) to determine the amount of tracer in the artery and vein quantitatively. \u0000Results: The parenchymal venous system participated in CSF tracer clearance following ICM infusion of different MRI tracers with different concentrations of iron. Parenchymal venous participation was more obvious when 75 μg iron was injected. In the parenchymal veins, the relative mean (±SE) value of the susceptibility increased by 13.5±1.0% at 15 min post-tracer infusion (p<0.01), and 33.6±6.7% at 45 min post-tracer infusion (p=0.01), compared to baseline. In contrast to the parenchymal veins, a negligible amount of CSF tracer entered the parenchymal arteries: 1.3±2.6% at 15 min post-tracer infusion (p=0.6), and 12±19% at 45 min post-tracer infusion (p=0.5), compared to baseline. \u0000Conclusions: MRI tracers can enter the parenchymal vascular system and more MRI tracers were observed in the cerebral venous than arterial vessels, suggesting the direct participation of parenchymal vascular system in CWC.","PeriodicalId":421508,"journal":{"name":"Veins and Lymphatics","volume":"5 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129841956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BACKGROUND: There is an urgent need for better detection and understanding of vascular abnormalities at the micro-level, where critical vascular nourishment and cellular metabolic changes occur. This is especially the case for structures such as the midbrain and hippocampus, where both the feeding and draining vessels are quite small. The hippocampus is a complex grey matter structure that plays an important role in spatial and episodic memory. It can be affected by a wide range of pathologies including vascular abnormalities. Being able to monitor vascular changes in normal aging in various hippocampal subfields will allow us to better understand vascular vulnerability across the hippocampus. METHODS: We recently introduced the concept of microvascular in-vivo contrast revealed origins (MICRO) protocol to image micro-cerebral vessels.1-3 MICRO uses ferumoxytol, an ultra-small superparamagnetic iron oxides (USPIO) agent, to induce susceptibility in the arteries and veins; and by imaging with high resolution (0.22×0.44×1 mm3) susceptibility weighted imaging sequence (SWI) at 3 T. Although the increased vascular susceptibility enhances the visibility of small sub-voxel vessels, the accompanying strong signal loss of the large vessels deteriorates the local tissue contrast. Hence, data are collected at different time points during a gradual administration (final concentration = 4 mg/kg) of ferumoxytol. Dynamically acquired SWI data were co-registered and combined (phase gradient-based adaptive combination or SWIPGAC) to reduce the blooming artifacts from large vessels, preserving the small-vessel contrast. RESULTS: The presence of ferumoxytol helped to enhance the microvasculature, something that has previously only been demonstrated in cadaver brain studies. Figure 1 shows the difference between the pre-contrast SWI and SWIPGAC data in visualizing the micro-vasculature across four healthy subjects. The intra-hippocampal and superficial major arteries (obtained through a non-linear subtraction method) and veins (obtained by averaging the T1-shortening map, pre-contrast quantitative susceptibility mapping (QSM) and pre-contrast R2* maps) are used as an overlay in the third column to better visualize the major vessels penetrating and draining the hippocampus. The hippocampal fissure, along with the fimbria, granular cell layer of the dentate gyrus and cornu ammonis layers (except for CA1), showed higher micro-vascular density than the other parts of hippocampus. The CA1 region exhibited a significant correlation with age (R=−0.37, p<0.05, n=37). demonstrating an overall loss of hippocampal vascularity in the normal aging process. Moreover, the vascular density reduction was more prominent than the age correlation with the volume reduction (R=−0.1, p>0.05, n=37) of the CA1 subfield. CONCLUSIONS: With this USPIO-induced increase in susceptibility comes the potential to study the cerebral micro-vasculature using high-resolution SWI. There was a strong
{"title":"In vivo vascular mapping of the human hippocampus using MICRO imaging","authors":"S. Buch, Y. Ge, E. M. E. Mark Haacke","doi":"10.4081/vl.2022.10944","DOIUrl":"https://doi.org/10.4081/vl.2022.10944","url":null,"abstract":"BACKGROUND: There is an urgent need for better detection and understanding of vascular abnormalities at the micro-level, where critical vascular nourishment and cellular metabolic changes occur. This is especially the case for structures such as the midbrain and hippocampus, where both the feeding and draining vessels are quite small. The hippocampus is a complex grey matter structure that plays an important role in spatial and episodic memory. It can be affected by a wide range of pathologies including vascular abnormalities. Being able to monitor vascular changes in normal aging in various hippocampal subfields will allow us to better understand vascular vulnerability across the hippocampus. \u0000METHODS: We recently introduced the concept of microvascular in-vivo contrast revealed origins (MICRO) protocol to image micro-cerebral vessels.1-3 MICRO uses ferumoxytol, an ultra-small superparamagnetic iron oxides (USPIO) agent, to induce susceptibility in the arteries and veins; and by imaging with high resolution (0.22×0.44×1 mm3) susceptibility weighted imaging sequence (SWI) at 3 T. Although the increased vascular susceptibility enhances the visibility of small sub-voxel vessels, the accompanying strong signal loss of the large vessels deteriorates the local tissue contrast. Hence, data are collected at different time points during a gradual administration (final concentration = 4 mg/kg) of ferumoxytol. Dynamically acquired SWI data were co-registered and combined (phase gradient-based adaptive combination or SWIPGAC) to reduce the blooming artifacts from large vessels, preserving the small-vessel contrast. \u0000RESULTS: The presence of ferumoxytol helped to enhance the microvasculature, something that has previously only been demonstrated in cadaver brain studies. Figure 1 shows the difference between the pre-contrast SWI and SWIPGAC data in visualizing the micro-vasculature across four healthy subjects. The intra-hippocampal and superficial major arteries (obtained through a non-linear subtraction method) and veins (obtained by averaging the T1-shortening map, pre-contrast quantitative susceptibility mapping (QSM) and pre-contrast R2* maps) are used as an overlay in the third column to better visualize the major vessels penetrating and draining the hippocampus. The hippocampal fissure, along with the fimbria, granular cell layer of the dentate gyrus and cornu ammonis layers (except for CA1), showed higher micro-vascular density than the other parts of hippocampus. The CA1 region exhibited a significant correlation with age (R=−0.37, p<0.05, n=37). demonstrating an overall loss of hippocampal vascularity in the normal aging process. Moreover, the vascular density reduction was more prominent than the age correlation with the volume reduction (R=−0.1, p>0.05, n=37) of the CA1 subfield. \u0000CONCLUSIONS: With this USPIO-induced increase in susceptibility comes the potential to study the cerebral micro-vasculature using high-resolution SWI. There was a strong","PeriodicalId":421508,"journal":{"name":"Veins and Lymphatics","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131341125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Evidence of the benefits of aerobic exercise training (AET) on brain structure, function, and perfusion in older adults is inconclusive. Methods: We conducted two randomized controlled trials (RCT) in sedentary older adults with or without mild cognitive impairment (MCI) to address this question.1-3 The trial’s intervention arm was a progressive moderate-to-vigorous intensity AET, and the active control arm was stretching-and-toning (SAT). Outcome measures included neurocognitive function focused on memory and executive function, global and regional brain volume and cortical thickness measured with structural magnetic resonance imaging (MRI), cerebral blood flow (CBF) and CBF pulsatility measured in the large cerebral arteries (the internal carotid artery, the vertebral artery, and the middle cerebral artery) with 2D duplex ultrasonography and transcranial Doppler, central arterial stiffness measured with arterial applanation tonometry, and cardiorespiratory fitness measured with treadmill peak oxygen consumption (V̇O2peak). The duration of both trials was one year. Results: In both studies, we observed that AET increased V̇O2peak significantly by ∼10% while it did not change with SAT. Cognitive composite scores and domain-specific scores improved in both the AET and SAT groups, although no group differences were observed (likely reflected by cognitive test practice effects). Total brain and hippocampal volume and mean cortical thickness decreased in both groups over one year. Conversely, AET increased CBF, and decreased central arterial stiffness and CBF pulsatility. Increases in V̇O2peak with AET were correlated with increases in CBF and decreases in cerebrovascular resistance (CVR). Further, the improved memory score in the AET group was associated with decreased CVR and central arterial stiffness measured with carotid β-stiffness index. Conclusions: Taken together, these findings demonstrated that one-year moderate-to-vigorous intensity AET increased CBF and decreased central arterial stiffness in older adults with or without MCI. We speculate that improvement in cerebrovascular function with AET may precede its potential effects on brain structure and neurocognitive function in older adults. (The research findings presented herein were supported by the National Institutes of Health R01AG033106 and R01HL102457)
{"title":"Aerobic exercise training reduces central arterial stiffness and improves cerebral blood flow in older adults","authors":"Rong Zhang","doi":"10.4081/vl.2022.10962","DOIUrl":"https://doi.org/10.4081/vl.2022.10962","url":null,"abstract":"Background: Evidence of the benefits of aerobic exercise training (AET) on brain structure, function, and perfusion in older adults is inconclusive. \u0000Methods: We conducted two randomized controlled trials (RCT) in sedentary older adults with or without mild cognitive impairment (MCI) to address this question.1-3 The trial’s intervention arm was a progressive moderate-to-vigorous intensity AET, and the active control arm was stretching-and-toning (SAT). Outcome measures included neurocognitive function focused on memory and executive function, global and regional brain volume and cortical thickness measured with structural magnetic resonance imaging (MRI), cerebral blood flow (CBF) and CBF pulsatility measured in the large cerebral arteries (the internal carotid artery, the vertebral artery, and the middle cerebral artery) with 2D duplex ultrasonography and transcranial Doppler, central arterial stiffness measured with arterial applanation tonometry, and cardiorespiratory fitness measured with treadmill peak oxygen consumption (V̇O2peak). The duration of both trials was one year. \u0000Results: In both studies, we observed that AET increased V̇O2peak significantly by ∼10% while it did not change with SAT. Cognitive composite scores and domain-specific scores improved in both the AET and SAT groups, although no group differences were observed (likely reflected by cognitive test practice effects). Total brain and hippocampal volume and mean cortical thickness decreased in both groups over one year. Conversely, AET increased CBF, and decreased central arterial stiffness and CBF pulsatility. Increases in V̇O2peak with AET were correlated with increases in CBF and decreases in cerebrovascular resistance (CVR). Further, the improved memory score in the AET group was associated with decreased CVR and central arterial stiffness measured with carotid β-stiffness index. \u0000Conclusions: Taken together, these findings demonstrated that one-year moderate-to-vigorous intensity AET increased CBF and decreased central arterial stiffness in older adults with or without MCI. We speculate that improvement in cerebrovascular function with AET may precede its potential effects on brain structure and neurocognitive function in older adults. (The research findings presented herein were supported by the National Institutes of Health R01AG033106 and R01HL102457)","PeriodicalId":421508,"journal":{"name":"Veins and Lymphatics","volume":"6 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123851026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background. Reduced cerebrovascular flow and localized hypoperfusion have been widely associated with various forms of cognitive impairment. Vascular cognitive impairment has also been associated with arterial stiffening and arteriosclerotic development. The linkages between cerebrovascular arteriosclerosis and localized cerebral ischemia, as dictated by the physics of fluid flow, while relatively unaddressed, are vascular contributions to cognitive impairment. Methods. The physics of fluid dynamics, particularly that of wave propagation in compliant vessels, was applied to the analysis of blood flow in a complex cerebrovascular tree, consisting of hundreds of thousands of arterial junctions. Each of these arterial junctions or bifurcations may partially reflect antegrade pulsatile flow into retrograde flow, resulting in reduced peripheral cerebral pulsatile flow. Results. The physics of fluid dynamics predicts1 that, at each bifurcation in the complex cerebrovascular maze, the percentage of antegrade flow which is reflected in retrograde flow is determined by the quotient of the arterial stiffnesses ratio and cross-sectional areas ratio on each side of each bifurcation. Physics predicts that, if the arterial stiffness/area ratios quotient is equal to unity then, ideally, there is no pulsatile retrograde flow. A ten percent pulsatile reflection would result from an arterial mismatch (in the quotation of trunk to branch artery stiffnesses to areas ratios) of about twenty percent. In other words, if a trunk artery at a bifurcation stiffens with aging by twenty percent relative to the bifurcations branch arteries, and the dimensions are unchanged, then the pulsatile antegrade flow reduces by about ten percent. In progressing from the extracranial arteries into the cerebral capillaries this pulsatile flow reduction process may be repeated at each bifurcation tier, causing an accumulating reduction in pulsatile flow into the capillaries. If the amplitude of the pulsatile retrograde flow is sufficiently large, the collision of the retrograde and antegrade pulsatile flows may result in transient flow reversal at select locations in the vascular bed. Such flow reversals may occur where a maximum in the retrograde flow pattern coincides with a minimum in the antegrade flow pattern, resulting in localized diastolic flow reversal. Persistent blood cell flow reversal, with its “scrubbing effect” on endothelial cells, combined with the flow’s associated pulse pressure amplification, may cause lifting of endothelial cells, thereby exposing the underlying intima and media to deposition of foreign materials, such as lipids and calcium. Hence, localized retrograde flow may induce arteriosclerotic development, which in turn, may increase bifurcation arterial stiffness ratios, which may further increase pulsatile flow reversals, increase arteriosclerotic development, decrease peripheral flow and increase arteriole ischemia at select cerebral locations. Conclusio
{"title":"Physics linkages between arterial stiffness, cerebrovascular flow and cognitive impairment","authors":"Trevor Tucker","doi":"10.4081/vl.2022.10958","DOIUrl":"https://doi.org/10.4081/vl.2022.10958","url":null,"abstract":"Background. Reduced cerebrovascular flow and localized hypoperfusion have been widely associated with various forms of cognitive impairment. Vascular cognitive impairment has also been associated with arterial stiffening and arteriosclerotic development. The linkages between cerebrovascular arteriosclerosis and localized cerebral ischemia, as dictated by the physics of fluid flow, while relatively unaddressed, are vascular contributions to cognitive impairment. \u0000Methods. The physics of fluid dynamics, particularly that of wave propagation in compliant vessels, was applied to the analysis of blood flow in a complex cerebrovascular tree, consisting of hundreds of thousands of arterial junctions. Each of these arterial junctions or bifurcations may partially reflect antegrade pulsatile flow into retrograde flow, resulting in reduced peripheral cerebral pulsatile flow. \u0000Results. The physics of fluid dynamics predicts1 that, at each bifurcation in the complex cerebrovascular maze, the percentage of antegrade flow which is reflected in retrograde flow is determined by the quotient of the arterial stiffnesses ratio and cross-sectional areas ratio on each side of each bifurcation. Physics predicts that, if the arterial stiffness/area ratios quotient is equal to unity then, ideally, there is no pulsatile retrograde flow. A ten percent pulsatile reflection would result from an arterial mismatch (in the quotation of trunk to branch artery stiffnesses to areas ratios) of about twenty percent. In other words, if a trunk artery at a bifurcation stiffens with aging by twenty percent relative to the bifurcations branch arteries, and the dimensions are unchanged, then the pulsatile antegrade flow reduces by about ten percent. In progressing from the extracranial arteries into the cerebral capillaries this pulsatile flow reduction process may be repeated at each bifurcation tier, causing an accumulating reduction in pulsatile flow into the capillaries. If the amplitude of the pulsatile retrograde flow is sufficiently large, the collision of the retrograde and antegrade pulsatile flows may result in transient flow reversal at select locations in the vascular bed. Such flow reversals may occur where a maximum in the retrograde flow pattern coincides with a minimum in the antegrade flow pattern, resulting in localized diastolic flow reversal. Persistent blood cell flow reversal, with its “scrubbing effect” on endothelial cells, combined with the flow’s associated pulse pressure amplification, may cause lifting of endothelial cells, thereby exposing the underlying intima and media to deposition of foreign materials, such as lipids and calcium. Hence, localized retrograde flow may induce arteriosclerotic development, which in turn, may increase bifurcation arterial stiffness ratios, which may further increase pulsatile flow reversals, increase arteriosclerotic development, decrease peripheral flow and increase arteriole ischemia at select cerebral locations. \u0000Conclusio","PeriodicalId":421508,"journal":{"name":"Veins and Lymphatics","volume":"151 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114638566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nicholas Young, R. Zivadinov, M. Dwyer, N. Bergsland, B. Weinstock-Guttman, D. Jakimovski
Background: Both greater retinal neurodegenerative pathology and greater cardiovascular burden have been seen in persons with multiple sclerosis (pwMS).1,2 Moreover, studies have described multiple extracranial and intracranial vasculature changes in pwMS.3 However, only a few studies have examined the retinal vasculature in multiple sclerosis (MS). Objectives: To determine if there are differences in retinal vasculature between pwMS and healthy controls (HCs) and their relationship to peripapillary retinal nerve fiber layer (pRNFL) thickness. Materials and methods: A total of 167 pwMS (113 relapsing-remitting MS (RRMS) and 54 progressive MS (PMS)) and 48 HCs were scanned using optical coherence tomography (OCT). Earlier OCT scans were available in a smaller sample size of 101 pwMS and 35 HCs for additional longitudinal 5-year follow-up analysis. The semiautomated segmentation of the retinal vasculature was performed in a blinded manner on peripapillary scans using the optical coherence tomography segmentation and evaluation GUI (OCTSEG) in MatLab. (Figure 1). Automated segmentation of the pRNFL was performed in the native Heidelberg OCT software. The sum of bilateral measures of total retinal vessel diameter, the total number of retinal vessels and average vessel diameter were calculated. Independent sample t-test and paired t-test were used for cross-sectional and longitudinal analyses, respectively and non-parametric Spearman’s test for determining correlations. Results: PwMS had a significantly smaller total vessel diameter (2.5 cm vs 2.7 cm, age-adjusted p=0.017) and numerically fewer number of retinal vessels when compared to HCs (35.1 vs 36.8, age-adjusted p=0.167). No significant differences between the pwRRMS and pwPMS were found. Over the follow-up, pwMS had significant decrease in number of retinal vessels (36.7 vs. 33.0, p<0.001) and significant increase in the average vessel diameter (0.072cm vs. 0.081cm, p<0.001). No longitudinal changes in the HCs were noted. Only in pwMS, lower pRNFL was associated with fewer retinal vessels and total vessel diameter (r=0.191, p=0.018 and r=0.216, p=0.007). Conclusions: PwMS have retinal vasculature that results in smaller and fewer retinal vessels when compared to HCs that were related to reduced pRNFL. Over time, a reduction of retinal vasculature occurred. Future investigations should determine the relevance of retinal vasculature in regards to MS disease outcomes, presence of cardiovascular abnormalities and cerebral/retinal perfusion.
背景:多发性硬化症(pwMS)患者的视网膜神经退行性病理和心血管负担均加重。此外，研究已经描述了多发性颅外和颅内脉管系统的改变然而，只有少数研究检查视网膜血管系统在多发性硬化症(MS)。目的:探讨pwMS与健康对照组(hc)视网膜血管是否存在差异及其与乳头周围视网膜神经纤维层(pRNFL)厚度的关系。材料和方法:采用光学相干断层扫描(OCT)对167例pwMS(113例复发缓解型MS (RRMS)和54例进行性MS (PMS))和48例hc进行扫描。早期的OCT扫描可用于101个pwMS和35个hc的较小样本量，用于额外的纵向5年随访分析。采用MatLab中的光学相干断层扫描分割和评估GUI (OCTSEG)，在盲法下对乳头周围扫描进行视网膜血管的半自动分割。(图1)。在本地海德堡OCT软件中对pRNFL进行自动分割。计算双侧视网膜血管总直径、视网膜血管总数和平均血管直径之和。横断面分析和纵向分析分别采用独立样本t检验和配对t检验，非参数Spearman检验确定相关性。结果:与hc相比，PwMS的血管总直径明显更小(2.5 cm vs 2.7 cm，年龄校正p=0.017)，视网膜血管数量也更少(35.1 vs 36.8，年龄校正p=0.167)。pwRRMS与pwPMS之间无显著差异。随访期间，pwMS组视网膜血管数量显著减少(36.7 vs. 33.0, p<0.001)，平均血管直径显著增加(0.072cm vs. 0.081cm, p<0.001)。没有观察到hcc的纵向变化。只有在pwMS中，较低的pRNFL与较少的视网膜血管和总血管直径相关(r=0.191, p=0.018和r=0.216, p=0.007)。结论:与pRNFL降低相关的hc相比，PwMS的视网膜血管更小、更少。随着时间的推移，视网膜血管减少。未来的研究应确定视网膜血管与MS疾病结局、心血管异常和脑/视网膜灌注的相关性。
{"title":"Retinal blood vessel analysis using optical coherence tomography in multiple sclerosis","authors":"Nicholas Young, R. Zivadinov, M. Dwyer, N. Bergsland, B. Weinstock-Guttman, D. Jakimovski","doi":"10.4081/vl.2022.10961","DOIUrl":"https://doi.org/10.4081/vl.2022.10961","url":null,"abstract":"Background: Both greater retinal neurodegenerative pathology and greater cardiovascular burden have been seen in persons with multiple sclerosis (pwMS).1,2 Moreover, studies have described multiple extracranial and intracranial vasculature changes in pwMS.3 However, only a few studies have examined the retinal vasculature in multiple sclerosis (MS). \u0000Objectives: To determine if there are differences in retinal vasculature between pwMS and healthy controls (HCs) and their relationship to peripapillary retinal nerve fiber layer (pRNFL) thickness. \u0000Materials and methods: A total of 167 pwMS (113 relapsing-remitting MS (RRMS) and 54 progressive MS (PMS)) and 48 HCs were scanned using optical coherence tomography (OCT). Earlier OCT scans were available in a smaller sample size of 101 pwMS and 35 HCs for additional longitudinal 5-year follow-up analysis. The semiautomated segmentation of the retinal vasculature was performed in a blinded manner on peripapillary scans using the optical coherence tomography segmentation and evaluation GUI (OCTSEG) in MatLab. (Figure 1). Automated segmentation of the pRNFL was performed in the native Heidelberg OCT software. The sum of bilateral measures of total retinal vessel diameter, the total number of retinal vessels and average vessel diameter were calculated. Independent sample t-test and paired t-test were used for cross-sectional and longitudinal analyses, respectively and non-parametric Spearman’s test for determining correlations. \u0000Results: PwMS had a significantly smaller total vessel diameter (2.5 cm vs 2.7 cm, age-adjusted p=0.017) and numerically fewer number of retinal vessels when compared to HCs (35.1 vs 36.8, age-adjusted p=0.167). No significant differences between the pwRRMS and pwPMS were found. Over the follow-up, pwMS had significant decrease in number of retinal vessels (36.7 vs. 33.0, p<0.001) and significant increase in the average vessel diameter (0.072cm vs. 0.081cm, p<0.001). No longitudinal changes in the HCs were noted. Only in pwMS, lower pRNFL was associated with fewer retinal vessels and total vessel diameter (r=0.191, p=0.018 and r=0.216, p=0.007). \u0000Conclusions: PwMS have retinal vasculature that results in smaller and fewer retinal vessels when compared to HCs that were related to reduced pRNFL. Over time, a reduction of retinal vasculature occurred. Future investigations should determine the relevance of retinal vasculature in regards to MS disease outcomes, presence of cardiovascular abnormalities and cerebral/retinal perfusion.","PeriodicalId":421508,"journal":{"name":"Veins and Lymphatics","volume":"19 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114216243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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