Types Of Vascular Lesions Research Articles

Placental histopathology associated with pre-eclampsia: systematic review and meta-analysis.

Pre-eclampsia (PE) is associated with impaired trophoblastic invasion and typical villous and vascular placental lesions. The primary aim of this study was to quantify the prevalence of placental histopathological lesions in pregnancies complicated by PE. MEDLINE, EMBASE and CINAHL were searched electronically, and relevant articles reporting on placental histopathological lesions were assessed according to the following criteria: study design, number of pregnancies included, severity of PE and whether the pathologist was blinded to the clinical information. Prospective and retrospective case-control studies including ≥ 100 pregnancies were included in the systematic review. The incidence of each type of histological lesion according to the Perinatal Section of the Society for Pediatric Pathology classification in pre-eclamptic and normal pregnancies was identified, and lesions were categorized into two main groups: villous lesions and vascular lesions. Random-effects meta-analysis of proportions was used for analysis. Between-study heterogeneity was assessed using the I2 statistic. The search yielded 717 citations, and a total of eight studies (four blinded and four non-blinded) were included in the review. In unblinded studies, the pooled prevalence of villous lesions was 11.6% and 48.2% in normal and pre-eclamptic pregnancies, respectively, giving a pooled odds ratio (OR) of 7.59. In blinded studies, the pooled prevalence of villous lesions was 18.5% and 42.0% in normal and pre-eclamptic pregnancies, respectively, giving a pooled OR of 4.28. In unblinded studies, the pooled prevalence of vascular lesions was 8.1% and 37.3% in normal and pre-eclamptic pregnancies, respectively, giving a pooled OR of 20.34. In blinded studies, the pooled prevalence of vascular lesions was 9.8% and 38.9%, in normal and pre-eclamptic pregnancies, respectively, giving a pooled OR of 7.08. In blinded studies, the incidence of both placental villous and vascular histopathological lesions is four- to seven-fold higher in pre-eclamptic than in normal pregnancies. Greater differences are reported in unblinded studies. Despite the higher probability (point prevalence) of finding abnormal placental pathology in pregnancies with PE, placental lesions are not specific to the diagnosis of PE. Copyright © 2017 ISUOG. Published by John Wiley & Sons Ltd.

Imaging of Vascular Lesions in Pediatric

Background: The most common soft tissue tumors during infancy and childhood are vascular lesions. Although the vast majority of these lesions have typical clinical features with no need for any further exam, but sometimes atypical superficial or deeply located lesions require complementary studies to be diagnosed and classified. In that way it is also very important to exclude very less common malignant soft tumors. Imaging studies play an essential role for categorization of vascular lesions before taking any therapeutic decision. Methods: Vascular tumors such as hemangiomas and vascular malformations have their own imaging characteristics to be classified. Although MRI is the best imaging modality because of its excellent soft tissue resolution, but Ultrasound and Color Doppler studies are the first step and sometimes preferred imaging approach in most of the cases. This is a review article to describe different types of vascular lesions in childhood and infancy and explain various imaging findings of each one.

Endovascular coil oclusion of spontaneous ruptured vertebral artery dissecting aneurysm

Abstract Spontaneous dissecting aneurysm of vertebral artery is known as a rare pathological condition causing a subarachnoid hemorrhage in the posterior circulation. The treatment of ruptured vertebral artery dissecting aneurysms is still an important subject of debates in the literature. We present a particular case of ruptured vertebral artery dissecting aneurysms that was treated by only endovascular Guglielmi detachable coils occlusion. A brief review of technical possibilities of treatment of these types of vascular lesions, with their advantages and disadvantages are discussed.

Impaired Neovascularization and Reduced Capillary Supply in the Malignant vs. Non-malignant Course of Experimental Renovascular Hypertension.

Malignant hypertension develops in some cases of hypertension but not in others. We hypothesized that an impaired neovascularization and a reduced capillary supply characterizes the malignant course of experimental hypertension. Two-kidney, one-clip renovascular hypertension was induced in rats; controls (sham) were sham operated. To distinguish malignant hypertension from non-malignant hypertension, we considered two factors: weight loss, and the number of typical vascular lesions (onion skin lesions and fibrinoid necroses) per kidney section of the nonclipped kidney. Animals in the upper half for both criteria were defined as malignant hypertensives. After 5 weeks, mean arterial blood pressure was elevated to the same degree in malignant hypertension and non-malignant hypertension whereas plasma renin and aldosterone were significantly higher in malignant hypertensives. The expression of plasminogen activator inhibitor-1 was elevated (up to 14-fold) in non-malignant but significantly more increased (up to 36-fold) in malignant hypertensive rats, compared to sham. As a bioassay for neovascularization, the area of granulation tissue ingrowth in polyvinyl discs (implanted subcutaneously) was reduced in malignant hypertension compared to non-malignant hypertension and sham, while there was no difference between non-malignant hypertension and sham. The number of renal and left ventricular capillaries was significantly lower in malignant hypertension compared to non-malignant hypertension, as was the number of proliferating endothelial cells. We conclude that an impaired neovascularization and capillarization occurs in malignant renovascular hypertension but not in the non-malignant course of the disease despite comparable blood pressure levels. This might contribute to the unique vascular lesions and progressive target organ damage observed in malignant hypertension.

Lymph vessels: the forgotten second circulation in health and disease.

The lymphatic circulation is still a somewhat forgotten part of the circulatory system. Despite this, novel insights in lymph angiogenesis in health and disease, application of immune markers for lymphatic growth and differentiation and also the introduction of new imaging techniques to visualize the lymphatic circulation have improved our understanding of lymphatic function in both health and disease, especially in the last decade. These achievements yield better understanding of the various manifestations of lymph oedemas and malformations, and also the patterns of lymphovascular spread of cancers. Immune markers that recognize lymphatic endothelium antigens, such as podoplanin, LYVE-1 and Prox-1, can be successfully applied in diagnostic pathology and have revealed (at least partial) lymphatic differentiation in many types of vascular lesions.Electronic supplementary materialThe online version of this article (doi:10.1007/s00428-016-1945-6) contains supplementary material, which is available to authorized users.

Iatrogenic vascular injuries during arthroplasty of the hip.

Vascular injuries during total hip arthroplasty (THA) are rare but when they occur, have serious consequences. These have traditionally been managed with open exploration and repair, but more recently there has been a trend towards percutaneous endovascular management. We performed a systematic review of the literature to assess if this change in trend has led to an improvement in the overall reported rates of morbidity and mortality during the last 22 years in comparison with the reviews of the literature published previously. We found a total of 61 articles describing 138 vascular injuries in 124 patients. Injuries because of a laceration were the most prevalent (n = 51, 44%) and the most common presenting feature, when recorded, was bleeding (n = 41, 53.3%). Delay in diagnosis was associated with the type of vascular lesion (p < 0.001) and the clinical presentation (p = 0.002). Open exploration and repair was the most common form of management, however percutaneous endovascular intervention was used in one third of the injuries and more constantly during the last 13 years. The main overall reported complications included death (n = 9, 7.3%), amputation (n = 2, 1.6%), and persistent ischaemia (n = 9, 7.3%). When compared with previous reviews there was a similar rate of mortality but lower rates of amputation and permanent disability, especially in patients managed by endovascular strategies.

Impact of local vascular lesions assessed with optical coherence tomography and ablation points on blood pressure reduction after renal denervation

Local vascular injury is detectable with optical coherence tomography (OCT) after catheter-based renal denervation (RDN). However, it is unclear whether the number and type of vascular lesions or the number of ablation points could affect blood pressure (BP) reduction. The aim of the study was to assess the impact of vascular injury induced by RDN detected with OCT and the number of ablation points on BP response after 1, 3 and 6 months. RDN was either performed with a Simplicity catheter or an EnligHTNTM multielectrode basket followed by OCT. BP was recorded prospectively as office measurement and 24-hour ambulatory blood pressure monitoring (24-h ABPM) at each time point. Correlations between type and number of vascular lesions, as well as ablation points, on BP reduction were performed. Out of 16 patients, two were lost to BP follow-up. We documented a BP reduction at 1, 3 and 6 months in both office and 24-h ABPM. The Δmean office systolic BP (SBP) reduction was -18.75 ± 24.55 mm Hg, -20.58 ± 16.92 mm Hg and -18.75 ± 29.39 mm Hg, respectively, and the Δmean 24h-ABPM SBP reduction was -6.50 ± 23.45 mm Hg, -16.88 ± 26.64 mm Hg and -13.89 ± 21.20 mm Hg, respectively. The number of vascular lesions did not correlate with office and 24h-SBP and diastolic BP reduction. However, there was a correlation between ablation points and office Δmean SBP reduction at 6 months (p <0.02). Our study demonstrates for the first time that the number and type of vascular lesions as assessed with OCT did not predict the success of BP reduction after RDN. However, we observed a substantial decrease in office SBP in relation to the number of ablation points at 6 months.

Clinical and Imaging Analysis of a Cerebellar Watershed Infarction

Objective: To investigate the characteristics of vascular lesions in patients with a cerebellar watershed infarction. Methods: Clinical data from 178 cases of cerebellar infarction were collected with magnetic resonance imaging (MRI) scan results, including diffusion weighted imaging (DWI), a magnetic resonance angiography (MRA), and computed tomography angiography (CTA). The cases were divided into cerebellar watershed and non-watershed infarctions based on lesion location, which was revealed by DWI. Forty-two cases met the criteria for a cerebellar watershed infarction. Based on the MRA/CTA results, the vertebrobasilar artery stenoses were divided into four categories (i.e., intracranial, extracranial, combined, and no detectable stenosis) to compare the vascular lesion characteristics from patients with a cerebellar watershed infarction and patients with a non-watershed infarction. Results: Patients with cerebellar watershed infarcts presented mild symptoms at onset and had a favorable prognosis. However, 90.5% of these patients had a vascular stenosis, which was higher than for patients with a cerebellar non-watershed infarction (74.3%). The four types of vascular lesions, intracranial, extracranial, combined, and no detectable stenosis, were 14.3%, 52.4%, 23.8%, and 9.5% in patients with a cerebellar watershed infarction and 33.8%, 16.2%, 24.3%, and 25.7% in patients with a non-watershed cerebellar infarction, respectively. Conclusion: Although patients with cerebellar watershed infarcts often had comparatively benign clinical manifestations and prognoses, such patients also had a high stenosis prevalence in major blood vessels, especially the extracranial segment in the vertebral artery, which required early intervention and treatment.

Dental considerations of capillary malformation

Hemangiomas and vascular malformations (VMs) are the two types of vascular lesions. VMs are further subdivided according to the type of involved vessels present as arterial, arterio-venous, venous, and capillary or lymphatic malformations. The capillary malformation (CM) previously was considered to be a hemangioma and was known as port wine stain, and hereby presenting a case report on the orodental manifestations of CM.

Surgical management of cervical radiculomedullary arterial aneurysm with subarachnoid haemorrhage: A case report

The aim of this paper was to report an unusual case of a 30-year-old woman admitted to the emergency department for a subarachnoid spinal haemorrhage. Clinical presentation was typical and the initial CT-scan did not show any intracranial lesions. Diagnosis was then confirmed by a full-spinal MRI that revealed a cervical radiculomedullary artery aneurysm. The diagnosis was also confirmed by an arteriography that showed a left C6 radiculomedullary artery aneurysm. Surgical management was performed and included a direct approach of the vascular lesion using an anterolateral cervicotomy and occlusion of the parent vessel. Histological examination confirmed the typical aspect of the aneurysm. The postoperative course was uneventful and the patient was discharged from hospital at day 15. This type of vascular lesion is very uncommon and requires a prompt diagnosis. Initial MRI can confirm the presence of a subarachnoid haemorrhage related to the aneurysm, which can be also visualized by an arteriography. Management of these vascular disorders requires a multidisciplinary specialized spine-team and is commonly performed using a direct surgical approach.

Isolated anti‐β2‐glycoprotein I antibodies in neurology: a frontier syndrome between multiple sclerosis and antiphospholipid syndrome?

Anti-β2-glycoprotein I (anti-β2-GPI) antibodies are part of the heterogeneous family of antiphospholipid antibodies and seem to be present in various neurological manifestations in addition to antiphospholipid syndrome (APS). Our objective was to analyse the clinical, radiological and therapeutic characteristics of neurological patients with positive anti-β2-GPI antibodies and without the Sapporo criteria for APS. The medical records were retrospectively reviewed of 28 consecutive patients hospitalized in the Neurology Department of Strasbourg University Hospital, France, in whom anti-β2-GPI antibodies (immunoglobulin G and/or immunoglobulin M) were positive and other antiphospholipid antibodies negative, from November 2005 to July 2011. Clinical, radiological, biological and therapeutic data and clinical course were studied. Positive anti-β2-GPI antibodies were present in 28 patients. The predominant physiopathological process was mainly inflammatory (25% with myelitis, 14.3% with optic neuritis) or vascular (14.3% with cerebral ischaemia, 7.1% with cerebral vasculitis). Brain magnetic resonance imaging was performed in 89.3% of patients: atypical lesions were observed in 44% and typical inflammatory and vascular lesions in 16% and 12%, respectively. The anti-β2-GPI antibody seems to be involved in two types of neurological disease: vascular or inflammatory 'multiple sclerosis-like' disease. These two types of patients frequently develop an autoimmune disease (multiple sclerosis, systemic lupus erythematosus, APS). However, a large proportion of the patients had an undefined profile with aspecific cerebral lesions and required monitoring. This study raises questions about a separate entity at the border between APS and multiple sclerosis which remains to be better defined in a larger cohort.

Formation of typical vascular lesions in a new experimental model of pulmonary arterial hypertension

Formation of typical vascular lesions in a new experimental model of pulmonary arterial hypertension

Multiphase post-mortem computed tomography angiography in seven lethal cases of great height falls: Preliminary results of a French experience

Background The use of enhanced multislice computed tomography (MSCT) in forensic sciences has been recently developed in order to improve radiological vascular and organs injuries detection. Methods Seven suicidal cases of great height falls (4 women, and 3 men) underwent a multiphase post-mortem computed tomography angiography (MPMCTA) before medico-legal autopsy. The estimated height falls varied from 5 to 15 m. All corpses were prepared with a surgical cannulation of femoral vessels. After a non-MSCT exploration, a controlled perfusion device (Virtangio ® machine) was used with paraffin oil mixed with specific contrast agent (Angiofil ® ), allowing three time-different acquisitions (arterial, venous, dynamic). Two radiologists proceeded to images analysis. The forensic pathologist undergoing autopsies knew preliminary imaging results. Results The results of MPMCTA explorations and autopsies differed concerning detection of gas, bone fractures, and vascular ruptures (mainly cerebral), with a superiority of the MPMCTA. Autopsies were superior to MPMCTA for detection of some superficial skin lesions, which were easily accessible to external examination. Discussion Both techniques were able to diagnose some classical and typical bone, visceral and vascular lesions. Additionally, some rare injuries were found like coronary desinsertion, double thoracic aortic ruptures, inferior vena cava laceration extended to the right atrium, and pulmonary vein disruption. These findings were found with both techniques, but MPMCTA permitted better in situ lesions' illustration and documentation. Furthermore, realization of different-time acquisitions was essential for detection and comprehension of abnormal traumatic communication between cardiac cavities. Conclusion This study illustrates the complementarity of MPMCTA and autopsy in traumatic cases, and especially for cases of lethal great height falls.

Bone morphogenetic protein receptor 2 in patients with idiopathic portal hypertension

In idiopathic portal hypertension (IPH) typical vascular lesions are present in the branches of the portal vein or in the perisinusoidal area of the liver. Similar histological alterations have been reported in the pulmonary vasculature of patients with idiopathic pulmonary artery hypertension (IPAH). As IPAH is associated with mutations of the bone morphogenetic protein receptor 2 (BMPR2) gene, the aim of this study was to investigate whether this association might also be found in patients with IPH. Twenty-three samples belonging to 21 unrelated caucasian patients with IPH followed in the hepatic haemodynamic laboratory of the Hospital Clinic in Barcelona were included in the study. All patients were studied for the entire open reading frame and splice site of the BMPR2 gene by direct sequencing and multiple ligation probe amplification (MLPA) in order to detect large deletions/duplications. None of the 23 patients had pulmonary artery hypertension. Four patients presented one single nucleotide polymorphism (SNP) in intron 5, four patients had a SNP in exon 12 and a SNP in exon 1 was found in two cases. Two patients had both intron 5 and exon 12 polymorphisms. All SNPs were previously described. Except for these three SNPs, neither mutations nor rearrangements have been identified in the BMPR2 gene in this population. We did not detect mutations or rearrangements in the coding region of the BMPR2 gene in our patients with IPH. These findings suggest that, in contrast to IPAH, mutations in BMPR2 are not involved in the pathogenesis of IPH.

Vascular dementia: Different forms of vessel disorders contribute to the development of dementia in the elderly brain

The diagnosis of vascular dementia (VaD) describes a group of various vessel disorders with different types of vascular lesions that finally contribute to the development of dementia. Most common forms of VaD in the elderly brain are subcortical vascular encephalopathy, strategic infarct dementia, and the multi infarct encephalopathy. Hereditary forms of VaD are rare. Most common is the cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Sporadic forms of VaD are caused by degenerative vessel disorders such as atherosclerosis, small vessel disease (SVD) including small vessel arteriosclerosis, arteriolosclerosis, and lipohyalinosis, and cerebral amyloid angiopathy (CAA). Less frequently inflammatory vessel disorders and tumor-associated vessel lesions (e.g. angiocentric T-cell or angiotropic large cell lymphoma) can cause symptoms of dementia. Here, we review and discuss the impact of vessel disorders to distinct vascular brain tissue lesions and to the development of dementia in elderly individuals. The impact of coexisting neurodegenerative pathology in the elderly brain to VaD as well as the correlation between SVD and CAA expansion in the brain parenchyma with that of Alzheimer's disease (AD)-related pathology is highlighted. We conclude that “pure” VaD is rare and most frequently caused by infarctions. However, there is a significant contribution of vascular lesions and vessel pathology to the development of dementia that may go beyond tissue damage due to vascular lesions. Insufficient blood blow and alterations of the perivascular drainage mechanisms of the brain may also lead to a reduced protein clearance from extracellular space and subsequent increase of proteins in the brain parenchyma, such as the amyloid β-protein, and foster, thereby, the development of AD-related neurodegeneration. As such, it seems to be important for clinical practice to consider treatment of potentially coexisting AD pathology in cognitively impaired patients with vascular lesions.

Postcricoid vascular lesions

Postcricoid vascular lesions are a rare cause of dysphagia and stridor in the pediatric population. Currently, there is no clear consensus on what type of vascular lesions are common in the postcricoid area because adequate histological or immunohistochemistry studies are lacking. This study aimed to describe the histology and immunohistochemistry of postcricoid masses in our institutions' experience, and consolidate available data on the symptoms, management, and histology of these unusual malformations with a comprehensive literature review. Retrospective patient and literature review. A retrospective review of patients with postcricoid vascular lesions was performed at two pediatric tertiary care institutions. Histology and immunohistochemistry studies were performed in patients undergoing a lesion biopsy. A complete literature review of the English language was completed for cases involving vascular lesions of the postcricoid area. Four patients were identified in our study with postcricoid vascular lesions. All patients presented with symptoms of dysphagia and intermittent stridor. Histology and immunohistochemistry studies were performed in three patients. GLUT-1 was negative in all three patients, and CD34 was positive in all patients tested. Lewis Y antigen was performed in one patient and was negative. A description of 19 cases reported in the English literature is included. Patients with postcricoid vascular lesions usually present with mild to moderate feeding difficulties, and stridor or dyspnea with agitation. Histopathology and immunohistochemistry results suggest that postcricoid vascular lesions may often represent congenital vascular malformations instead of infantile hemangiomas.

Abortive hemangiomas. Description of clinical and pathological findings with special emphasis on dermoscopy

Infantile hemangiomas (IH) are the most commonly found benign neoplasia in childhood. Up to a third of IH may be present at birth and develop in 3 clearly defined stages. In their endothelial cells, IH express an erythocyte type glucose transport protein (GLUT-1), highly specific to this type of lesion, which enables them to be differentiated from other types of vascular lesions, including congenital hemangiomas (RICH or NICH) and capillary malformations. We present clinical, dermoscopic and histological descriptions of two patients with vascular lesions present at birth whose immunohistochemical GLUT-1 confirmed that they were IH, although their course was not characteristic of this type of lesion. These IH have been called abortive or minimal-growth hemangiomas (AH). We believe that this is the first dermoscopic description of AH and suggest that this technique is a useful diagnostic tool that enables diagnosis to be made without the need for a biopsy.

The neuroanatomical model of post-stroke depression: Towards a change of focus?

One third of all stroke survivors develop post-stroke depression (PSD). Depressive symptoms adversely affect rehabilitation and significantly increase risk of death in the post-stroke period. One of the theoretical views on the determinants of PSD focuses on psychosocial factors like disability and social support. Others emphasize biologic mechanisms such as disruption of biogenic amine neurotransmission and release of proinflammatory cytokines. The “lesion location” perspective attempts to establish a relationship between localization of stroke and occurrence of depression, but empirical results remain contradictory. These divergences are partly related to the fact that neuroimaging methods, unlike neuropathology, are not able to assess precisely the full extent of stroke-affected areas and do not specify the different types of vascular lesions. We provide here an overview of the known phenomenological profile and current pathogenic hypotheses of PSD and present neuropathological data challenging the classic “single-stroke”-based neuroanatomical model of PSD. We suggest that vascular burden due to the chronic accumulation of small macrovascular and microvascular lesions may be a crucial determinant of the development and evolution of PSD.

Donepezil in patients with subcortical vascular cognitive impairment

Introduction: Studies of the effect of cholinesterase inhibitors in vascular dementia have been hampered by clinical heterogeneity in terms of type of vascular lesions, location of lesions, and degree of concomitant Alzheimer’s disease (AD) pathology. In a meta-analysis of eight double-blind, placebo-controlled trials in vascular dementia, including three with donepezil, one with rivastigmine, two with galantamine, and two with memantine, the extent of severe white matter lesions ranged from 18% to 64%, and the presence of cortical lesions was 12% to 46% in the cholinesterase-inhibitor groups [ 1 ]. These trials showed a consistent modest benefi t of 1 to 2 points on the Alzheimer’s Disease Assessment Scale–cognitive subscale (ADAS-Cog), which was derived from improvement in the treated group rather than worsening of the placebo group. However, there was no corresponding improvement in the clinical global or activity of daily living (ADL) measures, which is a requirement for regulatory approval. The mechanism by which cholinesterase inhibitors might improve cognition in vascular dementia is unknown. Cholinesterase inhibitors may act by increasing postsynaptic acetylcholine caused by disruption (infarction) of subcortical or cortical cholinergic pathways [ 2 , 3 ]. Memantine has also been shown to be effective in a pooled analysis, specifi cally in patients with vascular dementia with small vessel disease compared with placebo [ 4 ]. The similar benefi t of cholinesterase inhibitors and memantine in both AD and vascular dementia suggests that the mechanism of action could be due to the effects on AD pathology. Because so many individuals with vascular dementia also have AD pathology, it is diffi cult to determine the potential mechanism for improvement. Treatment of cerebral, autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), which is caused by a mutation in the NOTCH3 gene [ 5 ], provides an opportunity to determine the extent to which treatment with cholinesterase inhibitors might affect a more pathologically homogeneous entity. Executive function and attention are the most commonly affected domains, and these impairments may occur early, prior to overt stroke. CADASIL has been shown to be a good model for sporadic cerebral small vessel disease because the pattern of cognitive impairment, particularly executive dysfunction, is similar [ 6 ] and because dementia occurs at a younger age in CADASIL, making the presence of AD pathology less likely. Disruption of ascending cholinergic pathways from the nucleus basalis of Meynert through the external capsule to the cortex without concomitant AD pathology in the nucleus basalis of Meynert or cortex has been demonstrated in CADASIL [ 7 ].

An Unusual Cause of Young Hypertension

AbstractA 16‐year‐old male was evaluated for hypertension. On clinical examination, he had features suggestive of type 1 neurofibromatosis (NF1). Further, he had feeble pulse over both lower limbs, with arterial bruit over the abdomen. A magnetic resonance angiogram revealed constriction of the abdominal aorta with bilateral renal artery stenosis. This type of vascular lesion in NF1 is a rare entity. It may be progressive and requires timely intervention to control hypertension and prevent ischemic nephropathy.