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Venous Anomalies (venous + anomaly)

Distribution by Scientific Domains
Medical Sciences88%

Kinds of Venous Anomalies

  • developmental venous anomaly
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    Selected Abstracts

    Development of a Posterior Fossa Cavernous Malformation Associated With Bilateral Venous Anomalies: Case Report

    JOURNAL OF NEUROIMAGING, Issue 4 2002
    Jason Sheehan MD
    ABSTRACT Venous angiomas (VAs) and cavernous malformations (CMs) are common cerebrovascular malformations. Frequently, these lesions are found in close proximity. The interrelationship between VAs and CMs has not yet been adequately defined. The authors report a case of a 48-year-old man with progressive dysarthria, dysmetria, and ataxia. Eight years previously, magnetic resonance imaging (MRI) revealed a solitary CM and bilateral posterior fossa VAs. Later imaging after neurological progression revealed the presence of 2 rather than 1 CMadjacent to the VAs. The sequential imaging suggests a causal relationship between VAs and some CMs. Furthermore, the detailed MRI permitted radiosurgical treatment of these CMs. The occurrence of de novo CMs adjacent to VAs on future imaging studies in other patients may help confirm the etiology of at least a subset of CMs. [source]

    Genetics, epigenetics and pharmaco-(epi)genomics in angiogenesis

    JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 6b 2008
    Ian Buysschaert
    ,,Introduction ,,Angiogenesis is genetically pre-determined ,,Mutations causing vascular anomalies -,Venous anomalies -,Haemangiomas -,The transforming growth factor-ß in vascular anomalies -,Cerebral cavernous malformations ,,Translocations reveal novel angiogenic genes ,,Single nucleotide polymorphisms shape the angio-genome -,SNPs in VEGF and their association with cancer -,SNPs in VEGF pathway genes associated with other diseases -,Genetic variability in VEGFR-2 -,Genetic variability in HIF-1, -,SNPs in VEGFR-1 integrate angiogenesis within the P53 pathway -,Variations in angiogenic genes are linked with neurodegeneration -,Angiogenic factors in genome-wide association studies ,,Copy number variability affects angiogenesis ,,Epigenetic regulation of angiogenesis -,Methylation of anti-angiogenic factors -,Methylation as a second hit event in cancer -,Histone modifications determine angiogenesis ,,Micromanagers of angiogenesis ,,Perspectives Abstract Angiogenesis is controlled by a balance between pro- and anti-angiogenic factors. Studies in mice and human beings have shown that this balance, as well as the general sensitivity of the endothelium to these factors, is genetically pre-determined. In an effort to dissect this genetic basis, different types of genetic variability have emerged: mutations and translocations in angiogenic factors have been linked to several vascular malformations and haemangiomas, whereas SNPs have been associated with complex genetic disorders, such as cancer, neurodegeneration and diabetes. In addition, copy number alterations of angiogenic factors have been reported in several tumours. More recently, epigenetic changes caused by aberrant DNA methylation or histone acetylation of anti-angiogenic molecules have been shown to determine angiogenesis as well. Initial studies also revealed a crucial role for microRNAs in stimulating or reducing angiogenesis. So far, most of these genetic studies have focused on tumour angiogenesis, but future research is expected to improve our understanding of how genetic variants determine angiogenesis in other diseases. Importantly, these genetic insights might also be of important clinical relevance for the use of anti-angiogenic strategies in cancer or macular degeneration. [source]

    Abnormal venous and arterial patterning in chordin mutants

    DEVELOPMENTAL DYNAMICS, Issue 9 2007
    Emmanučle C. Délot
    Abstract Classic dye injection methods yielded amazingly detailed images of normal and pathological development of the cardiovascular system. However, because these methods rely on the beating heart of diffuse the dyes, the vessels visualized have been limited to the arterial tree, and our knowledge of vein development is lagging. In order to solve this problem, we injected pigmented methylsalicylate resins in mouse embryos after they were fixed and made transparent. This new technique allowed us to image the venous system and prompted the discovery of multiple venous anomalies in Chord,/, mutant mice. Genetic inactivation of Chordin, an inhibitor of the Bone Morphogenetic Protein signaling pathway, results in neural crest defects affecting heart and neck organs, as seen in DiGeorge syndrome patients. Injection into the descending aorta of Chrd,/, mutants demonstrated how a very severe early phenotype of the aortic arches develops into persistent truncus arteriosus. In addition, injection into the atrium revealed several patterning defects of the anterior cardinal veins and their tributaries, including absence of segments, looping and midline defects. The signals that govern the development of the individual cephalic veins are unknown, but our results show that the Bone Morphogenetic Protein pathway is necessary for the process. Developmental Dynamics 236:2586,2593, 2007. © 2007 Wiley-Liss, Inc. [source]

    Isolated right-sided varicocele as a salvage pathway for portal hypertension

    INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 6 2005
    G-M. Pinggera
    Summary Retrograde blood flow can occur in the testicular veins and in the pampiniformis plexus in the absence of valves or if the valves are incompetent, resulting in tortuosity and dilatation of the veins. These abnormal alterations in the anatomy of the veins, termed varicoceles, are associated with infertility in the male. Most varicoceles occur on the left. We report the case of a rare isolated right-sided varicocele in a male evaluated for infertility in whom extensive work-up revealed venous anomalies and a spontaneous porto-systemic shunt. In such cases, standard approaches to infertility treatment are fruitless. [source]

    Cerebral developmental venous anomalies: Current concepts,

    ANNALS OF NEUROLOGY, Issue 3 2009
    Diego San Millán Ruíz MD
    Cerebral developmental venous anomalies are the most frequently encountered cerebral vascular malformation, and as such, are frequently reported as fortuitous findings in computed tomography (CT) and magnetic resonance imaging (MRI) studies. Developmental venous anomalies (DVAs) are generally considered extreme anatomical variations of the cerebral vasculature, and follow a benign clinical course in the vast majority of cases. Here we review current concepts on DVAs with the aim of helping clinicians understand this complex entity. Morphological characteristics that are necessary to conceptualize DVAs are discussed in depth. Images modalities used in diagnosing DVAs are reviewed, including new MRI or CT techniques. Clinical presentation, association with other vascular malformations and cerebral parenchymal abnormalities, and possible physiopathological processes leading to associated imaging or clinical findings are discussed. Atypical forms of DVAs are also reviewed and their clinical significance discussed. Finally, recommendations as to how to manage asymptomatic or symptomatic patients with a DVA are advanced. Ann Neurol 2009;66:271,283 [source]

    Vascular anomalies in Proteus syndrome

    CLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 3 2004
    P. H. Hoeger
    Summary Proteus syndrome (PS) is a complex hamartomatous disorder defined by local overgrowth (macrodactyly or hemihypertrophy), subcutaneous tumours and various bone, cutaneous and/or vascular anomalies (VA). VA are manifold in PS, but their prevalence is unknown so far. In order to further characterize PS, we studied the prevalence of VA in 22 PS patients presenting to our outpatient clinic and reviewed 100 PS patients previously reported between 1983 and 2001. The diagnosis of vascular abnormalities was made on clinical grounds and supported with imaging studies and/or histology in 12 and seven patients out of 22, respectively. Thirty-five VA were identified in 22/22 (100%) of our patients, and more than one type of VA were present in 10 of them. Vascular tumours, portwine stains (PWS), and venous anomalies (varicosities, prominent veins) were equally common. A total of 118 VA were previously reported in 70/100 (70%) PS patients; vascular hamartomas were more prevalent (56/118 = 47.5%), whilst PWS (21.2%) and venous anomalies (22.9%) were slightly less common than in our series, but there is the possibility of under-reporting. Unlike Klippel,Trenaunay syndrome, where VA are mostly confined to the hypertrophic limb, major arteriovenous anomalies are rare, and ,,similar to the other hamartomas and naevi observed in PS (pigmentary naevi, epidermal naevi, subcutaneous tumours, exostoses) , VA appear to be distributed at random sites on the body. We conclude that VA are among the most common findings in PS. Their varying type and distribution lend further support to the concept of somatic mosaicism. [source]

    Pyogenic abscess complicating a resolving cerebral haematoma secondary to a cavernous haemangioma: Computed tomography and magnetic resonance imaging findings

    JOURNAL OF MEDICAL IMAGING AND RADIATION ONCOLOGY, Issue 2 2005
    AD Borsaru
    Summary A case is discussed of a brain abscess complicating an intracerebral haemorrhage occurring in a cavernous haemangioma. A young child presented with focal seizures as a result of a large intracerebral haemorrhage, occurring in a cavernous haemangioma. The only clue to the underlying vascular malformation was the presence of an associated developmental venous anomaly. The case was complicated by the development of a brain abscess at the site of the intracranial haematoma. The CT and MRI findings are discussed. [source]

    Persistent Left Superior Vena Cava-Inferior Vena Caval Communication Complicating Implantation of an Implantable Cardioverter Defibrillator

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 11 2005
    SANJEEV GOYAL
    A persistent left superior vena cava has been observed in 0.3% of the general population on autopsy. Its presence can complicate left-sided device implantation. Commonly, a LSVC connects to the right atrium via the coronary sinus. A LSVC-accessory hemiazygous-hemiazygous-inferior vena caval communication has not been described previously. The presence of such a congenital venous anomaly will prohibit a left-sided device implant. [source]