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Results for “Neovascularization, Pathologic”

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PubMed2007

Early vitrectomy for fundus-obscuring dense vitreous haemorrhage from presumptive retinal tears.

BACKGROUND: Published literature on the management of patients with fundus-obscuring dense vitreous haemorrhage due to presumptive retinal tears is sparse and advocates waiting for spontaneous resolution. Surgery is indicated only when a definite retinal tear or retinal detachment is identified. METHODS: A retrospective review of all patients who underwent early vitrectomy for vitreous haemorrhage associated with posterior vitreous detachment was carried out. A comparison of initial visual acuity versus final visual acuity after vitrectomy was performed. The number of eyes that were found to have retinal tears and retinal detachment were documented. Initial and final Snellen acuities were used for statistical analysis. Categorical data were analysed using Fisher's exact test and statistical significance was considered to be p < 0.05. RESULTS: Sixteen eyes were identified and all these patients presented or were referred soon after the onset of vitreous haemorrhage. Associated ocular pathology (choroidal neovascular membrane, retinal branch vein occlu-sion, macroaneurysm) was suspected to be the source of the haemorrhage in 4 eyes. Vitrectomy was carried out in 12 eyes soon after presentation (mean time 6.3 days, range 1-28 days). Nineteen retinal breaks were seen in these eyes and 5 eyes had more than two breaks. None of the eyes were found to have proliferative vitreoretinopathy at the time of surgery. Two eyes needed repeat surgery for new retinal breaks. Excluding the eyes found to have an ocular pathology as the cause of vitreous haemorrhage, the mean visual acuity improved from hand movements to 6/12 (p < 0.001). CONCLUSIONS: Early vitrectomy for spontaneous dense fundus-obscuring vitreous haemorrhage and posterior vitreous detachment is safe. Since the number of patients in this study was small, a prospective randomised controlled study comparing early versus late vitrectomy is needed to see whether early surgery also prevents proliferative vitreoretinopathy formation.

Aged↗

PubMed1994

[Color Doppler flow data of breast tumors].

The recent development of high-quality colour Doppler instruments allows flow detection in small vessels below the resolution of B-mode imaging. Therefore, Doppler is now frequently used for flow detection in tumours. For breast examinations, CW Doppler has been in use for many years, which allows a sufficient definition of diagnostic criteria. Nevertheless, it is surprising that new studies using colour Doppler try to define different diagnostic criteria. To characterise the vascularity of breast lesions by colour Doppler we investigated 127 symptomatic patients. In 54 carcinomas the average flow velocity was 32 cm/s and 12.6 cm/s in 73 benign conditions (p > 0.0001). Total tumour vascularisation was characterised by a new parameter: the sum of all flow velocities in all tumour vessels. In carcinomas the mean total flow as 197.9 cm/s, and 52.7 cm/s in benign pathologies (p > 0.0001). Mean RI (resistance index) and PI (pulsatility index) were calculated to describe the flow profiles. The wide variation did not allow for a differentiation between benign and malignant lesions.

Arteries↗

PubMed2006

Ultrasound guided electrocoagulation in patients with chronic non-insertional Achilles tendinopathy: a pilot study.

BACKGROUND: High resolution colour Doppler ultrasound shows intratendinous Doppler activity in patients with chronic Achilles tendinopathy. Treatment of this neovascularisation with sclerosing therapy seems to relieve the pain. However, the procedure often has to be repeated. OBJECTIVE: To investigate the effect of electrocoagulation of the neovessels on tendon pain and tendon vascularity in patients with chronic Achilles tendinopathy. METHODS: Colour Doppler ultrasound guided electrocoagulation was used on vessels in the ventral portion of the Achilles tendon in 11 patients (seven men, four women, mean age 41 years) with painful chronic mid-portion Achilles tendinosis. A unipolar coagulation device was used. RESULTS: One patient dropped out after two months (dissatisfied with the results). The remaining 10 patients (91%) were satisfied. These 10 patients were still satisfied at six months of follow up and had returned to their previous level of activity. All 10 patients were "cured" after one treatment. The patient who dropped out received two treatments because of lack of progress. There was significantly reduced pain (Likert pain scale, 0-10) during activity, from a median of 7 (range 4 to 10) at baseline to 0 (0 to 8) at six months' follow up (p<0.005); and at rest, from 1.5 (1 to 5) to 0 (0 to 8) (p = 0.005). In all patients, vascularisation was unchanged at the six months follow up, with no significant change in semiquantitative or quantitative colour scoring. CONCLUSIONS: Coagulation in the area with vessels entering the tendon appears to be effective treatment for painful chronic mid-tendinous Achilles tendinopathy. No effect on the intratendinous Doppler activity could be detected, suggesting that the effect is independent of changes in blood flow. Localisation of hyperaemia appears to be the key to the pathology and for targeting the treatment. One explanation could be that the effect is obtained by destruction of nerves accompanying the vessels.

Achilles Tendon↗

PubMed2005

Angiogenic and lymphangiogenic microvessel density in breast carcinoma: correlation with clinicopathologic parameters and VEGF-family gene expression.

Angiogenesis and lymphangiogenesis are essential for breast cancer progression and are regulated by vascular endothelial growth factors (VEGF). To determine clinical and molecular correlates of these processes, we measured blood and lymphatic vascular microvessel density in 29 invasive carcinomas (22 ductal, six lobular, one papillary), using the vascular marker CD31 and the novel lymphatic marker D2-40. Microvessel density was assessed microscopically and by image cytometry, and was compared with tumor histology, grade, stage, lymph node metastasis, hormone receptors, HER2/neu status, and expression of VEGF, VEGF-C and VEGF-D by immunohistochemistry or quantitative RT-PCR. Strong correlation was observed between visual and image cytometric microvessel density using D2-40 but not CD31 (P=0.016 and 0.1521, respectively). Image cytometric CD31 microvessel density correlated with tumor size, grade, stage and lymph node metastasis (P=0.0001, 0.0107, 0.0035 and 0.0395, respectively). D2-40 microvessel density correlated with tumor stage (P=0.0123 by image cytometry) and lymph node metastasis (P=0.0558 by microscopy). Immunohistochemical VEGF signal in peritumoral blood vessels correlated with image cytometric CD31 and D2-40 microvessel density (P=0.022 and 0.0012, respectively), consistent with the role of VEGF in blood and lymphatic vascular growth. Intratumoral VEGF-C and VEGF-D expression by quantitative RT-PCR correlated with D2-40 (P=0.0291 by image cytometry) but not with CD31 microvessel density, which could suggest a selective role of VEGF-C and VEGF-D in lymphangiogenesis. CD31 and D2-40 microvessel density correlated significantly with several prognostic factors, including lymph node metastasis. Thus, measurements of angiogenesis and lymphangiogenesis may have utility for breast cancer pathology, particularly for estimation of metastatic risk.

Adult↗

PubMed1998

Microvascular invasion in prostate cancer: prognostic significance in patients treated by radical prostatectomy for clinically localized carcinoma.

OBJECTIVE: To investigate the clinical significance of vascular invasion in prostate cancer patients treated by radical prostatectomy for clinically localized and locally advanced disease. MATERIALS AND METHODS: Vascular invasion was determined during a routine work-up of radical prostatectomy specimens of 273 patients who underwent surgery for prostatic carcinoma. The correlation with other pathological variables was investigated. The prognostic influence for clinical progression, local recurrence, distant metastases, biochemical progression, overall survival and cancer-specific survival was determined. RESULTS: Vascular invasion was present in 33 patients (12%). Vascular invasion correlated significantly with capsular perforation, seminal vesicle invasion, positive margins of resection, perineural invasion, high grade, and pathological stage. Vascular invasion was a significant prognostic factor for clinical progression (p < 0.001), local recurrence (p = 0.007), distant metastases (p < 0.001), biochemical progression (p < 0.001), overall survival (p = 0.02), and cancer-specific survival (p < 0.001). Multivariate analysis, adjusting for capsular perforation, high grade, and positive margins of resection, showed that vascular invasion was associated with a 2.5-fold increased risk for clinical progression. This relative risk was 2.3 for biochemical progression, and 2.7 for cancer-specific survival. CONCLUSION: Vascular invasion is a very important pathological variable for progression and survival, and must be evaluated on a routine basis during the work-up of radical prostatectomy specimens.

Aged↗

PubMed2003

Power Doppler analysis of tendon vascularization.

Forty-nine patients with tendonitis (patellar in 16, quadriceps in two, Achilles in 12, rotator cuff disease in 19) and 47 patients with tenosynovitis (acute tenosynovitis in 25, stenosing tenosynovitis in 22) underwent ultrasound (US) and Power Doppler (PD)-US examination. Spectral analysis of flow signals was performed in all patients. Ten patients (six with tendonitis, four with tenosynovitis) were rewired after medical therapy. Six healthy volunteers were also examined for control purposes. Three different patterns of flow distribution were found in patients with tendonitis and active tenosynovitis. The vessels of tendons without tendon sheaths began with great peduncles at the level of the peritendinous soft tissues and were then distributed inside the tendon (pattern I). A clear peritendinous hypervascular pattern was found in all active tenosynovitis, but no vessels were found inside the tendons (pattern II). In some cases of intratendinous or partial lesions PD-US revealed some vessels located near or inside the lesion (pattern II). On spectral analysis these vessels corresponded to arteries with a low resistance index or small venules. PD-US revealed a significant reduction of flow signals in patients rewired after medical therapy. No pathological flow signals were found either in patients with stenosing tenosynovitis or in the control group. PD-US gives us an in vivo confirmation of tendon vascularity. Spectral analysis adds further information to gray-scale US.

Adolescent↗

PubMed2004

Vascular endothelial growth factor: basic science and clinical progress.

Vascular endothelial growth factor (VEGF) is an endothelial cell-specific mitogen in vitro and an angiogenic inducer in a variety of in vivo models. Hypoxia has been shown to be a major inducer of VEGF gene transcription. The tyrosine kinases Flt-1 (VEGFR-1) and Flk-1/KDR (VEGFR-2) are high-affinity VEGF receptors. The role of VEGF in developmental angiogenesis is emphasized by the finding that loss of a single VEGF allele results in defective vascularization and early embryonic lethality. VEGF is critical also for reproductive and bone angiogenesis. Substantial evidence also implicates VEGF as a mediator of pathological angiogenesis. In situ hybridization studies demonstrate expression of VEGF mRNA in the majority of human tumors. Anti-VEGF monoclonal antibodies and other VEGF inhibitors block the growth of several tumor cell lines in nude mice. Clinical trials with various VEGF inhibitors in a variety of malignancies are ongoing. Very recently, an anti-VEGF monoclonal antibody (bevacizumab; Avastin) has been approved by the Food and Drug Administration as a first-line treatment for metastatic colorectal cancer in combination with chemotherapy. Furthermore, VEGF is implicated in intraocular neovascularization associated with diabetic retinopathy and age-related macular degeneration.

Animals↗

PubMed2005

Anti-angiogenic activity of the mutant Dutch A(beta) peptide on human brain microvascular endothelial cells.

Cerebral amyloid angiopathy is a common pathological feature of patients with Alzheimer's disease (AD) and it is also the hallmark of individuals with a rare autosomal dominant disorder known as hereditary cerebral hemorrhage with amyloidosis-Dutch type. We have shown previously that wild type A(beta) peptides are anti-angiogenic both in vitro and in vivo and could contribute to the compromised cerebrovascular architecture observed in AD. In the present study, we investigated the potential anti-angiogenic activity of the Dutch A(beta)(1-40) (E22Q) peptide. We show that compared to wild type A(beta), freshly solubilized Dutch A(beta) peptide more potently inhibits the formation of capillary structures induced by plating human brain microvascular endothelial cells onto a reconstituted basement membrane. Aggregated/fibrillar preparations of wild type A(beta) and Dutch A(beta) do not appear to be anti-angiogenic in this assay. The stronger anti-angiogenic activity of the Dutch A(beta) compared to wild type A(beta) appears to be related to the increased formation of low molecular weight A(beta) oligomers in the culture medium surrounding human brain microvascular endothelial cells. Using oligonucleotide microarray analysis of human brain microvascular endothelial cells, followed by a genome-scale computational analysis with the Ingenuity Pathways Knowledge Base, networks of genes affected by an anti-angiogenic dose of Dutch A(beta) were identified. This analysis highlights that several biological networks involved in angiogenesis, tumorigenesis, atherosclerosis, cellular migration and proliferation are disrupted in human brain microvascular endothelial cells exposed to Dutch A(beta). Altogether, these data provide new molecular clues regarding the pathological activity of Dutch A(beta) peptide in the cerebrovasculature.

Amyloid beta-Peptides↗

PubMed2000

CD36 and atherosclerosis.

CD36 has been associated with diverse normal and pathologic processes. These include scavenger receptor functions (uptake of apoptotic cells and modified lipid), lipid metabolism and fatty acid transport, adhesion, angiogenesis, modulation of inflammation, transforming growth factor-beta activation, atherosclerosis, diabetes and cardiomyopathy. Although CD36 was identified more than 25 years ago, it is only with the advent of recent genetic technology that in-vivo evidence has emerged for its physiologic and pathologic relevance. As these in-vivo studies are expanded, we will gain further insight into the mechanism(s) by which CD36 transmits a cellular signal, and this will allow the design of specific therapeutics that impact on a particular function of CD36.

Animals↗

PubMed1997

Bronchial vascular congestion and angiogenesis.

The bronchial vasculature is the systemic arterial blood supply to the lung. Although small relative to the pulmonary blood flow, the bronchial vasculature serves important functions and is modified in a variety of pulmonary and airway diseases. Congestion of the bronchial vasculature may narrow the airway lumen in inflammatory airway diseases, and formation of new bronchial vessels (angiogenesis) is implicated in the pathology of a variety of chronic inflammatory, infectious and ischaemic pulmonary diseases. The remarkable ability of the bronchial vasculature to remodel has implications for disease pathogenesis. The contributions of the bronchial vasculature to the pathogenesis of pulmonary disease are reviewed in this article.

Bronchi↗

PubMed2003

Vegfb gene knockout mice display reduced pathology and synovial angiogenesis in both antigen-induced and collagen-induced models of arthritis.

OBJECTIVE: To determine the role of vascular endothelial growth factor B (VEGF-B) in 2 mouse models of arthritis, antigen-induced arthritis (AIA) and collagen-induced arthritis (CIA). METHODS: For AIA studies, monarticular AIA was induced by methylated bovine serum albumin (mBSA) priming of Vegfb gene knockout (Vegfb(-/-)) and wild-type (Vegfb(+/+)) mice, followed by intraarticular injection of mBSA or saline control 8 days later. CIA was induced in Vegfb(-/-) and Vegfb(+/+) mice by intradermal injection of chick type II collagen in adjuvant. Arthritis was monitored in both models using defined criteria (clinical and histologic). Angiogenesis was measured by synovial vessel density in diseased and control joints. RESULTS: In AIA studies, Vegfb(+/+) mice displayed significant knee joint swelling and synovial inflammation 7 days after intraarticular injection of antigen. Synovial inflammation was associated with angiogenesis, since vessel density in AIA synovium was significantly higher in arthritic than in control joints from the same animal. Knee joint swelling, synovial inflammation, and inflammation-associated vessel density in arthritic joints were reduced in Vegfb(-/-) mice compared with arthritic joints from Vegfb(+/+) mice. Similarly, in CIA, both disease incidence and mean clinical severity scores were significantly reduced in Vegfb(-/-) mice compared with Vegfb(+/+) mice. Mean histologic severity scores and mean synovial vessel density were reduced in diseased joints from Vegfb(-/-) mice when compared with diseased joints from Vegfb(+/+) mice. CONCLUSION: The reduction in inflammation-associated synovial angiogenesis in Vegfb(-/-) mice implicates VEGF-B in pathologic vascular remodeling in inflammatory arthritis. VEGF-B may be an attractive target in the design of anti-angiogenic therapies for rheumatoid arthritis.

Angiogenesis Inducing Agents↗

PubMed2006

Hepatitis B virus promotes angiopoietin-2 expression in liver tissue: role of HBV x protein.

The progression of chronic hepatitis B (CHB) is related to fibrosis and to the emergence of intrahepatic anomalous vascular structures. Hepatitis B virus (HBV) X protein transactivator (HBx) may play a significant role in both processes. To analyze how HBV induces vascular growth and remodeling in vivo, we assessed the expression of angiopoietin-2 (Ang2) in liver biopsies from CHB patients by reverse transcriptase-polymerase chain reaction, Western blotting, and immunohistochemistry because of the relevant role of Ang2 in vascular development, remodeling, and tumor promotion. In addition, we analyzed the influence of HBx in the expression of Ang2 in HBx-expressing hepatocyte cell lines and in hepatic stellate cells stimulated with conditional medium from HBx-hepatocytes. Ang2 expression was clearly up-regulated at both mRNA and protein levels in the liver of CHB patients, showing an intense staining of inflammatory infiltrates and vascular structures at inflamed portal areas. HBx-expressing hepatocytes and stimulated stellate cells showed a significant induction of Ang2 expression. PI3K inhibitor and antioxidants repressed the 64-kd Ang2 form but further enhanced the inflammation-related 50-kd molecular species. Therefore, HBx could account for the induction of Ang2 observed in CHB, especially the 50-kd form, contributing to pathological angiogenesis and hepatocellular carcinoma progression.

Adult↗

PubMed1998

Increased apoptosis coincides with onset of involution in infantile hemangioma.

OBJECTIVE: Hemangioma is an endothelial cell tumor that grows rapidly during infancy and regresses slowly during childhood. However, little is known about the natural history of this common tumor. To gain insight into the cellular mechanisms that underlie the switch from uncontrolled growth to involution of endothelium, we investigated the extent of cellular apoptosis versus proliferation in hemangioma specimens that spanned the natural life cycle of the tumor. METHODS: We analyzed apoptosis and cellular proliferation in frozen sections from 16 hemangioma specimens using the TUNEL assay to detect apoptotic cells and the Ki67 antigen to detect dividing cells. RESULTS: Apoptosis was low in proliferative phase hemangiomas but increased fivefold in involutive phase specimens obtained from children one to four years of age. Immunofluorescence double-labeling experiments showed that at least one third of the apoptotic cells were endothelial. As expected, cellular proliferation was high in specimens up to 2 years of age but decreased significantly thereafter. Apoptosis was consistently low in nine normal skin tissues (newborn to 4 years of age) obtained from discarded pathology specimens. CONCLUSIONS: These results suggest that increased apoptosis during the second year of life can offset cellular proliferation and may be involved in initiating regression of hemangioma.

Age Factors↗

PubMedDate not supplied

Inhibition of angiogenesis as a strategy for tumor growth control.

Angiogenesis is a complex sequence of events leading to the formation of new capillaries. Although essential to maturation and wound healing, most angiogenesis in the adult is associated with pathological events, such as the development of solid tumors. One approach to the inhibition of angiogenesis is the antagonism of basic fibroblast growth factor, a major angiogenic protein. Evidence is reviewed to suggest that inhibiting angiogenesis results in the suppression of tumor growth.

Animals↗

PubMed2002

Insights into vascular pathology after intracoronary brachytherapy.

Post-angioplasty restenosis is a major limitation of interventional cardiology. A large body of evidence reveals that expression of myofibroblast activity promoters moves progressively from the neoadventitia to the neointima. Brachytherapy inhibits vascular cell activity (proliferation, migration), mitigates recruitment of intimal cells, and shows a favorable prophylactic effect on late vascular remodeling by preventing adventitial constriction at the injured site. These effects of brachytherapy are dose related. Clinical and experimental data demonstrate that restenosis is determined by the balance between arterial remodeling and intimal hyperplasia. Apparently, brachytherapy-induced positive remodeling plays the principal role in increasing the luminal diameter after PTCA and, in case of a lower dose or dose fall-off, to cause detrimental edge effects. With regard to clinical course, healing defects, endothelial dysfunction and stent-vessel wall malapposition are apparently important and possibly underestimated features of vascular pathology, since they may contribute to late thrombosis and delayed intimal hyperplasia in long-term course after intracoronary brachytherapy.

Angioplasty, Balloon, Coronary↗

PubMed2005

Femur window--a new approach to microcirculation of living bone in situ.

BACKGROUND: The processes of osteogenesis, bone remodelling, fracture repair and metastasis to bone are determined by complex sequential interactions involving cellular and microcirculatory parameters. Consequently studies targeting the analysis of microcirculatory parameters on such processes should mostly respect these complex conditions. However these conditions could not yet be achieved in vitro and therefore techniques that allow a long-term observation of functional and structural parameters of microcirculation in bone in vivo at a high spatial resolution are needed to monitor dynamic events, such as fracture healing, bone remodelling and tumor metastasis. METHODS: We developed a bone chamber implant (femur window) for long-term intravital microscopy of pre-existing bone and its microcirculation at an orthotopic site in mice preserving the mechanical properties of bone. After bone chamber implantation vascular density, vessel diameter, vessel perfusion, vascular permeability and leukocyte-endothelial interactions (LEIs) in femoral bone tissue of c57-black mice (n=11) were measured quantitatively over 12 days using intravital fluorescence microscopy. Furthermore a model for bone defect healing and bone metastasis in the femur window was tested. RESULTS: Microvascular permeability and LEIs showed initially high values after chamber implantation followed by a significant decrease to a steady state at day 6 and 12, whereas structural parameters remained unaltered. Bone defect healing and tumor growth was observed over 12 and 90 days respectively. CONCLUSION: The new femur window design allows a long-term analysis of structural and functional properties of bone and its microcirculation quantitatively at a high spatial resolution. Altered functional parameters of microcirculation after surgical procedures and their time dependent return to a steady state underline the necessity of long-term observations to achieve unaltered microcirculatory parameters. Dissection of the complex interactions between bone and microcirculation enables us to evaluate physiological and pathological processes of bone and may give new insights especially in dynamic events e.g. fracture healing, bone remodeling and tumor metastasis.

Animals↗

PubMed2005

Involvement of mast cells in angiogenesis and chronic inflammation.

Mast cells (MC) are granulated secretory cells that have long been recognized as a rich source of biologically highly active mediators such as biogenic amines, prostaglandins, leukotrienes, proteases, cytokines and chemokines. Most of their biological functions however has been rather elusive. There are now emerging data assigning these cells a relevant role in orchestrating angiogenesis, both in normal and pathological conditions. MC indeed synthesize and release a large array of proangiogenic factors upon different stimulation pathways. In addition, MC have been recognized as key cells in mediating host innate and adaptive immune responses. This review summarizes the most recent acquisitions concerning MC involvement in angiogenic processes and chronic inflammatory reactions.

Animals↗

PubMed2005

[Significance of proliferating cell nuclear antigen (PCNA) index and microvessel density (MVD) in endometrial carcinoma].

BACKGROUND & OBJECTIVE: Incidence of endometrial carcinoma (EC) is ascending, but its pathogenesis and prognosis are unclear. This study was designed to investigate correlation of proliferating cell nuclear antigen (PCNA) index, and microvessel density (MVD) to pathologic stage, and differentiation of endometrial carcinoma. METHODS: PCNA index and MVD in 62 specimens of endometrial carcinoma, and 22 specimens of normal endometrium were detected by SP immunohistochemistry. Correlation of PCNA index, and MVD to pathologic stage, and differentiation of endometrial carcinoma was statistically analyzed. RESULTS: PCNA index, and MVD in endometrial carcinoma were significantly higher than those in normal endometrium (54.5+/-9.3 vs. 32.7+/-7.7, and 49.0+/-8.6 vs. 32.4+/-11.0,P<0.05). PCNA index and MVD positively correlated with pathologic stage and differentiation of endometrial carcinoma (P<0.05). PCNA index positively correlated with MVD in endometrial carcinoma. CONCLUSIONS: The increase of PCNA index and MVD may enhance development of endometrial carcinoma. Angiogenesis might play a role in promoting cell proliferation.

Adenocarcinoma↗