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Venous Hypertension (venous + hypertension)
Selected AbstractsClosure of the Greater Saphenous Vein with Endoluminal Radiofrequency Thermal Heating of the Vein Wall in Combination with Ambulatory Phlebectomy: Preliminary 6-Month Follow-upDERMATOLOGIC SURGERY, Issue 5 2000Mitchel P. Goldman MD Background. Incompetence of the saphenofemoral junction with reflux into the greater saphenous vein is one cause of chronic venous hypertension which may lead to the development of varicose and telangiectatic leg veins. Therefore treatment is necessary. Objective. To evaluate a novel method for closing the incompetent greater saphenous vein at its junction with the femoral vein through an endoluminal approach. Methods. Ten patients with reflux at the saphenofemoral junction into the greater saphenous vein were treated with radiofrequency heating of the vein wall through an endoluminal catheter. Patients were evaluated at 3 and 6 months to determine treatment efficacy as well as adverse sequelae. Results. All treated patients achieved complete closure of the saphenofemoral junction and greater saphenous vein. Complete treatment took an average of 20 minutes. Adverse sequelae were minimal, with 2 of 12 patients having mild erythema for 2,3 days. Conclusion. Endoluminal radiofrequency thermal heating of an incompetent greater saphenous vein has been shown to be easily accomplished and efficacious throughout the 6-month follow-up period. [source] Regional distribution of collagen and haemosiderin in the lungs of horses with exercise-induced pulmonary haemorrhageEQUINE VETERINARY JOURNAL, Issue 6 2009F. J. Derksen Summary Reasons for performing study: Regional veno-occlusive remodelling of pulmonary veins in EIPH-affected horses, suggests that pulmonary veins may be central to pathogenesis. The current study quantified site-specific changes in vein walls, collagen and haemosiderin accumulation, and pleural vascular profiles in the lungs of horses suffering EIPH. Hypothesis: In the caudodorsal lung regions of EIPH-affected horses, there is veno-occlusive remodelling with haemosiderosis, angiogenesis and fibrosis of the interstitium, interlobular septa and pleura. Methods: Morphometric methods were used to analyse the distribution and accumulation of pulmonary collagen and haemosiderin, and to count pleural vascular profiles in the lungs of 5 EIPH-affected and 2 control horses. Results: Vein wall thickness was greatest in the dorsocaudal lung and significantly correlated with haemosiderin accumulation. Increased venous, interstitial, pleural and septal collagen; lung haemosiderin; and pleural vascular profiles occurred together and changes were most pronounced in the dorsocaudal lung. Further, haemosiderin accumulation colocalised with decreased pulmonary vein lumen size. Vein wall thickening, haemosiderin accumulation and histological score were highly correlated and these changes occurred only in the caudodorsal part of the lung. Conclusion: The colocalisation of these changes suggests that regional (caudodorsal) venous remodelling plays an important role in the pathogenesis of EIPH. Potential relevance: The results support the hypothesis that repeated bouts of venous hypertension during strenuous exercise cause regional vein wall remodelling and collagen accumulation, venous occlusion and pulmonary capillary hypertension. Subjected to these high pressures, there is capillary stress failure, bleeding, haemosiderin accumulation and, subsequently, lung fibrosis. [source] Clenbuterol administration does not attenuate the exercise-induced pulmonary arterial, capillary or venous hypertension in strenuously exercising Thoroughbred horsesEQUINE VETERINARY JOURNAL, Issue 6 2000M. MANOHAR Summary The present study was carried out to ascertain whether ,2 -adrenergic receptor stimulation with clenbuterol would attenuate the pulmonary arterial, capillary and venous hypertension in horses performing high-intensity exercise and, in turn, modify the occurrence of exercise-induced pulmonary haemorrhage (EIPH). Experiments were carried out on 6 healthy, sound, exercise-trained Thoroughbred horses. All horses were studied in the control (no medications) and the clenbuterol (0.8 ,g/kg bwt, i.v.) treatments. The sequence of these treatments was randomised for every horse, and 7 days were allowed between them. Using catheter-tip-transducers whose in-vivo signals were referenced at the point of the left shoulder, right heart/pulmonary vascular pressures were determined at rest, sub-maximal exercise and during galloping at 14.2 m/s on a 3.5% uphill grade - a workload that elicited maximal heart rate and induced EIPH in all horses. In the control experiments, incremental exercise resulted in progressive significant increments in right atrial as well as pulmonary arterial, capillary and venous (wedge) pressures and all horses experienced EIPH. Clenbuterol administration to standing horses caused tachycardia, but significant changes in mean right atrial or pulmonary vascular pressures were not observed. During exercise performed after clenbuterol administration, heart rate as well as right atrial and pulmonary arterial, capillary and wedge pressures also increased progressively with increasing work intensity. However, these values were not found to be statistically significantly different from corresponding data in the control study and the incidence of EIPH remained unaffected. Since clenbuterol administration also does not affect the transpulmonary pressure during exercise, it is unlikely that the transmural force exerted onto the blood-gas barrier of exercising horses is altered following i.v. clenbuterol administration at the recommended dosage. [source] The petrosquamosal sinus in humansJOURNAL OF ANATOMY, Issue 6 2006Diego San Millán Ruíz Abstract This article provides a comprehensive description of the morphology of the human petrosquamosal sinus (PSS) derived from original observations made on 13 corrosion casts of the cranial venous system combined with routine clinical imaging studies in two patients. The PSS is not a rare finding in the adult human. In particular, continuous developments in imaging techniques have made radiologists become increasingly aware of this anatomical entity in recent years. The role of the PSS as a major encephalic drainage pathway and its potential implication in pathological conditions such as intracranial venous hypertension are discussed. [source] Microcirculatory Dysfunction in Chronic Venous Insufficiency (CVI)MICROCIRCULATION, Issue S1 2000MICHAEL JÜNGER ABSTRACT The elevated ambulatory pressure in the peripheral venous system of chronic venous insufficiency (CVI) patients manifests itself not only in the form of disturbed macrocirculation but also and particularly in microangiopathic changes. For this reason, it is closely correlated with trophic disorders of the skin and can ultimately lead to ulceration. Using microcirculation research techniques, we are able to provide clear evidence of a typical microangiopathy in chronic venous insufficiency. Fifty CVI patients in Widmer stages I, II, and III were examined with fluorescence video microscopy, intravital video capillaroscopy, transcutaneous oxygen partial pressure measurement, TcpO2 and laser Doppler flowmetry. The effects of compression therapy with individually fitted compression stockings on capillary morphology were studied over a period of 4 weeks in 20 CVI patients in Widmer stages I and II. The capillary pressure was measured during simulated muscle contraction using a servo-null micropressure system. We periodically drew blood from the dorsalis pedis vein and a brachial vein of 11 healthy test persons and 8 patients with stage III CVI during experimental venous hypertension in order to evaluate the expression pattern of leukocyte adhesion molecules involved in inflammation: LFA-1 (CD11a), Mac-1 (CD11b), p150,95 (CD11c), CD18, VLA-4 (CD49d), and L-selectin (CD62L). In the same patients, we used immunohistochemical methods to examine clinically unaffected skin and the skin near an ulcer, focusing on the adhesion molecules ICAM-1, VCAM-1, and E-selectin. The microangiopathic changes observed with worsening clinical symptoms include a decrease in the number of capillaries, glomerulus-like changes in capillary morphology, a drop in the oxygen content (tcpO2) of the skin, increased permeability of the capillaries to low-molecular-weight substances, increased laser Doppler flux reflecting elevated subcutaneous flow, and diminished vascular reserve. These microangiopathic changes worsen in linear proportion to the clinical severity of chronic venous insufficiency. In patients with venous ulcerations, the baseline expression of LFA-1 and VLA-4 on lymphocytes, Mac-1 expression on the myeloid cell line, and L-selectin expression on all three cell lines was not significantly different from that in healthy controls. During orthostatic stress, there was a significant reduction in the expression of L-selectin in blood cells collected at foot level in the controls (p = 0.002), but not in the patients. Clinical improvement by compression therapy was accompanied by an increase in the number of nutritive capillaries, while the diameter of the capillaries and the dermal papillae was reduced. When ulcers healed in a short period (<6 weeks), we observed a concomitant increase in the number of capillaries (p < 0.05). Microangiopathy appears before trophic disorders of the skin develop. Even trophically normal skin areas may have dilated nutritive capillaries, an early sign of disturbed skin perfusion. These changes represent a plausible explanation for the development and to recurrency tendency of venous ulcers. The reduced expression of lymphocytic L-selectin in healthy controls during the orthostatic stress test may be an indication that the cells are activated by venous stasis. Clinically effective therapeutic measures improve the impaired microcirculation of the skin in the ankle area. [source] Experimental Models To Investigate Inflammatory Processes in Chronic Venous InsufficiencyMICROCIRCULATION, Issue S1 2000RONALD J. KORTHUIS ABSTRACT Chronic venous insufficiency (CVI) is characterized by leukocyte adhesion and infiltration, venous hypertension and dilatation, and valvular dysfunction. The fact that activated white cells can direct a powerful cytotoxic arsenal at parenchymal cells following their extravasation into the tissues led to the original proposal that leukocytes may play a causative role in the pathogenesis of venous disease. A large body of subsequent work indicates that white blood cells are indeed activated in CVI. However, identification of the factors responsible for initiating leukosequestration and activation in such disorders and determination of whether these activated cells then contribute to the progression of venous disease have been hampered by the lack of appropriate animal models that accurately mimic the human condition. Tantalizing evidence suggesting that cyclical periods of ischemia and reperfusion (I/R) may occur in diseased regions of the skin is beginning to accumulate. As is the case with CVI, leukocyte infiltration is a prominent feature in I/R and activated neutrophils play a causative role in the reperfusion component of tissue injury via the targeted release of reactive oxygen metabolites and hydrolytic enzymes. In light of these considerations, many investigators have suggested that examining the mechanisms of I/R injury in skin and skeletal muscle, where ischemia is produced by arterial occlusion, may provide a relevant model for studying the pathogenesis of CVI. Others have suggested that venous occlusion may represent a more appropriate model, as this approach also produces the venous hypertension that is characteristic of the disease. The purpose of this review is to summarize the evidence pointing to the involvement of I/R and venous hypertension as causative factors in CVI-induced leukocyte recruitment. In addition, we will describe the evidence in favor of the view that white blood cells contribute to the pathogenesis of CVI. Finally, we will describe several different experimental models that have been used to examine the role of I/R-induced microvascular dysfunction as it may pertain to the development of CVI, together with a discussion of the relative advantages and limitations of the various models. [source] Minimally Invasive Vein Surgery: Latest Options for Vein DiseaseMOUNT SINAI JOURNAL OF MEDICINE: A JOURNAL OF PERSONALIZED AND TRANSLATIONAL MEDICINE, Issue 3 2010FACPhArticle first published online: 20 MAY 2010, Steven Elias MD Abstract The goal of treatment for venous disease is to decrease ambulatory venous hypertension. Various strategies are employed. These can be divided into exogenous and endogenous treatments. Exogenous methods concern those employed from the outside of the limb, such as compression and elevation. Endogenous modalities treat from inside the limb the underlying venous pathology due to venous valvular dysfunction or venous obstruction. Traditional endogenous procedures include stripping, ligation, and phlebectomy. All these procedures require incisions, anesthesia, and perhaps hospitalization, and involve significant discomfort. Newer minimally invasive vein surgery procedures now exist. These are all same-day, outpatient procedures, usually involving local anesthesia. Most can be performed percutaneously without incisions. Patients ambulate the day of the procedure. Morbidity is less than 1%. This article summarizes the concept of minimally invasive vein surgery and summarizes new technologies to manage all forms of venous disease. Mt Sinai J Med 77:270,278, 2010. © 2010 Mount Sinai School of Medicine [source] Distal venous hypertension complicating a brachiocephalic arterovenous fistulaANZ JOURNAL OF SURGERY, Issue 6 2009Gianpiero Gravante MD No abstract is available for this article. [source] | ||||||||||