Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During chronic venous insufficiency (CVI), several microvascular functional abnormalities, due to venous hypertension, develop. To look for blood rheological consequences of venous hypertension "VH", whole blood viscosity and its main determinants were measured in 11 normal controls and 36 patients with CVI exposed to a short-term experimental VH. Patients were subdivided into 2 groups according to the severity of their disease. Blood was taken from a foot vein before and after VH, which was induced by appling a pneumatic tourniquet to 100 mmHg for 15 minutes. Whole blood viscosity at low and high shear rates, red blood cell (RBC) aggregation, RBC rigidity, plasma viscosity and proteins as well as red and white blood cell (WBC) counts were recorded. Patients at baseline, i.e., before application of the tourniquet, showed several hemorheological abnormalities such as an increased RBC aggregation, increased low shear rate viscosity, and a significant elevation in plasma fibrinogen level. Patients with more severe CVI had more marked hemorheological changes. The short term VH in patients led to further aggravation of these changes. There were also at baseline lower values, however not significantly, of hematocrit and RBC count, suggesting that hemoconcentration is not a feature of CVI. These same parameters were slightly, however not significantly, increased after VH, indicating a fluid escape into the extravascular space. A significant fall in WBC count was also observed after VH, in keeping with the white cell trapping hypothesis. In conclusion, even a short-term VH is able to induce several hemorheological impairments, which are probably involved in the failure of the microcirculation and hence the initiation of tissue damage in patients with CVI.
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PMID:Blood rheology as a marker of venous hypertension in patients with venous disease. 1525 59

Venous reflux is the most common cause of venous hemodynamic disorders. In this paper 2 issues are discussed: how and where does reflux arise and what are the hemodynamic consequences of retrograde flow. Pressure gradient and incompetent vein connecting both poles of the gradient are the prerequisite for venous reflux to arise. Ambulatory pressure gradient occurs during the activity of the calf muscle venous pump between deep veins of the thigh and the lower leg. Thus the incompetent reflux-carrying vein must connect the popliteal, femoral, profunda femoris, or iliac vein with 1 of the deep veins of the lower leg. Reflux can be considered as shunting of blood from thigh veins into the lower leg veins. The most frequently found incompetent veins are the long and short saphenous veins and perforators communicating with deep veins of the thigh. On the other hand, calf perforators emptying into the deep veins of the lower leg, where the lower pole of the pressure gradient is located, cannot be the feeding source of reflux. A physiological bidirectional flow takes place in calf perforators connecting superficial and deep veins of the lower leg and making them conjoined vessels. Venous reflux produces ambulatory venous hypertension. The quantity of reflux volume and not the localization of retrograde flow in superficial or deep veins is the most important hemodynamic factor. Reflux in superficial veins, when large enough, can cause the most serious symptoms of chronic venous insufficiency including leg ulcers. Plethysmographic findings have shown that incompetence of the femoral and calf perforating veins is hemodynamically unimportant. Large incompetent calf perforators are not the cause of venous abnormality but are the consequence of saphenous retrograde flow.
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PMID:The venous reflux. 1537 17

Although the presence of arteriovenous communications in patients with chronic venous ulcers has been confirmed in several studies, their role in the pathogenesis of venous ulcers is still uncertain. They possibly do play an important role in the aetiology of chronic venous insufficiency. There is also substantial evidence to suggest that arteriovenous communications develop as a result of chronic venous hypertension. The question raised in this pilot study was whether the importance of arteriovenous shunts in the genesis of venous ulcer disease is such that their obliteration might lead to long-term healing. This clinical study was also designed to determine whether therapeutic microembolization of nutritive arterial branches to arteriovenous fistulas, found in patients with venous ulcers, facilitates healing of venous ulcers resistant to previous conservative and/or classical surgical treatment. From 1997 to 1999, 34 patients (22 women and 14 men, mean age 51.3 years) with chronic venous ulcer resistant to classical treatment were included in the study. Arteriovenous shunting was demonstrated by digital subtraction angiography in 31 patients (31/34 = 91%). The embolization procedure of muscular arterial branches feeding the arteriovenous shunts with microspirals and microparticles led to ulcer healing in 13 patients (13/31). The results suggest that the role of arteriovenous shunting in chronic venous ulceration resistant to classical treatment is more important than previously suggested, and that their microembolization might lead to complete healing.
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PMID:Role of arteriovenous shunting in venous ulcers--therapeutic implications. 1550 14

An analysis was made of the results of an all-round clinical, ultrasound, phlebotonometric and phlebographic examination of 89 patients with the clinical evidence of chronic venous insufficiency (CVI) of the pelvis. It is established that small pelvis varicosis develops because of hemodynamic disorders in the system of the inferior vena cava, iliac and left renal veins. In men, blood reflux from the iliac vein to the parietal tributaries leads to the development of the atypical forms of varicosis. In women, the left- sided regional renal venous hypertension induces valvular insufficiency of the left ovarian vein with the extent of the renoovarian blood reflux to the pampiniform, uterovaginal, presacral, vesical and rectal venous plexus. The concomitant action of the caval and renoovarian blood refluxes causes the origination of the syndrome of the blood overfilling of the pelvic organs and varicosis of the pubis, perineum, vulva, and buttocks. The clinical, ultrasound and phlebographic appearance of small pelvis varicosis is described in detail.
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PMID:[The mechanisms of the natural history of small pelvis varicosis]. 1562 97

Initially, the progression of chronic venous insufficiency is related to venous hypertension. The earliest complaints or symptoms, as well as vessel wall deterioration, valve restructuring, and, eventually, varicose veins, result not only from elevation of pressure, but also from a cascade of biochemical events related to both the macro- and the microcirculation. Thickening and remodelling of the venous wall are influenced by two parameters: abnormal shear stress and hypoxia that activate the endothelium first at the level of valve cusps and then in large veins. Hypoxia leads to activation of the endothelium and leukocyte accumulation. By inhibiting endothelial activation, micronized purified flavonoid fraction (MPFF) (Daflon 500 mg), an edema-protective agent, can prevent the inflammatory cascade resulting from the leukocyte-endothelium interaction. This subsequently delays the appearance of reflux and inhibits the initiation of the vicious circle ending in enhanced venous pressure. This is how Daflon 500 mg relieves patients from symptoms and edema and possibly also prevents the appearance of varicose veins. Rheological disturbances also play a major role in the appearance of these disorders. Furthermore, venous hypertension provokes leakage from the vessels and capillaries exhibiting increased permeability, leading to increases in hydrostatic load, and overloading of the lymphatic network, which subsequently results fluid exudation causing edema. Microcirculatory dysfunction leads to capillary damage, skin changes and venous leg ulcers. The clinical efficacy of Daflon 500 mg in venous leg ulcers has been demonstrated by several randomised controlled studies, in which the rate of ulcer healing was significantly shortened. An explanation for the ability to speed ulcer healing comes from the protection Daflon 500 mg exerts on the microcirculation.
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PMID:Micronized purified flavonoid fraction (MPFF): a review of its pharmacological effects, therapeutic efficacy and benefits in the management of chronic venous insufficiency. 1564 40

We described the diagnosis and treatment for limb edema due to venous disease in this paper. Venous limb edema is caused by vein pressure elevation, which is induced by venous reflux, flow disturbance and overflow. Valve incompetence causes varicose vein and deep venous insufficiency of lower extremities. Deep vein thrombosis is the most popular disease among the venous obstruction morbidity. Arterio-venous fistula for hemodialysis sometimes induces venous arm edema due to overflow. Arm edema due to venous hypertension appears more clearly when it is associated by subclavian vein stenosis or occlusion. There are several causes for venous edema. So, we have to make an appropriate treatment based on the clear diagnosis.
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PMID:[Diagnosis and treatment for limb edema due to venous disease]. 1567 31

The aim of this independent study was to investigate differences in efficacy between HR, (0-[beta-hydroxyethyl]-rutosides) and D+H (500 mg, diosmin+hesperidin) in patients with chronic venous insufficiency (CVI). A first group of 90 patients with severe venous hypertension (CVI, ankle swelling) were randomized into an HR or a D+H group. The HR group received oral HR (2 g/day, 8 weeks); the D+H group received a 500 mg tablet 3 times daily for 8 weeks. A second group of comparable patients was included in a registry following the same study format. Patients were openly included; the 2 treatments were administered with the same methods and procedures. Clinical conditions were comparable to those described in the randomized study. Patients treated for at least 8 weeks were included in the registry. A number of physicians (specialists or general practitioners) included patients when they considered that clinical conditions were compatible with using 1 of the 2 treatments on the basis of their personal evaluation and experience. When cases were compatible with the registry, the prescribing physician communicated the case. Patients were evaluated without interfering with the treatment. Main targets of evaluation were skin flux at rest (RF), strain-gauge-derived rate of ankle swelling (RAS), and analogue symptoms score (ASLS). Ninety subjects completed the study in the first group; 122 in the second, registry group (total of 212 patients). The first and second (registry) groups and the 2 treatment groups were comparable for age and sex distribution. The pooled mean age was 42 years (SD +/-5.5) in the HR group (46+62 patients) and 41.5 (SD +/-6) in the D+H group (44+60 patients). Considering pooled data there were no differences in microcirculatory parameters between the pooled treatment groups at inclusion. A significant decrease (p<0.05) in RF and RAS was observed in the HR group at 8 weeks. The decrease in resting skin flux and in capillary filtration was associated with a significant improvement in signs/symptoms (analogue scale line) from an average of 9.4 (range 3-10) to 3.3 (4-6) (p<0.05). Significantly smaller variations were observed in the D+H group. The decrease in RF was 47.6% in the HR group vs 15.7% in the D+H group. The decrease in RAS was 40.9% in the HR group vs 12.8% in the D+H group. The decrease in ASLS was 64.8% in the HR group vs 12.9% in the comparative group. In conclusion venous microangiopathy and edema were improved by the treatment with HR both in the randomized study and in the pooled analysis. The comparison with D+H indicates that HR is comparatively more effective both on microcirculatory parameters and on signs/symptoms of CVI.
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PMID:HR, 0-(beta-hydroxyethyl)-rutosides, in comparison with diosmin+hesperidin in chronic venous insufficiency and venous microangiopathy: an independent, prospective, comparative registry study. 1567 50

Chronic venous insufficiency (CVI) is a pathologic condition caused by valvular incompetence, with or without associated venous outflow obstruction, which may affect both the superficial and the deep venous system, causing venous hypertension and stasis. The most common form of CVI is primary varicose veins due to the insufficiency of the saphenous system. Color-Doppler sonography (CDS) is actually the main diagnostic technique of imaging for CVI. In this article, we describe the anatomy, the technique, and the information necessary to the radiologist to perform CDS in chronic venous insufficiency. The knowledge of the venous anatomy is the cornerstone for an adequate sonographic examination. The venous network in the lower extremities is divided into three systems: superficial, deep, and perforating veins. Deep veins are "comitantes" to the corresponding arteries and run under the muscular fascia. Superficial veins course into the subcutaneous fat, superficially to the deep muscular fascia; the main superficial veins are the greater and lesser saphenous and their tributaries. Connection between the saphenous veins are defined as communicating veins. Superficial and deep veins are connected by perforating veins, with flow directed, under normal circumstances, from the superficial to the deep system. The main perforating are the Hunter in the mid thigh, the Dodd in the lower thigh, the Boyd in the upper calf, and the Cockett's in the middle and lower calf. Sonographic examination must be performed in the upright and supine position. Compression sonography and color and PW Doppler are systematically employed to assess the absence of deep venous thrombosis. Femoro-popliteal veins are evaluated with color and PW Doppler for valvular insufficiency with reflux by performing Valsalva maneuver and calf compression. The sapheno-femoral and sapheno-popliteal junctions are examined to identify type of junction, continence, accessory saphenous, and incompetent collaterals. Perforating veins are usually identified at the medial aspect of the thigh and at the medial, lateral, and posterior aspects of the leg. Outward flow (lasting more than 500 ms) in the perforating veins should be considered a sign of their incompetence. Several surgical and interventional procedures are now available for the treatment of the CVI, as follows: vein ligation and stripping, stab avulsion, endoluminal occlusion of the saphenous trunks, subfascial endoscopic perforator surgery, and valvuloplasty.
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PMID:Color-Doppler sonography in chronic venous insufficiency: what the radiologist should know. 1575 79

The aim of this independent study was to demonstrate the rapidity of the clinical action of HR 0-(beta-hydroxyethyl)-rutosides, Venoruton (Novartis Consumer Health) in patients with chronic venous insufficiency (CVI). Two groups of patients with venous hypertension and microangiopathy were treated with HR (1 or 2 g/day, for 8 weeks). Twelve patients (age 56.4; range 44-66; M:F = 6:6) were included in group 1 (1 g/day) (moderate CVI and microangiopathy); 10 patients (age 57.4; range 42-67; M:F = 5:5) in group 2 (2 g/day) with more severe CVI and microangiopathy. Average ambulatory venous pressure (AVP) was 58.6 (range 50-65) with a refilling time (RT) shorter than 10 seconds. There were no significant differences in AVP and RT between the 2 groups, but the duration of the disease was longer in group 2: 3.5 years (SD 2.0) in group 1 and 6.4 years (SD 3.3) in group 2. All included subjects completed the study and no dropouts were observed. In both dose groups there was a progressive decrease in laser Doppler resting flux (RF), indicating improvement in microangiopathy and a significant decrease in capillary filtration (RAS) associated with a significant improvement in analogue scale line score (ASLS) and edema. Although the effect in the 2 g dose group was more rapid on the microcirculatory parameters with a significant effect on RF and RAS after 4 days (effect of 1 g per day after 8 days and 6 days, respectively), there was no difference in the time to onset of a significant clinical improvement (ie, the ASLS and the edema score): 4 days in both groups. Venous microangiopathy and edema were improved by the treatment with HR within a few days. The effects were visible with both dosages, in both severity groups.
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PMID:HR, 0-(beta-hydroxyethyl)-rutosides; (Venoruton): rapid relief of signs/symptoms in chronic venous insufficiency and microangiopathy: a prospective, controlled study. 1579 6

Patients with venous leg ulcers usually have extensive symptoms both related to their venous insufficiency and to the wound itself, often combined with a reduced quality of life. Prevalence of venous leg ulcers varies from 0.1 to 1.0%. Treatment costs are high and may amount to 1.5% of a nation's total spending on health care. Venous hypertension is the common denominator for all patients with venous leg ulcers. Isolated superficial as well as deep or combined venous insufficiency with or without insufficient perforators may cause ulceration. In the microcirculation, inflammation is involved, but the exact mechanisms behind the ulcer formation remain unresolved. During the examination, a presence of superficial venous insufficiency accessible for superficial resection must be established. In addition to a clinical examination, venous pressure measurements/plethysmography and colour duplex scanning is recommended in order to locate and evaluate the significance of the venous insufficiency. The key element in the treatment of venous ulcers is to reduce oedema and venous hypertension by adequate compression and elevation. If primary superficial venous insufficiency is established, venous resection is recommended. This may improve healing and reduce recurrences. In selected patients, deep venous reconstruction is an alternative approach.
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PMID:[Venous leg ulcers]. 1581 37


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