scholarly journals Venous Valve Reconstruction in Patients with Secondary Chronic Venous Insufficiency

2008 ◽  
Vol 36 (4) ◽  
pp. 466-472 ◽  
Author(s):  
A. Rosales ◽  
J.J. Jørgensen ◽  
C.E. Slagsvold ◽  
E. Stranden ◽  
Ø. Risum ◽  
...  
2015 ◽  
Vol 30 (1_suppl) ◽  
pp. 50-58 ◽  
Author(s):  
A Rosales

The history of venous valve reconstruction extends back to 1968 when Robert L Kistner performed the first internal valve plasty to treat deep venous axial reflux. Throughout the past 50 years other techniques of reconstructive deep venous surgery (RDVS) were developed, not only to repair but also to replace venous valves. And the fact that several surgeons and centers have undertaken RDVS in the treatment of chronic venous insufficiency (CVI) reporting outcomes, has added knowledge to define more clearly the role of this kind of specialized surgery. Patients who may benefit from RDVS are among those where conventional treatment with compression stockings combined with superficial surgery has failed. Ulcer-healing rates of up to 70% have been reported after RDVS and ulcer-free periods of up to 36 months have been generated. But during five-year follow-up, freedom from ulceration period and clinical improvement rates were reduced significantly. This raises then the issue and challenge of durability of RDVS since the average age of patients who can benefit from it is about 50 years.


Angiology ◽  
2001 ◽  
Vol 52 (1_suppl) ◽  
pp. S27-S34 ◽  
Author(s):  
Geert W. Schmid-Schönbein ◽  
Shinya Takase ◽  
John J. Bergan

Chronic venous insufficiency (CVI) is inseparably linked to elevated venous pressure and is accompanied by vascular, dermal, and subcutaneous tissue damage and restructuring. Abundant evidence exists both in humans and in experimental models to suggest that the tissue damage may be initiated by generation of an inflammatory reaction. inflammatory indi cators include elevation of endothelial permeability; attachment of circulating leukocytes to the endothelium; infiltration of monocytes, lymphocytes, and mast cells into the connective tissue; and development of fibrotic tissue infiltrates and several molecular markers, such as growth factor or membrane adhesion molecule generation. Indicators of an inflammatory reaction are already detectable at early stages of CVI and may be involved in the development of primary venous valve dysfunction. One of the important questions is to identify trigger mechanisms for the inflammatory reaction in CVI. Current evidence suggests that, among several possible mechanisms (hypoxia, humoral stimulation), a shift in fluid shear stress from normal physio logical levels and endothelial distension under the influence of elevated venous pressure may serve as trigger mechanisms for inflammation.


1997 ◽  
Vol 173 (4) ◽  
pp. 301-307 ◽  
Author(s):  
Seshadri Raju ◽  
James D. Hardy

2006 ◽  
Vol 32 (5) ◽  
pp. 570-576 ◽  
Author(s):  
A. Rosales ◽  
C.E. Slagsvold ◽  
A.J. Kroese ◽  
E. Stranden ◽  
Ø. Risum ◽  
...  

2004 ◽  
Vol 74 (1-2) ◽  
pp. 34-39 ◽  
Author(s):  
Ramesh Tripathi ◽  
Kishore Sieunarine ◽  
Manzoor Abbas ◽  
Nazish Durrani

2017 ◽  
Vol 12 (2) ◽  
pp. 28-32
Author(s):  
Marilena SPIRIDON ◽  
◽  
Dana CORDUNEANU ◽  

Chronic venous insufficiency (CVI), frequent cause of lower limb edema, represents a severe consequence of the dysfunction of the venous valve, which results from the venous hypertension together with the degenerative processes at this level. CVI defines only the severe stages of the chronic venous disease (CVD), accompanied by morphological and functional damage, with significant alteration in quality of life. The treatment of CVI involves, depending on the severity of the case, a combination of general nonpharmacologic, pharmacologic, and surgical measures. Non-pharmacologic measures involve the use of a continuous and controlled external pressure represented by compression stockings which can significantly improve the venous return and lead to a major symptoms improvement. Pharmacologic treatment aims on one hand to alleviate hemodinamics by lowering blood viscosity, decreasing venous pressure and preventing intravascular thrombus formation and, on the other hand, restoring thevascular glycocalyx/endothelium, reducing parietal inflammation and increasing the venous wall tone. Within this pathology, sulodexide represents an innovative biological product with polypharmacological actions targeting more sites involved in the pathogenesis of CVD/CVI that alleviate hemodynamics and restore vascular structure which lead to a significant symptoms improvement and a slow disease progression. Surgery remains the procedure of choice in patients initially treated conservatively in whom symptoms persist or worsen, but also in case of those who already come to doctor in a severe stage of the disease.


1996 ◽  
Vol 23 (2) ◽  
pp. 357-367 ◽  
Author(s):  
Seshadri Raju ◽  
Ruth K. Fredericks ◽  
Peter N. Neglèn ◽  
J.David Bass

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