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ICVTS on-line discussion A Valves and primary varicose veins

University Hospital Sestre Milosrdnice, Zagreb 10000, Croatia

Role of saphenous vein wall in the pathogenesis of primary varicose veins

eComment: The authors stated that there are no available studies which compare the structural problems of varicose veins in the case of the presence of valvular incompetence and that they study findings of the histopathologic changes which support the theory of primary weakness of the vein wall as a cause of varicosity [1]. Studies on the pathophysiology of chronic venous insufficiency [CVI] should acknowledge that the valvular ‘chain’ is not limited to large veins, but extends down to the venular level where microscopic venous valves [MVVs] play an important role in venous hemodynamics. Role of MVVs was demonstrated in limbs afflicted with CVI by Photoplethysmography [2]. These findings evaluated the venous refilling time [VRT] in limbs with severe CVI [CEAP: C4-C6] and attributed to the increase in VRT exclusively to the transfer of MVV. The improvement of the local venous haemodynamics was also confirmed by the clinical results with no recurrent ulceration and no recurrent tissue lipodermatosclerosis up to 9 years. This data suggests that MVVs play a role in counteracting venous hypertension caused by valvular failure of larger veins. Therefore, MVV incompetence could explain the occurrence of skin changes associated with CVI in limbs with competence of proximal valves and a short VRT and in those without any relevant venous disease. Clinicians consider the venous bed as ‘valveless’ from the venular level up to 2 mm large veins.

The above mentioned statements demonstrate that MVVs are present in vascular territories with unfavourable venous haemodynamics to play a functional role which must be still comprehensively evaluated. The available evidence suggests that MVV incompetence could explain clinical syndromes characterized by signs and symptoms of CVI in limbs with competent venous valves in large veins. Investigation of the pathophysiology of CVI must take into account the possible haemodynamic role of a valvular ‘chain’ extending down to the venular level. In the future, the functional role of MVV in CVI will be investigated by techniques such as capillaroscopy, high frequency ultrasound probes, Laser Doppler and micro fibre angioscopy. The huge body of knowledge available concerning MVVs urges us to study further the combined histopathological changes of varicose vein walls and valves.

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1. Elsharawy MA, Naim MM, Abdelmaguid EM, Al-Mulhim AA. Role of saphenous vein wall in the pathogenesis of primary varicose veins. Interact CardioVasc Thorac Surg 2007; 6:219–224.[Abstract/Free Full Text]
2. Aharinejad S, Nedwed S, Michlitis W, Dunn R, Abraham D, Vernadakis A, Marks SC. Valvular density alone cannot account for sites of chronic venous insufficiency and ulceration in the lower extremity. Microcirculation 2001; 8:347–354.[CrossRef][Medline]

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Narcis Hudorovic Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Hudorovic, N. Search for Related Content PubMed PubMed Citation Articles by Hudorovic, N. Related Collections Related Article