Underperfusion of Valve Pockets and the Initiation of DVT


If the first stage in the aetiology of DVT is sustained underperfusion of the valve pockets (VVP) during extended periods of non-pulsatile flow, then the structure, function and pathology of venous valves are of crucial importance. The questions to be answered are: how might underperfusion of a VVP lead to thrombosis, and where in a valve would thrombus formation be initiated? This chapter reviews the accumulated evidence that VVP are indeed the sites of venous thrombogenesis, describes valve morphology and function, and considers how these may be changed under pathological conditions. At the end of the chapter we propose that hypoxaemia in long-underperfused VVP leads to endothelial hypoxia, specifically of the inner (parietalis) surface of the valve cusp(s), and that this may under certain conditions become the prelude to DVT. In the light of this proposal, we calculate the approximate time needed for non-pulsatile venous flow to become pathogenic.


Local hypoxaemia venous valve pocket valve cusp parietalis endothelium endothelial hypoxia 


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© Springer Science + Business Media B.V 2008

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