Valve Pathology The Formation of Nascent Thrombi within VVP

Saphir and Lev (1952a) studied femoral valvulitis and found that 'inflammatory injury' to venous valves is common. Since the appearance of an 'inflamed' valve cusp represents margination and sequestration of leucocytes/platelets, it could be considered that an 'inflamed valve' is indistinguishable from a 'white thrombus' in its earliest (Kopfteil) phase (cf. Chapter 7). Valve cusps can become necrotic, e.g. after (or perhaps during the pathogenesis of) endocarditis or other heart diseases, and such necrosis appears to be thrombogenic. Leukocytes congregate around the injured cusp, and sometimes the connective material of the cusp is thickened and coarsened. These findings suggest a possible mechanism for the formation of

Fig. 9.6 From Stone and Stewart (1988). These photographs show the constancy of what Franklin termed ostial valves at the mouths of tributary veins, attached/ anchored within the tributary vein as it joins the main venous trunk concerned. Franklin's parietal valves are the (predominantly) multi-cusp valves that intersect the main-vein lumen and hold up the blood column above them when the distal pressure below has fallen. In this illustration, a plastic was infused into the main vein lumen (and subsequently removed by a 'corrosion' technique). Very small protrusions of the solid ('cured') plastic are visible, retained by the ostial valve that had closed a few millimetres from the main vein orifice in each tributary (thus facilitating a valve thrombus at the junction, and manifest as a very short 'stump' of contained plastic). Copyright 1988 John Wiley and Sons. Reproduced with permission of Wiley-Liss Inc. on behalf or John Wiley and Sons Inc

Fig. 9.6 From Stone and Stewart (1988). These photographs show the constancy of what Franklin termed ostial valves at the mouths of tributary veins, attached/ anchored within the tributary vein as it joins the main venous trunk concerned. Franklin's parietal valves are the (predominantly) multi-cusp valves that intersect the main-vein lumen and hold up the blood column above them when the distal pressure below has fallen. In this illustration, a plastic was infused into the main vein lumen (and subsequently removed by a 'corrosion' technique). Very small protrusions of the solid ('cured') plastic are visible, retained by the ostial valve that had closed a few millimetres from the main vein orifice in each tributary (thus facilitating a valve thrombus at the junction, and manifest as a very short 'stump' of contained plastic). Copyright 1988 John Wiley and Sons. Reproduced with permission of Wiley-Liss Inc. on behalf or John Wiley and Sons Inc

Fig. 9.6 (continued)

pre-thrombotic nidi, but they are not consistent with the contention (Sevitt 1974a) that only some 10% of venous thrombi were observed to originate on the cusps.

This calls the exact site of nidus formation into question: is it the cusp itself (specifically, the luminalis or the parietalis endothelium), the neighbouring vein wall, or the sinus of the VVP? The studies of Saphir and Lev, Paterson and McLachlan, and Sevitt, led them to exclude the vein wall as the primary site of nidus thrombus formation. Leukocyte infiltration of cusps has subsequently been described in cases of venous insufficiency associated with injury to saphenous vein valves (Ono et al. 1998), and was beautifully demonstrated in scanning electron micrographs of the junctions between tributaries and jugular veins in dogs (Stewart et al. 1983, 1984; see Fig. 9.6). Notably, such infiltration is not immediately accompanied by fibrin deposition (cf. Aschoff 1924). Thrombosis can lead to the complete obliteration of venous valves in the lower extremities, leading to the major symptoms of post-thrombotic syndrome (Chapter 1; see below).

In a subsequent paper, Saphir and Lev (1952b) reported that ageing is associated with increased collagen and decreased elastin below the parietalis endothelium, where the crypts tend to become smaller. Also, the elastic material below the luminalis endothelium thickens with increasing age. Generally, the connective tissue and muscle contents of the valve sinus decrease and fat deposits increase. We may speculate about the significance of these findings for the increased incidence of DVT in older people: the cusp becomes less flexible, impairing the efficiency of valve function. In addition, perhaps the lower resting venous tone in older patients decreases local blood velocity, exacerbating underperfusion by attenuating the intravascular pressure changes during pulsatile flow (see below).

The weight of evidence therefore favours pro-thrombotic nidus formation on the valve leaflets; but if so, why did Sevitt, an eminent histopathologist, find so few thrombi anchored to cusp endothelia? We shall return to this question in Chapter 10.

It is well-attested that thrombi can also arise in venous sinuses in the soleal and gastrocnemius muscles (for reviews see, e.g. Mammen 1992; Hirsh et al. 1986), and these structures do not usually have manifest valves (Dodd and Cockett 1976). However, Chapple and Wood (1980) made a telling observation about venous sinuses in the legs of the monkey Macaca fascicularis: they contain 'flaps of endothelial tissue'. Similar flaps of endothelial tissue have been described in human venous sinuses (Cotton and Clark 1965). The mechanism we shall propose for the origin of pro-thrombotic nidi on the valve cusp parietalis endothelium could apply equally to the endothelial flaps of venous sinuses.5

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