Valvular Density Alone Cannot Account for Sites of Chronic Venous Insufficiency and Ulceration in the Lower Extremity

Aharinejad, Seyedhossein; Nedwed, Stephan; Michlits, Wolfgang; DUNN, RAYMOND; Abraham, Dietmar; VERNADAKIS, ADAM; Marks, Sandy C.

doi:10.1080/mic.8.5.347.354

Cited by 5 publications

(15 citation statements)

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“…2,4 One study has compared the density of microvenous valves in areas of the lower limb at low risk of venous ulceration with the density of valves in areas at high risk, concluding that differences in valvular density alone were not enough to explain the differences in ulceration risk at different sites of the lower leg. 6 While the variation in size and density of microvenous valves is noteworthy, it may be that the distribution of microvenous valves within the venous network is more pertinent to their normal role and their ability to prevent reflux. What happens to these microvalves in veins with superficial venous reflux and venous ulcer has not been described.…”

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confidence: 97%

Failure of microvenous valves in small superficial veins is a key to the skin changes of venous insufficiency

Vincent

Jones

Hill

et al. 2011

Journal of Vascular Surgery

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This study demonstrates that valvular incompetence can occur independently in small superficial veins in the absence of reflux within the GSV and the major tributaries. We have shown that once there is incompetence of the third generation "boundary" microvalves, reflux can extend into the microvenous networks in the skin. These effects are markedly worse in the presence of GSV incompetence. We propose that degenerative changes with valve incompetence are required in both the larger proximal vessels and the small superficial veins, in particular at the "boundary" valve level, for the severe skin changes in venous insufficiency to occur.

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confidence: 97%

Failure of microvenous valves in small superficial veins is a key to the skin changes of venous insufficiency

Vincent

Jones

Hill

et al. 2011

Journal of Vascular Surgery

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“…Only when these two elements are working correctly is venous return successful (Stegall, ; Stick et al., ). The valvular insufficiency of superficial veins, frequently encountered in humans, results, during muscle contraction, in the return of blood from the deep to superficial veins, therefore leading to an accumulation of blood and an increase in hydrostatic pressure in these veins (Aharinejad et al., ; Mühlberger et al., ). This ‘blowout’ is an important risk factor in the development of varicose veins in humans (Aharinejad et al., ).…”

Section: Discussionmentioning

confidence: 99%

“…The valvular insufficiency of superficial veins, frequently encountered in humans, results, during muscle contraction, in the return of blood from the deep to superficial veins, therefore leading to an accumulation of blood and an increase in hydrostatic pressure in these veins (Aharinejad et al., ; Mühlberger et al., ). This ‘blowout’ is an important risk factor in the development of varicose veins in humans (Aharinejad et al., ). The valvular hyperdensity in the superficial veins in horses, unlike in humans where deep veins have more venous valves than their superficial veins (Shepherd and Vanhoutte, ; Pang, ), probably decreases the risk of varicose veins in horses.…”

Section: Discussionmentioning

confidence: 99%

“…The venous valves enable fluid to circulate in one direction only towards the heart and from the superficial veins of limb to the deep veins through anastomosis or perforating veins that normally drain blood from superficial to depth (Shepherd and Vanhoutte, ; Pang, ; Winokur and Khilnani, ). Preliminary studies in human medicine have shown that the majority of the venous valves are bicuspid, and are rarely tricuspid (Harmon and Edwards, ; Shima et al., ; Aharinejad et al., ).…”

Section: Introductionmentioning

confidence: 99%

“…In addition to inflammatory (Belknap et al., ) and metabolic abnormalities (Moore et al., ; Kyaw‐Tanner et al., ), vascular dysfunctions, particularly, at the digital venous level, were described to play a pivotal role in the development of laminitis (Allen et al., ; Peroni et al., ; Moore and Belknap, ; Katz and Bailey, ). The pathological modifications of venous valves have been reported to produce venous hemodynamic disorders, including venous stasis and local oedema especially in the distal portion of the limbs (Aharinejad et al., ; Shaolian and von Hoffmann, ).…”

Section: Introductionmentioning

confidence: 99%

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Venous Valvular Distribution in the Thoracic and Pelvic Limbs of the Horse

Harfoush

Guintard

Desfontis

et al. 2015

Anat. Histol. Embryol.

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Dysfunction of venous valves can lead to hemodynamic disorders causing venous stasis, which would favour the occurrence of equine laminitis. However, very few studies have investigated venous valves in the horse digit. The purpose of this study was to compare valvular density between thoracic and pelvic limbs and to study the relationship between valvular density of veins and their location, diameter and wall thickness. After dissection, valvular density was calculated based on the number of valves counted in the principal veins of 7 thoracic and 7 pelvic limbs from 7 horses. Our results showed that the valvular density was higher in thoracic limbs, which probably reflects the adaptation to the consequences of hydrostatic pressure. The superficial veins have a higher valvular density that would prevent the varicose risk in the horse. The lower valvular density in the thick veins can be explained by the high density of the smooth muscular cells contained, which would cause an important vasoconstriction via the sympathetic nervous system. The veins with a large diameter also have a lower valvular density; these veins are not exposed to important changes in hydrostatic pressure. Other valvular characteristics may also be involved in the vascular disorders that may be related to the pathophysiology of laminitis.

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Valves in Small Veins and Venules

Caggiati

Phillips

Lametschwandtner

et al. 2006

European Journal of Vascular and Endovascular Surgery

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It is commonly believed that valves are absent in veins smaller than two millimetres in diameter. Consequently, current investigations on the pathophysiology of chronic venous disease (CVD) consider and evaluate only the valvular competence of large veins. The authors review literature from their own collections as well as from medical database searches to assess the functional relevance of these valves. Microscopic venous valves (MVVs) were first described in 1934 in the human digits and have subsequently been demonstrated in other parts of the human body as well as in many tissues and organs of animals. Their location and arrangement suggests that MVVs prevent blood reflux in small sized veins and restrict flow from postcapillary venules back into the capillary bed. This haemodynamic role of MVVs is strongly supported by the clinical finding that grafting skin rich in MVVs results in long-lasting healing leg ulcers attributable to CVD. The huge body of knowledge available concerning MVVs urges us to correct textbooks of anatomy. Studies on the pathophysiology of CVI should acknowledge that the valvular "chain" is not limited to large veins, but extends down to the venular level where MVVs play an important role in venous haemodynamics.

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Valvular Density Alone Cannot Account for Sites of Chronic Venous Insufficiency and Ulceration in the Lower Extremity

Cited by 5 publications

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Failure of microvenous valves in small superficial veins is a key to the skin changes of venous insufficiency

Failure of microvenous valves in small superficial veins is a key to the skin changes of venous insufficiency

Venous Valvular Distribution in the Thoracic and Pelvic Limbs of the Horse

Valves in Small Veins and Venules

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