Venous valve incompetence: the first culprit in the pathophysiology
of primary chronic venous insufficiency

CHRONIC VENOUS INSUFFICIENCY (CVI) IS MANIFESTED IN THE
lower extremities. Its most obvious sign is protuberant, saccular
varicose veins. These fail to fulfill their assigned function of transporting
blood from the lower extremities to the heart. Instead, they
allow the weight of the column of blood from the right atrium as it is transmitted through the
valveless vena cava and iliac veins to be expressed in the thigh and leg. There, the venous hypertension
initiates a cascade of inflammatory reactions that may progress to edema, venous eczema,
ankle skin hyperpigmentation, atrophie blanche, and other manifestations such as lipodermatosclerosis
and venous leg ulcers.
Recently, considerable progress has been made in understanding the pathophysiological processes
at the cellular and molecular level that cause these diverse manifestations. These may become
targets for preventative pharmacologic intervention. If so, there will be a change in focus
from ablation to preservation. The goal of this editorial is to explain how the processes of venous
insufficiency begin because of initial venous valve failure and how they are perpetuated by that
valve failure.
Venous hypertension
In spite of the diversity of signs and symptoms associated with CVI, it is likely that they are all
related to venous hypertension. Venous hypertension involves reflux through incompetent
valves.1,2 Pressure in the veins of the leg is determined by two components, a hydrostatic component,
described above, and a hydrodynamic component related to pressure generated by contraction
of the skeletal muscles of the leg that is transmitted to the venular capillary network. Both
components are profoundly modified by the action of the venous valves. During standing without
skeletal muscle activity, venous pressures in the leg are determined by the hydrostatic component
and capillary flow. Skeletal muscle contractions, as during ambulation or exercise, increase
pressure within the deep leg veins. Competent venous valves ensure that the resulting
blood flow is toward the heart, leading to emptying of the deep and superficial venous systems
and a fall in venous pressure. Even quite small leg movements can provide significant pumping
action. However, in the absence of competent valves, venous pressure fails to fall with leg movements,
and the pressures generated by muscle contraction are transmitted to the skin microcirculation.
Skin changes in CVI stem from venous pressures in the leg that reach higher than
normal levels and are elevated for abnormally prolonged periods of time.
Valvular incompetence
Venous valve incompetence is a central feature of venous hypertension that in turn underlies most
of the signs characteristic of chronic venous disease (CVD). Alterations and damage to valves have
been noted angioscopically. These include stretching, splitting, tearing, thinning, and adhesion
of valve leaflets.3 Reduction in the number of valves has been observed in segments of saphenous

veins from patients with CVI.4

These observations do not reveal the mechanism of valvular disappearance or how such remodeling
fits into the pathophysiological sequence of events in CVD. However, an important step
forward came when we examined valves from great saphenous veins removed from patients with
CVD.5 Using a monoclonal antibody specific for monocytes and tissue macrophages, we found
infiltration of valve leaflets and the venous wall by monocytes and macrophages in all vein specimens
from CVD patients and in none from controls with normal veins. Infiltration was greater
in the valve sinus and proximal venous wall than in the distal aspect of the valve leaflet and distal
vein wall (Figure 1A). This suggested a link with elevated venous pressure. Further investigations
have shown that inflammation and subsequent remodeling of the venous valves and wall
are the fundamental mechanisms underlying valve damage and the lesions seen angioscopically.6

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