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Theoretical concept of a diastolic compression device is presented. The device could have a form of a pneumatic cuff or a rubber sleeve. Its objective is to exert external pressure below the knee, which would compress the great saphenous vein during the diastolic phase of the calf pump activity, and hinder thereby the saphenous reflux and the occurrence of ambulatory venous hypertension. Based on the results of venous pressure measurements, it is supposed that pressure of about 35 mm Hg would be able to fulfill this therapeutic aim. If tolerated and accepted by the patients, the device could offer, in addition to the current invasive methods and compression stocking therapy, a simple conservative, nonetheless effective treatment of primary varicose veins. It would keep the dividing line of the ambulatory pressure gradient below the knee, as is the case with healthy people, and prevent thereby the progression of the disease. In addition, this conservative method would preserve the great saphenous vein for possible use as a bypass graft in the future.

In this article, the CHIVA and ASVAL methods are assessed from the hemodynamic point of view. The CHIVA method comprises complicated, unusual terminology and new perceptions, such as closed and open shunts, fractionation of the hydrostatic pressure, subdivision of the venous network. The principal part of the CHIVA theory is the drainage of venous blood from the thigh saphenous system into the deep lower leg veins through the preserved saphenous trunk after high ligation at the saphenofemoral junction, which is considered as a beneficial, physiological phenomenon. In reality, this is recurrent reflux producing ambulatory venous hypertension. The main impact of the CHIVA procedure is the elimination of the saphenous reflux by high ligation at the saphenofemoral junction; thus it can be presumed that the CHIVA procedure yields similar results like the crossectomy.The ASVAL procedure is de facto the modification of the old Madelung method that was the prevalent surgical procedure before the Trendelenburg era in the 19th century. The results after ASVAL were not checked by plethysmography; there is a good case to suppose that the results after the ASVAL method would comply with those after sclerotherapy.

The hemodynamic assessment of the bidirectional flow within calf perforators and in the conductive veins in varicose vein disease is presented. The bidirectional streaming within calf perforators is induced by the changing polarity of the systolic and diastolic pressure gradients arising during calf pump activity between the deep veins and the saphenous system of the lower leg, as documented by simultaneous pressure measurements in the posterior tibial vein and the great saphenous vein. This bidirectional flow makes the deep and superficial veins of the lower leg conjoined vessels. The vector of the bidirectional streaming in varicose vein patients is oriented inward, into the deep veins. The enlarged calf perforators are the consequence of the saphenous reflux; after elimination of saphenous reflux the diameter of calf perforators diminishes significantly. Results of venous pressure, plethysmographic and electromagnetic flow measurements rebut the still prevalent opinion that the outward flow within calf perforators is a reflux. There is an up-and-down flow in the conductive veins during calf pump activity with a prevailing systolic centripetal (orthograde) flow in the popliteal/femoral axis and a diastolic centrifugal (retrograde) flow in the incompetent great saphenous vein. The popliteal vein represents actually the drain pipe of the calf muscle pump. The ambulatory venous pressure gradient arising during the diastolic phase of the calf pump activity resembles the diastolic pressure difference between the aorta and the left ventricle.

The following features characterize varicose vein disease: 1) Venous reflux, 2) Inherent weakness of the vein wall, 3) Tendency to recurrence. Venous reflux is the most important pathological hemodynamic phenomenon causing ambulatory venous hypertension and evoking chronic venous insufficiency; it is released by the ambulatory pressure gradient, which arises during calf pump activity between thigh and lower leg veins. Inherent weakness of the vein wall entails increased vein distensibility. The impaired vein wall structure is not able to resist the dilatation force of the hydrostatic and intra-abdominal pressure; the veins in the lower extremity subsequently dilate, become incompetent, and tend to form varicose veins. Abolition of saphenous reflux removes the hemodynamic disturbance but it simultaneously generates preconditions for reflux recurrence. This run of events is triggered by the drainage of venous blood from the thigh saphenous system into deep lower leg veins, which occurs during calf pump activity. The dividing line of the ambulatory pressure gradient that is located in healthy people just below the knee joint is displaced into the thigh between the femoral vein and the incompetent thigh saphenous system; in this way, pressure gradient between the femoral vein and the incompetent saphenous system occurs and starts the chain of events that evokes reflux recurrence. Hindrance of the untoward drainage at the knee level would prevent generation of this prerequisite for reflux recurrence.

Saphenous reflux interferes with the physiological decrease in pressure and induces ambulatory venous hypertension. Elimination of reflux is achieved by flush ligation at the incompetent saphenofemoral junction and stripping of the great saphenous vein, which is the basis of the conventional surgical therapy. Endovenous ablative methods substitute stripping by thermal of chemical destruction of the saphenous trunk; they usually refrain from saphenofemoral junction ligation. Short-term and medium-term results up to 5 years, achieved after endovenous ablation without high ligation, are comparable with those after conventional surgery, which questioned the necessity to ligate the incompetent saphenofemoral junction. Nevertheless, clinical symptoms caused by recurrent reflux occur as a rule not earlier than 8 to 10 years after efficient abolition of reflux. Consequently, randomized studies with long-term follow-ups exceeding 10 years are necessary for trustworthy assessment whether it is justified to abstain from saphenofemoral junction ligation.

Calf muscle pump is the motive force enhancing return of venous blood from the lower extremity to the heart. It causes displacement of venous blood in both vertical and horizontal directions, generates ambulatory pressure gradient between thigh and lower leg veins, and bidirectional streaming within calf perforators. Ambulatory pressure gradient triggers venous reflux in incompetent veins, which induces ambulatory venous hypertension in the lower leg and foot. Bidirectional flow in calf perforators enables quick pressure equalization between deep and superficial veins of the lower leg; the outward (into the superficial veins) oriented component of the bidirectional flow taking place during calf muscle contraction is no pathological reflux but a physiological centripetal flow streaming via great saphenous vein into the femoral vein. Calf perforators are communicating channels between both systems making them conjoined vessels; they are not involved in the generation of pathological hemodynamic situations, nor do they cause ambulatory venous hypertension. The real cause why recurrences develop has not as yet been cleared. Pressure gradient arising during calf pump activity between the femoral vein and the saphenous remnant after abolition of saphenous reflux triggers biophysical and biochemical events, which might induce recurrence. Thus, abolition of saphenous reflux removes the hemodynamic disturbance, but at the same time it generates precondition for reflux recurrence and for the comeback of the previous pathological situation; this chain of events has been called hemodynamic paradox.

Varicose vein disease is characterized by tenacious tendency to recur. Measures recommended to prevent recurrences (flush ligation at the saphenofemoral junction, removal of incompetent great saphenous vein in the thigh, and insertion of mechanical barriers in the fossa ovalis) did not succeed in preventing recurrence. Reflux recurrence is triggered by the hemodynamic phenomenon called hemodynamic paradox. Abolition of saphenous reflux removes the hemodynamic disturbance of any degree of severity but at the same time it releases the pathological process leading to recurrent reflux. This process is induced by drainage of venous blood from incompetent superficial thigh veins into deep lower leg veins during calf pump activity, which evokes the development of ambulatory pressure gradient between the femoral vein and incompetent segments of the saphenous system in the thigh. The pressure gradient sets off biophysical and biochemical events inducing recurrent reflux. The designed therapeutic strategy consists of reliable abolition of saphenous reflux and of hindering the pathological drainage of venous blood at the knee level in order to preclude development of the hemodynamic preconditions for reflux recurrence. In this way, the dividing line of the ambulatory pressure gradient would be kept below the knee, as is the case with healthy people.

The pathophysiology of calf perforators is presented. Bidirectional flow within calf perforators with a prevailing inward, into deep veins oriented component arises during calf pump activity in varicose vein patients, as evidenced by venous pressure measurements, plethysmographic findings, duplex ultrasonography, and electromagnetic flow measurements. Reflux within calf perforators is an inward, not outward, flow; the opinion that the outward flow within calf perforators is a reflux is at odds with the reality. During calf muscle contraction, the pressure in the posterior tibial vein is higher than in the great saphenous vein; it induces the harmless outward flow within calf perforators, which runs further via great saphenous vein in the physiological direction toward the heart. Deep and superficial veins of the lower leg form conjoined vessels, as documented by nearly equal pressure curves registered simultaneously in the posterior tibial and great saphenous veins both in varicose vein patients and in healthy people. Calf perforators do not entail ambulatory venous hypertension or any other hemodynamic disorder, even if enlarged and incompetent; their ligation is needless. The diameter of calf perforators is influenced by the intensity of saphenous reflux; it enlarges with increasing intensity of saphenous reflux and diminishes after the abolition of reflux.

Background: Neovascularization is an important cause of venous reflux recurrence after high ligation of the long saphenous vein. The pathogenesis of this phenomenon is so far obscure. It is possible that a hemodynamic factor – a pressure gradient between the femoral vein and the residual long saphenous vein – could be the trigger initiating the process of neovascularization. Patients and methods: Venous pressure measurements on eight patients with primary varicose veins were performed in the erect position in the insufficient long saphenous vein on the thigh. Mean pressures in the quiet standing position and ambulatory pressures were considered. By interrupting the saphenous reflux either distally or proximally to the point of measurement the pressure conditions either in the femoral or in the crural veins were simulated. Results: With the tourniquet placed distally to the point of measurement, the venous pressure in the upper interrupted segment of the long saphenous vein (equivalent to the pressure in the femoral vein) remained uninfluenced during ambulation. In contrast, by interrupting the reflux proximally to the point of measurement, a marked decrease of the ambulatory pressure in the lower part of the long saphenous vein (equivalent to the pressure in the crural veins) was noted. Conclusions: A pressure difference occurs between the veins of the thigh and the lower leg during the activation of the muscle venous pump. This fact may explain the tendency of recurrencies of varicose veins after high ligation of the long saphenous vein as well as the initiation of reflux.

A curious hemodynamic phenomenon emerging as a consequence of the treatment of varicose veins can offer a reasonable explanation why varicose vein and reflux recurrences occur tenaciously irrespective of the applied therapeutic procedure. Saphenous reflux is the most important hemodynamic factor in varicose vein disease: it is responsible for the hemodynamic disturbance, ambulatory venous hypertension, clinical symptoms, and chronic venous insufficiency. Abolition of saphenous reflux eliminates the hemodynamic disturbance and restores physiological hemodynamic and pressure conditions, but at the same time it unavoidably evokes a pressure difference between the femoral vein and the incompetent superficial veins in the thigh during calf pump activity. The pressure difference increases flow and enhances fluid shear stress on the endothelium in pre-existing minor communicating channels between the femoral vein and the saphenous system in the thigh, which triggers release of biochemical agents nitride oxide and vascular endothelial growth factor; the consequence is enlargement (vascular remodeling) of the communicating channels, and ultimately reflux recurrence. Hence, the abolition of saphenous reflux creates preconditions for the comeback of the previous pathological situation. This phenomenon-starting the same trouble while fixing the problem-has been called hemodynamic paradox; is explains why varicose vein and reflux recurrence can occur after any mode of therapy.