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Hemodynamics of "critical" venous stenosis and stent treatment.
BACKGROUND: The concept of "critical" stenosis at which there is a sharp reduction in forward flow is derived from arterial disease. The critical element in venous stenoses is upstream pressure, not downstream flow. Many venous symptoms and microvascular injury are related to venous hypertension. We studied the effect of venous stenosis on upstream pressure using a mechanical model and with clinical measurements after stenting of iliac vein segments (common and external).
METHODS: The experimental model consisted of a Starling Resistor - Penrose tubing enclosed in a pressurized plastic chamber to simulate abdominal venous flow. Clinical measurements included time-averaged velocity, area, rate of flow, and quantified phasic flow volume in the common femoral vein before and after iliac vein stenting. Traditional air plethysmography and occlusion plethysmography were also performed.
RESULTS: The mechanical model showed that upstream pressure varied based on (1) volume of venous inflow, (2) abdominal pressure, (3) outflow pressure, and (4) outflow stenosis. Upstream pressure changes were inverse to flow as kinetic energy was converted to pressure as required. A venous stenosis of as little as 10% raised upstream pressure in the model when the abdominal pressure was low, but high grades of stenosis had no contribution when abdominal pressure was high. Stenting of the Penrose moderated or nullified upstream pressure changes related to abdominal pressure. There was significant decompression of the common femoral vein, implying pressure reduction after stenting; median area reduction was 15% and 10% in erect and supine, respectively. Air plethysmography showed improvement in venous volume and in other parameters in confirmation of venous decompression. There was significant prolongation of phasic flow duration and quantitative phasic flow increased (median, 16%) after stenting in the erect position. There was no increase in arterial inflow.
CONCLUSIONS: The criticality of iliac vein stenosis is based on peripheral venous hypertension, which is controlled by more confounding factors than in arterial stenosis. The experimental model clarifies the interplay of the many variables. Clinical measurements indicate that iliac vein stenting results in decompression of the limb veins and, by inference, a reduction in venous pressure. Venous flow is improved less consistently and, in part, is related to an increase in duration of phasic flow. Limb arterial flow is not increased, and the venous flow changes are likely the result of rearrangement of the velocity and pressure components of venous flow.
METHODS: The experimental model consisted of a Starling Resistor - Penrose tubing enclosed in a pressurized plastic chamber to simulate abdominal venous flow. Clinical measurements included time-averaged velocity, area, rate of flow, and quantified phasic flow volume in the common femoral vein before and after iliac vein stenting. Traditional air plethysmography and occlusion plethysmography were also performed.
RESULTS: The mechanical model showed that upstream pressure varied based on (1) volume of venous inflow, (2) abdominal pressure, (3) outflow pressure, and (4) outflow stenosis. Upstream pressure changes were inverse to flow as kinetic energy was converted to pressure as required. A venous stenosis of as little as 10% raised upstream pressure in the model when the abdominal pressure was low, but high grades of stenosis had no contribution when abdominal pressure was high. Stenting of the Penrose moderated or nullified upstream pressure changes related to abdominal pressure. There was significant decompression of the common femoral vein, implying pressure reduction after stenting; median area reduction was 15% and 10% in erect and supine, respectively. Air plethysmography showed improvement in venous volume and in other parameters in confirmation of venous decompression. There was significant prolongation of phasic flow duration and quantitative phasic flow increased (median, 16%) after stenting in the erect position. There was no increase in arterial inflow.
CONCLUSIONS: The criticality of iliac vein stenosis is based on peripheral venous hypertension, which is controlled by more confounding factors than in arterial stenosis. The experimental model clarifies the interplay of the many variables. Clinical measurements indicate that iliac vein stenting results in decompression of the limb veins and, by inference, a reduction in venous pressure. Venous flow is improved less consistently and, in part, is related to an increase in duration of phasic flow. Limb arterial flow is not increased, and the venous flow changes are likely the result of rearrangement of the velocity and pressure components of venous flow.
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