Lower extremity arterial inflow is adversely affected in patients with venous disease

Background Lower extremity chronic venous disease is due to venous hypertension resulting from reflux and/or obstruction. Studies of venous valvular function have validated and quantified valve closure times defining normal and abnormal valve function, and investigators have categorized the amount of venous reflux with validated criteria. However, hemodynamics of venous outflow obstruction remains poorly defined. The purpose of this study is to assess whether chronic venous disease alters arterial inflow at rest or during hyperemic limb challenge, and whether there are differences in patients with primary chronic venous insufficiency (1° CVI) versus those with postthrombotic venous disease. Methods Twenty-two normal limbs and 32 limbs in patients with chronic venous disease (C-3 or greater) were examined between September 2006 and January 2008. Chronic venous disease patients consisted of 22 postthrombotic patients and 10 with 1° CVI. Arterial inflow was measured at rest using venous occlusion plethysmography and after induced arterial inflow using postocclusive reactive hyperemia (PORH). Volume changes were recorded with volume plethysmography. A minimum of 10 minutes elapsed between the resting and PORH measurements of arterial inflow. Results Resting arterial inflow was greater in patients with 1° CVI when compared to normal patients (2.81 vs 1.26, P = .008) and to patients with postthrombotic venous disease (2.81 vs 1.13, P = .03). There was a 7.3-fold increase in maximal arterial inflow in normal patients during PORH versus a 4.8-fold increase in patients with postthrombotic venous disease ( P = .015). Patients with 1° CVI had a marked attenuation of maximal arterial inflow during hyperemic limb challenge, demonstrating only a twofold increase relative to their baseline resting arterial inflow ( P = .08). Conclusion Increases in arterial inflow during a hyperemic limb challenge are less robust in patients with postthrombotic venous disease than in normal volunteers. These data suggest that the pain of venous claudication may in part be due to a diminished arterial inflow response.