Platelet-monocyte aggregates in patients with chronic venous insufficiency remain elevated following correction of reflux.Cardiovasc Surg. 2002 Oct; 10(5):464-9.CS
An increased number of circulating platelet-monocyte aggregates (PMAs) is present in patients with all clinical classes of chronic venous insufficiency (CVI). The purpose of this study was to determine whether patients with CVI maintain elevated levels of PMAs following complete surgical correction of chronic venous insufficiency.
Patients with superficial venous insufficiency and a normal deep venous system documented by duplex scan were included in the study. Venous blood was drawn from a superficial vein in the leg and an antecubital vein prior to vein stripping and again six weeks postoperatively. Control subjects without evidence of venous disease had blood drawn from an antecubital vein. Whole blood flow cytometry was used to analyze the samples for the presence of platelet-monocyte aggregates following incubation with buffer or 0.5 microM adenosine diphosphate (ADP).
Postoperative duplex scanning demonstrated elimination of venous reflux in the superficial venous system and normal deep vein physiology in all nine patients. Preoperatively, patients with CVI had significantly elevated levels of circulating PMAs in both arm and leg samples without stimulation by an agonist compared to controls (15.2+/-1.1 and 14.3+/-1.3 vs 7.4+/-0.3 for controls, p<0.02 for each), and after stimulation by 0.5 microM ADP (33.7+/-4.7 and 34.3+/-5.2 vs 12.5+/-3.8 for controls, p<0.04 for each). There was no significant change in the number of PMAs in either patient arm or leg blood samples six weeks following correction of venous reflux by removal of the diseased veins.
Complete correction of chronic venous insufficiency did not diminish the elevated circulating levels of platelet-monocyte aggregates. We conclude that the presence of an increased number of PMAs identified in patients with CVI is not secondary to the presence of venous reflux, but may be involved with the primary etiology of chronic venous insufficiency. This finding also suggests that a stimulus other than venous hypertension may be important in triggering the leukocyte activation seen in patients with chronic venous disease.