title: Pulsatile venous insufficiency in severe tricuspid regurgitation: does pulsatility protect against complications of venous disease?
abstract: Prior observations showed that the consequences of venous hypertension depend not only on the magnitude of the venous pressure but also on the efficiency of compensatory mechanisms that protect against the effects of excessive pressures on the microcirculation. Pulsatile venous insufficiency (PVI) associated with severe tricuspid regurgitation (TR) provides the opportunity to investigate the effect of the pulsatile shear stress on the outcome of venous insufficiency. The authors conducted a study to assess the flow characteristics and clinical outcome of PVI associated with TR. Five patients were evaluated, presenting venous insufficiency associated with ectasia, varices, and visible systolic pulsations of the leg veins. Characteristics of the venous flow were assessed by duplex ultrasound. In two patients, flow in the distal calf veins was evaluated by power Doppler sonography, and the supine-to-sitting leukocyte trapping was calculated. Results of the latter measurements were compared with measurements in five control patients who presented chronic nonpulsatile venous insufficiency. A survey of complications of PVI was conducted. On follow-up for 6 to 15 years (average 9.4 years) none of the patients developed venous thrombosis, phlebitis, or cutaneous ulcer. Flow in the distal calf vessels was increased in PVI (12-20 vessels/field) as compared with nonpulsatile venous insufficiency (0-7 vessels/field). Leukocyte trapping in the upright position was diminished in PVI (0.8-3%) as compared with nonpulsatile venous insufficiency (7-22%). In conclusion, PVI is characterized by increased flow in the distal calf veins, diminished leukocyte trapping, and a benign clinical course. These data are in agreement with experimental studies showing that pulsatile shear stress enhances secretion of cytokines by venous endothelial cells and, consequently, counteracts a predisposition to platelet aggregation, hypercoagulability, and white cell adhesion and promotes healing of leg ulcers.
authors.affiliation: Department of Internal Medicine A, Bnai Zion Medical Center, Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa.
authors.forename: J E
authors.initials: JE
authors.lastname: Naschitz
authors.forename: V
authors.initials: V
authors.lastname: Wolfson
authors.forename: I
authors.initials: I
authors.lastname: Tsikonova
authors.forename: D
authors.initials: D
authors.lastname: Keren
authors.forename: E
authors.initials: E
authors.lastname: Barmeir
authors.forename: D
authors.initials: D
authors.lastname: Yeshurun
mesh_terms: D000208:Acute Disease; D000368:Aged; D002908:Chronic Disease; D004452:Echocardiography / Q000379:methods; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology; D006801:Humans; D007866:Leg / Q000098:blood supply / Q000000981:diagnostic imaging; D008297:Male; D008875:Middle Aged; D011673:Pulsatile Flow / Q000502:physiology*; D014262:Tricuspid Valve Insufficiency / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D014689:Venous Insufficiency / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*