Prostaglandin (PG) metabolism in chronic venous disease can be assessed by quantitative analysis of prostacyclin (PGI2, an antiaggregatory vasodilator) and thromboxane A2 (TXA2, a proaggregatory vasoconstrictor). The authors corre lated the biochemical and noninvasive evaluation (Doppler ultrasound, pho toplethysmography [PRG], and phleborheography [PRG]) of 20 patients with normal and varicose veins, using operative specimens for biochemical analysis. Ten-mg segments of vein were incubated with 10 μM 14C-PGH2 and separated by thin-layer chromatography. Formation of 6-keto-PGF1a and TXB2 was in creased in varicose vein compared with normal vein: 157 ± 11 vs 230 ± 19 picograms 6-keto-PGF1a (p <.05) and 23 ± 2 vs 34 ± 4 picograms TXB2 (p <.05). All patients with varicose veins displayed evidence of venous insufficiency by all examinations. Of 13 patients with clinically normal veins, 8 were normal by all noninvasive criteria. Five were abnormal by two or more noninvasive critera, yet had normal biochemical findings. Increased PGI2 formation in patients with varicose veins indicated increased activity of PGI 2 synthase, possibly associated with chronic venous insufficiency . Noninvasive testing may indicate those patients at risk for developing chronic venous disease before clinical or biochemical changes occur.
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