Is the nihilistic approach to surgical reduction of superficial and perforator vein incompetence for venous ulcer justified?

OBJECTIVE: Twenty-five years ago, the senior author showed a 55% postoperative ulcer recurrence rate after open perforator ligation. Those data contributed to a nihilistic attitude toward incompetent perforating veins. Conversely, since the introduction of subfascial endoscopic perforator surgery (SEPS), we have undertaken ablation of superficial and perforator reflux as initial treatment in patients with ulcers (C6) or healed ulcers (C5). This report outlines our long-term results. METHODS: Between December 1994 and November 1999, SEPS was performed on 51 limbs in 45 patients with C5/C6 disease. Sixteen limbs underwent SEPS alone, and 35 had additional surgery on the greater saphenous vein (GSV), the lesser saphenous vein, or the tributary varicies. Data were collected according to the reporting standards in venous disease. Preoperative duplex scan of deep, superficial, and perforating veins was performed. Data were analyzed with Kaplan-Meier method, Mantel-Cox log-rank test, or t test. RESULTS: Of the 51 limbs that underwent SEPS, the GSV was stripped in 28. Twenty-nine were C6, and 22 were C5. Etiology was primary (Ep) in 25 limbs and secondary (Es) in 26 limbs. All limbs had duplex scan evidence of perforator incompetence (Ap), and deep insufficiency (A(D)) was seen in 39 cases (76%). Reflux predominated (P(R)). The clinical follow-up period was 0 to 82 months (median, 38 months). Venous disability scores improved from 9.8 before surgery to 4.2 at last follow-up (P <.05). Kaplan-Meier analysis showed 74% healing at 6 months. The presence of an ulcer more than 2 cm in diameter, secondary etiology, and SEPS without concomitant GSV stripping were associated (P <.05) with delayed healing. Among patients in whom ulcers healed or who were seen with healed ulcers, the 5-year ulcer recurrence rate was 13%. Lesser saphenous vein reflux was the only factor that correlated with increased ulcer recurrence. Deep system reflux as measured with duplex scan valve closure times did not correlate with the rate of ulcer healing or recurrence. CONCLUSION: Nihilism has no place in the management of venous disease in the 21st century. An aggressive approach to superficial and perforating vein reflux in this cohort of patients with C5 and C6 disease resulted in rapid ulcer healing and low 5-year recurrence rates. Prior saphenous vein stripping, large ulcers, and secondary etiology were associated with delayed healing. A less aggressive posture toward lesser saphenous vein reflux contributed to a higher recurrence rate in this subgroup of patients. These risk factors are useful in counseling patients as to their expected postoperative course; however, no combination of factors should a priori preclude surgical intervention in this group of patients.

Estrogen receptor-alpha mediates the protective effects of estrogen against vascular injury.

Blood vessel cells express the 2 known estrogen receptors, alpha and beta (ERalpha, ERbeta), which are thought to mediate estrogen inhibition of vascular injury and atherosclerosis, but the relative role of ERalpha and ERbeta in these events is controversial. Estrogen inhibits the vascular injury response to the same extent in ovariectomized female wild-type mice and in the original single gene knockout mice for ERalpha (ERalphaKO(Chapel Hill) [ERalphaKO(CH)]) and ERbeta (ERbetaKO(Chapel Hill) [ERbetaKO(CH)]). In double gene knockout mice generated by crossing these animals (ERalpha,betaKO(CH)), estrogen no longer inhibits medial thickening after vascular injury, but still inhibits vascular smooth muscle cell proliferation and increases uterine weight. The partial retention of estrogen responsiveness in ERalpha,betaKO(CH) mice could be due either to the presence of a novel, unidentified estrogen receptor or to functional expression of an estrogen receptor-alpha splice variant in the parental ERalphaKO(CH) mice. To distinguish between these possibilities, we studied recently generated mice fully null for estrogen receptor alpha (ERalphaKO(Strasbourg) [ERalphaKO(St)]) and examined the effect of estrogen on the response to vascular injury. In the present study, we show that after vascular injury in ovariectomized ERalphaKO(St) mice, estrogen has no detectable effect on any measure of vascular injury, including medial area, proteoglycan deposition, or smooth muscle cell proliferation. These data demonstrate that estrogen receptor-alpha mediates the protective effects of estrogen on the response to vascular injury.