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  Vol. 137 No. 3, March 2002 TABLE OF CONTENTS
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Inhibition of Intimal Hyperplasia Using the Selective Estrogen Receptor Modulator Raloxifene

Craig H. Selzman, MD; A. Simon Turner, BVSc; Jaime S. Gaynor, DVM; Stephanie A. Miller, MD; Eric Monnet, DVM; Alden H. Harken, MD

Arch Surg. 2002;137:333-336.

Hypothesis  The selective estrogen receptor modulator raloxifene hydrochloride inhibits intimal hyperplasia.

Design  Controlled laboratory experiment.

Setting  Experimental animal model.

Intervention and Main Outcome Measures  Forty-three senile female sheep were randomized to sham operation, ovariectomy, or ovariectomy followed by treatment with 17{beta}-estradiol or raloxifene. Six months after initial operation, we performed necropsy with histological assessment of the aortic bifurcation and bone mineral densitometry and assayed serum lipids.

Results  After 6 months, serum triglyceride and total and high-density lipoprotein cholesterol levels were similar among groups and within the reference range. Ovarian ablation alone resulted in intimal hyperplasia, which was attenuated with estradiol and raloxifene therapy. Furthermore, estradiol and raloxifene therapy reversed ovariectomy-induced decreases in bone mineral density measured using spine morphometry.

Conclusions  Raloxifene attenuates ovariectomy-induced aortic intimal hyperplasia independent of serum lipid levels. These data suggest that raloxifene, in addition to its beneficial influence on bone density, has direct, beneficial cardiovascular effects.


From the Division of Cardiothoracic Surgery, Department of Surgery, University of Colorado Health Sciences Center, Denver (Drs Selzman, Miller, and Harken) and the College of Veterinary Medicine, Colorado State University, Fort Collins (Drs Turner, Gaynor, and Monnet).



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ABSTRACT | FULL TEXT  





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