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Volume 205, Issue 1, Pages 325-330 (July 2009)


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Changes in remnant and high-density lipoproteins associated with hormone therapy and progression of coronary artery disease in postmenopausal women

Stefania Lamon-FavaaCorresponding Author Informationemail address, David M. Herringtonb, David M. Reboussinc, Michelle Shermana, Katalin Horvatha, Ernst J. Schaefera, Bela F. Asztalosa

Received 24 June 2008; received in revised form 17 October 2008; accepted 9 December 2008. published online 20 January 2009.

Abstract 

Objective

This study examined the effect of hormone therapy (HT) on the plasma concentration of remnant lipoprotein cholesterol (RLP-C) and high-density lipoprotein (HDL) subpopulations and the contribution of HT-related changes in these lipoproteins to the progression of coronary heart disease (CHD) in postmenopausal women.

Methods

Study participants were 256 women who completed the Estrogen Replacement and Atherosclerosis (ERA) trial, a placebo-controlled, randomized trial that examined the effects of 3.2 years of conjugated equine estrogen (CEE, 0.625mg/day) or CEE (0.625mg/day) plus medroxyprogesterone acetate (MPA, 2.5mg/day) on postmenopausal women with established coronary atherosclerosis. Quantitative coronary angiography and plasma RLP-C and HDL subpopulations were assessed at baseline and at follow-up.

Results

Relative to placebo, both CEE and CEE+MPA caused a significant reduction in plasma RLP-C concentrations and a significant increase in α1 and α2 HDL subpopulations. However, in the HT-treated subjects, faster progression of coronary atherosclerosis was observed in women who experienced the greatest reductions in RLP-C and in preβ1 HDL subpopulations.

Conclusions

Our data suggest that individual variability in RLP-C and HDL subpopulation response to HT is a predictor of CHD progression. Lipoprotein response to HT may be an indirect marker of susceptibility to other harmful effect of HT in postmenopausal women with established CHD or an indication of formation of dysfunctional lipoproteins.

a Lipid Metabolism Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston, MA 02111, United States

b Department of Internal Medicine – Cardiology, Wake Forest University School of Medicine, Winston-Salem, NC, United States

c Department of Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, NC, United States

Corresponding Author InformationCorresponding author. Tel.: +1 617 556 3105; fax: +1 617 556 3103.

PII: S0021-9150(08)00901-5

doi:10.1016/j.atherosclerosis.2008.12.020


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