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Individual and combined effects of estrogen/progestin therapy and lovastatin on lipids and flow-mediated vasodilation in postmenopausal women with coronary artery disease

David M. Herrington, MD, MHS, FACC^*, Brian L. Werbel, MD^*, Ward A. Riley, PhD, Benjamin E. Pusser, BA^* and Timothy M. Morgan, PhD

^* Department of Internal Medicine/Cardiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA
Department of Neurology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA
Department of Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA

View larger version (25K): [in a new window]   Figure 1 Plot of brachial artery diameter at baseline and 2 min after release of the blood pressure cuff. The maximum diameter observed over 2 min was used to calculate the vasodilator response. AUC = area under the diameter curve.

View larger version (29K): [in a new window]   Figure 2 Plot of mean (SE) lipid levels at baseline and at the end of each treatment period. Numbers at the top of each bar are the percent change from baseline. Both = HMG plus HRT; HDL = high density lipoprotein; HMG = lovastatin; HRT = conjugated equine estrogen and medroxyprogesterone acetate; LDL = low density lipoprotein. P values for all pair-wise comparisons are found in Table 1. *p < 0.05 vs. baseline.