Does elevated body mass modify the influence of postmenopausal estrogen replacement on atherosclerosis progression: results from the estrogen in the prevention of atherosclerosis trial.
OBJECTIVE
To determine whether the estrogen-related reduction in atherosclerosis progression demonstrated in the estrogen in the prevention of atherosclerosis trial (EPAT) is modified by body mass index (BMI).


METHODS
Subgroup analyses were performed using data from EPAT, a randomized, double-blind, placebo-controlled trial designed to determine whether unopposed 17beta-estradiol administered for a 2-year treatment period reduces the progression of subclinical atherosclerosis in healthy postmenopausal women. The primary trial endpoint was the rate of change of common carotid artery intima-media thickness (IMT). In this subgroup analysis, the sample was divided into 122 women with BMI<30 kg/m(2) and 77 women with BMI> or =30 kg/m(2). Statistical analysis was performed using mixed general linear models to evaluate whether the treatment effects on IMT progression rates differed in the two BMI groups.


RESULTS
There was no significant difference in the estradiol treatment effect on IMT progression rates between postmenopausal women with BMI<30 vs. > or =30 kg/m(2) (P=0.52). In the 77 subjects who did not use lipid-lowering therapy, there was significant improvement in IMT with estradiol treatment that was evident in both BMI groups (P=0.48 for differences between BMI groups).


CONCLUSIONS
In contrast to the epidemiological observation that obese postmenopausal women do not derive benefit from estrogen replacement therapy, results of this study indicate that estradiol treatment is beneficial in preventing progression of atherosclerosis regardless of initial BMI.


CONCLUSIONS
Estradiol treatment is beneficial in preventing progression of atherosclerosis in postmenopausal women not receiving lipid-lowering therapy, regardless of their initial body mass index.
Mack
Wendy J
WJ
Department of Preventive Medicine, University of Southern California, Los Angeles, USA. wmack@usc.edu
Hameed
Afshan B
AB
Xiang
Min
M
Roy
Subir
S
Slater
Cristin C
CC
Stanczyk
Frank Z
FZ
Lobo
Rogerio A
RA
Liu
Chao-ran
CR
Liu
Ci-hua
CH
Hodis
Howard N
HN
D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000502:physiology; D015992:Body Mass Index; D017536:Carotid Artery, Common / Q000473:pathology; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003324:Coronary Artery Disease / Q000188:drug therapy* / Q000517:prevention & control; D018450:Disease Progression; D004311:Double-Blind Method; D004958:Estradiol / Q000097:blood / Q000627:therapeutic use; D015914:Estrogen Replacement Therapy; D004967:Estrogens / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D008875:Middle Aged; D011372:Progestins / Q000627:therapeutic use; D012016:Reference Values; D013223:Statistics as Topic; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood; D017539:Tunica Intima / Q000473:pathology; D016387:Women's Health
D015415:Biomarkers; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D004967:Estrogens; D000960:Hypolipidemic Agents; D011372:Progestins; D014280:Triglycerides; D004958:Estradiol