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Premenopausal antimüllerian hormone concentration is associated with subsequent atherosclerosis

Appt, Susan E. DVM1; Chen, Haiying PhD2; Clarkson, Thomas B. DVM1; Kaplan, Jay R. PhD1

Menopause:
doi: 10.1097/gme.0b013e31825b4fe2
Brief Reports
Abstract

Objective: The aim of this study was to determine if premenopausal ovarian reserve is associated with susceptibility for atherosclerosis.

Methods: Female cynomolgus macaques (n = 66, women’s equivalent age = 45 y) consumed an atherogenic diet for ∼5 months before the measurement of a marker of ovarian reserve (antimüllerian hormone [AMH]), plasma lipids, follicular phase estradiol, and body weight (BW). Monkeys were then ovariectomized (OVX; n = 17), remained premenopausal (n = 20), or were induced to have reduced ovarian reserve (ROR, n = 29). After 26 additional months consuming the diet, atherosclerosis measurements and risk variables were reassessed.

Results: No differences in baseline AMH, plasma lipids, BW, and estradiol or postdiet lipids and BW were observed among the groups subsequently assigned to the OVX, premenopausal control, or reduced ovarian reserve conditions. Postdiet measurements of atherosclerosis extent did not differ among the groups. However, analysis of plaque size by tertile of baseline AMH revealed that plaques were largest in monkeys that began the experiment with the lowest baseline AMH, followed by those in the middle and high tertiles (plaque extent: low AMH, 0.76 ± 0.12 mm2; mid AMH, 0.46 ± 0.1 mm2; high AMH, 0.34 ± 0.08 mm2; P = 0.02). Baseline AMH and plaque size were also correlated negatively (r = −0.31, P = 0.01). Plasma lipids were also correlated significantly with plaque extent (all P < 0.01) but not with AMH.

Conclusions: We report for the first time an inverse relationship between a marker of ovarian reserve (AMH) and subsequent atherosclerosis risk.

Author Information

From the 1Wake Forest Primate Center and Department of Pathology/Comparative Medicine, Wake Forest School of Medicine, Winston-Salem, NC; and 2Public Health Sciences, Section on Biostatistics, Wake Forest School of Medicine, Winston-Salem NC.

Received February 7, 2012; revised and accepted April 19, 2012.

Funding/support: This work was supported by the National Institute on Aging (R01AG027847-SEA).

Financial disclosure/conflicts of interest: None reported.

Address correspondence to: Susan E. Appt, DVM, Wake Forest Primate Center, Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1040. E-mail: sappt@wakehealth.edu

©2012The North American Menopause Society