Objective: Women of perimenopause age experience an upward transition of cardiovascular risk possibly in association with changing hormonal status. We examined the cross-sectional relationships between the atherosclerotic plaque within the coronary and carotid arteries and aorta and the menopausal hormone levels among asymptomatic perimenopausal women.
Methods: The Assessment of the Transition of Hormonal Evaluation with Noninvasive Imaging of Atherosclerosis was a prospective substudy of the Prospective Army Coronary Calcium project. We screened 126 asymptomatic perimenopausal women (mean age, 50 y) using contrast-enhanced CT angiography (multidetector CT) and carotid ultrasound. Women had coronary calcium data from 5 to 10 years earlier. The measures included cardiovascular risk factors, serum hormone levels, 64-slice multidetector CT, and carotid ultrasound.
Results: The prevalence of any coronary plaque was 35.5%. The prevalence of noncalcified plaque was 30.2%, and noncalcified plaque was the only manifestation of coronary artery disease in 10.7%. Markers of androgenicity (increased free testosterone and reduced sex hormone–binding globulin) were associated with an increased extent of calcified and noncalcified coronary artery plaque and aortic plaque. However, these relationships were not independent of cardiovascular risk factors. Follicle-stimulating hormone was directly associated with the number of aortic plaques. The levels of estrogen hormones were unrelated to plaque presence or extent.
Conclusions: Coronary, aortic, and carotid arterial plaque is prevalent in perimenopausal women without cardiac symptoms. The assessment of perimenopausal hormone status was not independently associated with subclinical atherosclerosis beyond standard cardiovascular risk factors.
Markers of androgenicity (increased free testosterone and reduced sex hormone–binding globulin) were associated with increased extent of calcified and noncalcified coronary artery plaque and aortic plaque. However, these relationships were not independent of cardiovascular risk factors.
From the Departments of Medicine and Cardiology Service, Walter Reed Army Medical Center, Washington, DC.
Received March 9, 2011; revised and accepted April 27, 2011.
Funding/support: This study was supported by the Congressionally Directed, Peer Reviewed Medical Research Program, Grant ERMS 00239017-00216.
Financial disclosure/conflicts of interest: None reported.
The views expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Department of the Army, Department of Defense, or the US Government.
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Address correspondence to: Allen J. Taylor, MD, Cardiology Section, Washington Hospital Center, 110 Irving St, NW, Room 1E12, Washington, DC 20010. E-mail: firstname.lastname@example.org