Menopause: The Journal of The North American Menopause Society Vol. 19, No. 12, pp. 000/000 DOI: 10.1097/gme.0b013e318259c04e * 2012 by The North American Menopause Society Low-dose rosuvastatin improves the functional and morphological markers of atherosclerosis in asymptomatic postmenopausal women with dyslipidemia Michiya Igase, MD, PhD, 1,2 Katsuhiko Kohara, MD, PhD, 1,2,3 Yasuharu Tabara, PhD, 2,3,4 Tokihisa Nagai, MD, PhD, 1 Namiko Ochi, MD, PhD, 1,2 Tomoko Kido, MD, 1,2 Masayuki Ochi, MD, PhD, 1 and Tetsuro Miki, MD, PhD 1,2,3 Abstract Objective: Several large-scale studies have shed light on the primary preventive efficacy of statins against atherosclerotic diseases in the course of treatment of dyslipidemia. However, this efficacy in the management of dyslipidemia in relatively low-risk patients, particularly in women, has not been clarified. Here, we investigated the efficacy of dyslipidemia treatment with a statin on three indices that are widely used to assess atherosclerosis in postmenopausal women: carotid intima-media thickness (CIMT), arterial stiffness index A of the common carotid artery (carotid stiffness A), and brachial artery pulse wave velocity (baPWV). Methods: The study enrolled 51 postmenopausal women aged 55 years or older with dyslipidemia. The partic- ipants were randomly divided into two treatment groups and received a single daily administration of 2.5 mg of rosuvastatin or no statin therapy as control. Results: At baseline, the groups did not significantly differ with regard to the three indices. At the third and 12th months of treatment, both carotid stiffness A and baPWV values were significantly lower than those of the control group. As for CIMT, the value was significantly lower in the statin group than in the control group at 12 months of treatment. These changes were in conjunction with a significant decrease in low-density lipoprotein cholesterol. Interestingly, changes in CIMT during the 12-month period were significantly correlated with changes in high- sensitivity C-reactive protein during the 3-month period independently of lipid profile. Conclusions: The potent statin improves baPWV and carotid stiffness A, in addition to CIMT (surrogate markers of coronary artery disease), in postmenopausal women with low-risk dyslipidemia. Further studies to clarify the common mechanisms underlying the link between cholesterol-lowering therapy and atherosclerosis in post- menopausal women are required. Key Words: Postmenopausal women Y Dyslipidemia Y Statin Y Carotid intima-media thickness Y Carotid stiffness A Y baPWV. A therosclerosis is a leading cause of atherosclerotic diseases such as coronary artery diseases (CADs). Given the important role of dyslipidemia in the pro- gression of these diseases, 1 improvement in lipid profile rep- resents an important risk reduction strategy. Statins, which inhibit 3-hydroxy-3-methylglutaryl coenzyme A reductase, are standard therapeutic treatments for patients with dyslip- idemia. Several recent large-scale clinical trials have demon- strated that the treatment of dyslipidemia with statins plays a role in the secondary prevention of atherosclerotic diseases. 2,3 With regard to the primary prevention of atherosclerotic dis- eases through management of dyslipidemia, the Kyushu Lipid Intervention Study demonstrated that pravastatin at 10 to 20 mg/day reduced atherosclerotic diseases in these patients. 4 However, little is known about the effect of lipid-lowering therapy with statins on atherosclerosis in healthy postmen- opausal women. Because women have conventionally been considered to be at lower risk for atherosclerotic diseases during periods of menstrual activity, most large randomized controlled studies of lipid-lowering therapy carried out to date have predom- inantly involved men. Because of an increase in the levels of low-density lipoprotein cholesterol (LDL-C), however, the rate of CADs in postmenopausal women has sharply in- creased. Given the probable role of the reduced levels of Received December 9, 2011; revised and accepted April 4, 2012. From the 1 Department of Geriatric Medicine, Ehime University Graduate School of Medicine, Toon, Ehime, Japan; 2 Antiaging Center, Ehime University Hospital, Toon, Ehime, Japan; 3 Proteo-Medicine Research Center, Ehime University, Toon, Ehime, Japan; and 4 Department of Fundamental Medical Science, Ehime University Graduate School of Medicine, Toon, Ehime, Japan. Funding/support: This study was supported by a grant-in-aid for scien- tific research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan. Financial disclosure/conflicts of interest: None reported. Address correspondence to: Michiya Igase, MD, PhD, Department of Geriatric Medicine, Ehime University Graduate School of Medicine, Toon, Ehime 791-0295, Japan. E-mail: migase@m.ehime-u.ac.jp Menopause, Vol. 19, No. 12, 2012 1