Key result
Low-dose rosuvastatin (2.5 mg daily) significantly improved carotid stiffness β, baPWV, and CIMT compared to no statin therapy over 12 months in postmenopausal women with dyslipidemia.
Why the study?
Does rosuvastatin 2.5 mg once daily improve surrogate markers of atherosclerosis in postmenopausal women aged 55 years or older with dyslipidemia?
RCT (n=51)
Randomly divided
Does rosuvastatin 2.5 mg once daily improve surrogate markers of atherosclerosis in postmenopausal women aged 55 years or older with dyslipidemia?
Low-dose rosuvastatin (2.5 mg daily) significantly improves surrogate markers of atherosclerosis, including CIMT and arterial stiffness, in asymptomatic postmenopausal women with dyslipidemia.
Supports low-dose rosuvastatin in postmenopausal dyslipidemia; extends statin evidence to vascular surrogates in this RCT population.
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 β of the common carotid artery (carotid stiffness β), and brachial artery pulse wave velocity (baPWV). METHODS: The study enrolled 51 postmenopausal women aged 55 years or older with dyslipidemia. The participants 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 β 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 β, 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 postmenopausal women are required.
No takes yet. Share an insight, caveat, or question.
Igase et al. (2012) conducted an RCT in Dyslipidemia (n=51). Rosuvastatin vs. No statin therapy was evaluated on Carotid intima-media thickness (CIMT), arterial stiffness index β, and brachial artery pulse wave velocity (baPWV). Low-dose rosuvastatin (2.5 mg daily) significantly improved carotid stiffness β, baPWV, and CIMT compared to no statin therapy over 12 months in postmenopausal women with dyslipidemia.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: