Why the study?
Does atorvastatin improve flow-mediated dilatation, inflammatory cytokines, and carotid arterial stenosis in normocholesterolemic patients with stroke or TIA and carotid stenosis?
Does atorvastatin improve flow-mediated dilatation, inflammatory cytokines, and carotid arterial stenosis in normocholesterolemic patients with stroke or TIA and carotid stenosis?
Atorvastatin 10 mg daily improves endothelial function (FMD) in normocholesterolemic patients with carotid stenosis and prior stroke/TIA, despite no significant change in stenosis severity or cytokines at 4 months.
Answers are grounded in this paper and cite their sources.
May support endothelial benefit of atorvastatin in normocholesterolemic carotid stenosis; leaves open effects on lesions or inflammation.
BACKGROUND: Aggressive statin therapy to reduce low-density lipoprotein (LDL) cholesterol in patients with normal LDL-cholesterol levels reduces the incidence of future cardiovascular events and enhances atherosclerotic regression in the common carotid artery. We tried to quantify changes in flow-mediated dilatation (FMD), inflammatory cytokines, and the severity of carotid arterial stenosis, after aggressive statin administration to patients with normal LDL-cholesterol levels, and stroke or transient ischemic attack ipsilateral to carotid arterial stenosis. METHODS: Twenty patients with at least a 50% reduction in the diameter of the carotid artery were studied. Atorvastatin 10 mg daily was prescribed for 4 months. Serial changes in the severity of carotid arterial stenosis, and brachial-artery FMD were evaluated by high-resolution ultrasound. Tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), vascular cell adhesion molecule (VCAM), intracellular adhesion molecule (ICAM), soluble endothelin-1 (ET-1), and high-sensitivity C-reactive protein (hs-CRP), were measured before, and after 2 and 4 months of, atorvastatin treatment. RESULTS: Atorvastatin significantly decreased plasma levels of total cholesterol and LDL-cholesterol after 1, 2 and 4 months of treatment (p < 0.01). FMD showed significant improvement after only 4 months (10.0% vs 6.8% at baseline; p = 0.019). The overall severity of carotid arterial lesions was not significantly reduced by atorvastatin. Changes in TNF-alpha, IL-1beta, IL-6 and ET-1 showed trends towards a progressive decline after atorvastatin, but none of the cytokines was reduced significantly. FMD did not correlate with the severity of carotid arterial stenosis, lipid profile, or cytokine levels. CONCLUSION: Atorvastatin effectively reduced plasma concentrations of total cholesterol and LDL-cholesterol, and had beneficial effects on endothelial function, in Chinese patients with carotid arterial stenosis and normal LDL-cholesterol levels.
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Hsu et al. (2005) studied this question.
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