阿托伐他汀强化治疗可使颈动脉粥样硬化斑块缩小
Intensive Atorvastatin Therapy Reduces Carotid Atherosclerotic PlaqueNEW YORK (Reuters Health) Aug 07 - Intensive atorvastatin therapy is associated with regression of carotid atherosclerotic disease and reduction of C-reactive protein (CRP) levels, according to findings published in the August issue of Heart.
In an earlier study, high dose (80 mg daily) atorvastatin therapy prevented increase in coronary artery plaque volume, the authors explain, and regression of carotid intimal-medial thickness (IMT) with statin therapy has been demonstrated in patients with familial hypercholesterolemia.
Dr. Cheuk-Man Yu from The Chinese University of Hong Kong, Shatin, and colleagues investigated whether intensive atorvastatin therapy causes regression of atherosclerosis by assessing carotid IMT in 112 patients with coronary heart disease.
LDL cholesterol declined by 21.3% in patients treated for 26 weeks with low-dose atorvastatin (10 mg daily) and by 37.2% in patients treated with intensive atorvastatin (80 mg daily), the authors report.
Reductions in total cholesterol and triglyceride levels were also greater in the intensive atorvastatin group.
Intensive atorvastatin therapy brought a significant reduction in carotid IMT, the report indicates, whereas low-dose atorvastatin showed an insignificant trend.
CRP levels decreased significantly in the intensive atorvastatin group, the investigators write, but there was a nonsignificant trend toward increased CRP in the low-dose atorvastatin group.
All proinflammatory cytokines measured (IL-6, IL-8, IL-18, and TNF-alpha) were significantly reduced in the high-dose atorvastatin group, and all but IL-6 were also decreased in the low-dose group.
There was a modest correlation between the changes in carotid IMT and CRP levels.
"Therefore," the researchers conclude, "secondary prevention by high-dose atorvastatin therapy is able to reduce carotid atherosclerotic plaque burden, which is associated with the decrease in inflammatory activity of the plaque, as reflected by the reduced CRP and proinflammatory cytokine levels
Heart 2007;93:933-939.
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