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Source: Arthroscopy  |  Posted 5 years ago

Atorvastatin Improves Endothelial Function, May Prevent Vascular Damage in Patients With Type 2 Diabetes

By Cameron Johnston

BARCELONA, SPAIN -- September 7, 2006 -- High-dose atorvastatin therapy can lead to improved endothelial function among diabetic patients, even if they have no history of atherosclerotic disease and a normal lipid profile.

Magdalena Misiorna-Boehme, MD, department of medical research, Funen Hospital, Svendborg, Denmark, said deteriorating endothelial function is known to occur in diabetic patients.

In a presentation here on September 4[]th[] at the European Society of Cardiology World Congress of Cardiology, Dr. Misiorna-Boehme said that even before signs of endothelial damage begin to manifest themselves, damage to the endothelium may indicate early-stage atherosclerosis. In addition, she said, lowering cholesterol to levels below what is considered normal could help prevent early-stage damage.

In a study of 186 diabetic patients who were treated for 1 year with atorvastatin and/or an antihypertensive agent (amlodipine, perindopril, or doxazosin) or placebo, researchers used high-resolution ultrasound to measure endothelial function through nitric oxide-dependent (flow-mediated) and nitric oxide-independent (nitroglycerin-mediated) dilation of the brachial artery.

The study patients had no history of atherosclerotic disease and no visible indications of elevated cholesterol levels, Dr. Misiorna-Boehme said.

After 1 year of treatment with atorvastatin and/or antihypertensive drugs, lipid profiles were markedly improved among patients in both treatment arms but not those receiving placebo.

In patients receiving atorvastatin alone total cholesterol was reduced by a mean of 2.03 mmol/L. Low-density lipoprotein (LDL)-cholesterol was reduced by 1.93 mmol/L, and high-density lipoprotein (HDL)-cholesterol was increased by 0.18 mmol/L. Systolic and diastolic blood pressure were improved by 7.1 mm Hg and 4.4 mm Hg, respectively.

Flow-mediated dilation of the brachial artery was increased by 1.33% at the end of 1 year in patients receiving atorvastatin alone, and by 0.98% in patients receiving atorvastatin plus antihypertensive. These changes were both significant from baseline, but the between-group differences were not significant.

There were no significant changes in nitroglycerine-mediated dilation of the brachial artery in either treatment arm.

Dr. Misiorna-Boehme said in an interview that clinicians are now "leaning toward" adopting the idea that atorvastatin could be used as a preventive measure for some patients. These findings indicate that it should be considered, especially since the endothelial damage may be irreversible once it becomes detectable, and this is a potential means to prevent this damage. However, she added, this was a physiological study and such studies often have difficulty being translated into clinical practice.

[Presentation title: Improvement of Endothelial Dysfunction After Long Time Intensive Cholesterol Lowering Treatment in Type 2 Diabetes. Poster 3101]

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