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Back to Conference Highlights

ACTOS® (pioglitazone) reverses thickening of carotid artery wall in type 2 diabetes

6/11/04 - 10/11/04, New Orleans, LA

 

Scientific Sessions, the largest cardiovascular meeting in the world, is being held in New Orleans Nov. 6–10.

 
 

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  American Heart Association  
   

Mainz, Germany, November 9, 2004 – Clinical study results presented today in New Orleans, Louisiana, during the American Heart Association's Scientific Sessions 2004 proceedings, have shown that the drug pioglitazone (ACTOS®, Takeda) significantly reduced the thickness of the carotid (neck) artery in patients with type 2 diabetes.

By contrast, no change in carotid thickness was seen in a group of patients who received glimepiride, an older drug for type 2 diabetes.

"These results are provocative, because both drugs showed similar effects on lowering blood glucose, the traditional principal target for type 2 diabetes therapy," noted principal investigator Thomas Forst, Professor for Internal Medicine, Institute for Clinical Research and Development in Mainz, Germany.

"The thickness of the carotid artery is an indicator of atherosclerotic disease, which may both reduce arterial blood flow and set the stage for unstable blood clots in the arteries to dislodge and potentially cause a heart attack or stroke. The reduction in thickness by pioglitazone, a member of a new class of type 2 diabetes drugs called thiazolidinediones (TZDs) suggests that this medication may have benefits beyond improving metabolic control in patients with diabetes mellitus type 2," continued Forst. "This substantial regression of carotid intima media thickness over just 12 or 24 weeks may have important prognostic implications for patients with type 2 diabetes."

Study Design and Results

In the study, B-mode ultrasound was used to measure the intima media thickness (IMT) of the carotid artery before and 12 and 24 weeks after 173 patients received oral therapy with either pioglitazone (45 mg/day) or glimepiride (1-6 mg/day). Baseline carotid IMT was 0.949 ± 0.149mm in the pioglitazone group and 0.924 ± 0.150mm in the glimepiride group (p=n.s.). Carotid IMT was reduced only in the pioglitazone group after 12 weeks (-0.033 ± 0.052mm) vs. -0.002 ± 0.047mm in the glimepiride-treated patients (p = 0.0002 between groups) and after 24 weeks of treatment (-0.054 ± 0.059mm vs. -0.011 ± 0.058mm, respectively, p < 0.0001 between groups). In addition, insulin resistance was significantly improved in the pioglitazone group (-2.21 ± 3.40 vs. -0.27 ± 3.30, p < 0.0001 between groups). Changes in IMT correlated with improvement in insulin resistance (r=0.29, p<0.001) and were independent from the improvement in metabolic control.

The population included 66 females and 107 males with type 2 diabetes aged 62.6 +/- 1 7.9 years, with a mean body mass index (BMI) of 31.8 (generally classified as obese). Both treatments were generally well tolerated.

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Sources

American Heart Association - scientific sessions - 6/11/04 - 10/11/04, New Orleans, LA

Legal Disclaimer

The materials presented here were prepared by independent authors under the editorial supervision of The Doctors Lounge, and do not represent a publication of the American Heart Association. These materials and the related activity are not sanctioned by the American Heart Association or the commercial supporter of the conference, and do not constitute an official part of that conference.

The material presented here does not reflect the views of The Doctors Lounge or the companies providing unrestricted educational grants. These materials may discuss uses and dosages for therapeutic products that have not been approved by the United States Food and Drug Administration. A qualified health care professional should be consulted before using any therapeutic product discussed. All readers or continuing education participants should verify all information and data before treating patients or employing any therapies described in this educational activity.

Copyright © 2004 The Doctors Lounge.

Article reviewed by:

Dr. Tamer Fouad, M.D.

 

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