Apr. 4, 2007 An international study using ultrasound technology has found that the most potent cholesterol-lowering drug is also effective at halting early changes in the blood vessels that can lead to atherosclerosis.
"Rosuvastatin arrested the progression of thickened carotid arteries compared to a placebo," said John R. Crouse, M.D., lead researcher and a professor of endocrinology at Wake Forest University School of Medicine. "The findings show that the benefits of cholesterol management on arteries can be extended to low-risk patients."
Results from the study were reported today at the annual meeting of the American College of Cardiology in New Orleans and were published on-line by the Journal of the American Medical Association. The research involved people with moderately elevated cholesterol levels who didn't qualify for treatment under national guidelines.
Participants all had minimal thickening of their carotid arteries, which supply blood to the brain, and were considered at low risk for having a heart attack or dying from a heart-related event based on their age and other risk factors.
Over a two-year period, the therapy lowered low-density lipoprotein, or "bad" cholesterol, by 49 percent and increased high density lipoprotein, or "good" cholesterol, by 8 percent. Triglycerides were reduced by 16 percent and the progression of artery thickness was halted.
Rosuvastatin (sold under the trade name Crestor®) is the newest member of a family of drugs known as statins that work to lower levels of cholesterol and other fats in the blood. Other statins have been tested -- with similar results -- in patients who've already had a heart attack or who had high cholesterol levels. This was the first study to evaluate Crestor in a group of people at low risk for heart attacks.
"Atherosclerosis is often advanced before symptoms appear and it hasn't been clear whether treatment of low-risk individuals is beneficial," said Crouse. "This study shows that aggressive cholesterol management arrests the progress of even small changes in the arteries."
The study used ultrasound to assess whether Crestor was effective at halting progressive thickening of the carotid arteries. Vessel thickening is an early sign of atherosclerosis, the deposit of fatty material in blood vessels that can lead to heart attacks and strokes.
There were 984 study participants: 702 were randomly assigned to receive 40 mg of Crestor daily and 282 were randomly assigned to receive a placebo, or inactive tablet. Male participants were between 45 and 70 years old and females were between 55 and 70.
Crestor arrested the development of artery thickening overall and in all 12 sites of the carotid artery that were measured. Drug safety was assessed by vital signs, adverse events, laboratory tests and electrocardiograms. The frequency of adverse events was similar between the two groups and included muscle pain and gastrointestinal disorders.
"The drug was well tolerated during the two-year period and showed a similar safety profile to the placebo," said Crouse.
The study included 61 primary care practices in the United States and Europe and was conducted between August 2002 and May 2006. Each participant was followed for two years and received an ultrasound exam at the beginning and end of the study and every six months during the study period.
Participants were considered at low risk of a heart attack or death from a heart-related-event based on a formula developed by the National Cholesterol Education Program from the long-running Framingham Heart Study, which takes such factors as age, sex, blood pressure and cholesterol levels into account. Low risk was considered a heart disease risk of less than 10 percent over a 10-year period.
The study is known as METEOR (Measuring Effects on intima media Thickness: an Evaluation of Rosuvastatin).
Crouse said additional studies should be conducted to determine if the drug also affects the number of clinical events.
The research was funded by AstraZeneca. The final decision on manuscript content was exclusively retained by the authors. Co-researchers were Ward Riley, Ph.D., and Gregory Evans, M.A., both from Wake Forest, Joel Raichlen, M.D., and Mike Palmer, Ph.D., both with AstraZeneca, Macclesfield, England, Daniel O'Leary, M.D., Caritas Carney Hospital, Boston, Mass., and Diederick Grobbee and Michiel Bots, University Medical Center Utrecht, The Netherlands.
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