Statin Therapy Slows Progression of Arterial Thickening

Among low-risk middle-aged people with subclinical atherosclerosis, the cholesterol-lowering drug rosuvastatin reduces the rate of progression of arterial thickening and stops but does not reverse atherosclerotic disease, according to a study in the March 28 issue of JAMA. The study is being released early to coincide with its presentation at the American College of Cardiology's annual conference.

Lipid-lowering therapy has been shown to reduce cardiovascular events in a large number of studies. Statin drugs as well as other agents and lifestyle changes have also been shown to slow the progression of and even regress atherosclerosis, according to background information in the article. Atherosclerosis is the progressive thickening and hardening of the walls of medium-sized and large arteries as a result of fat deposits on their inner lining. Atherosclerosis is often advanced before symptoms appear, and it is not clear whether treatment is beneficial in middle-aged individuals with a low Framingham risk score (a measure used to predict the risk of cardiovascular disease) and mild to moderate subclinical atherosclerosis.

John R. Crouse III, M.D., of the Wake Forest University School of Medicine, Winston-Salem, N.C., and colleagues conducted a randomized study of 984 individuals. The Measuring Effects on Intima-Media Thickness: an Evaluation of Rosuvastatin (METEOR) study was designed to investigate the effect of a 40-mg. dose of rosuvastatin on carotid intima-media thickness (CIMT, a measure of the thickness of the middle layers of the carotid arteries) over two years in middle-aged individuals with low Framingham risk scores, but with evidence of subclinical atherosclerosis.

"Rosuvastatin treatment was associated with a 49 percent reduction in LDL-C ["bad" cholesterol] level, a 34 percent reduction in total cholesterol level, an eight percent increase in HDL-C ["good" cholesterol] level, and a 16 percent reduction in level of triglycerides," the authors write.

"Compared with placebo, rosuvastatin significantly slowed progression of the maximum CIMT for the 12 carotid sites," they continue, although the study did not demonstrate regression of disease with rosuvastatin. The authors point out, "In contrast to the significant progression of atherosclerosis in the placebo group, no significant progression was observed in the rosuvastatin group."

The 40-mg. dose of rosuvastatin was well tolerated during the two-year study period and showed a similar safety profile to that of placebo.

"In conclusion, the findings of METEOR demonstrate that in middle-aged adults with Framingham risk scores lower than ten percent and evidence of subclinical atherosclerosis, rosuvastatin treatment resulted in statistically significant reductions in the rate of progression of maximum CIMT during a two-year period compared with placebo. Rosuvastatin did not induce regression overall," the authors conclude. "Larger, longer-duration randomized trials focused on clinical events are needed to determine the practice implications of these findings."