on March 31, 2008
Published online before print March 31, 2008, doi: 10.1161/CIRCULATIONAHA.108.773747
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Submitted on February 15, 2008
From the Section of Atherosclerosis and Vascular Medicine, Department of Medicine, Baylor College of Medicine, and Center for Cardiovascular Disease Prevention, Methodist DeBakey Heart and Vascular Center, Houston, Tex (C.M.B.); AstraZeneca, Wilmington, Del (J.S.R., V.A.C.); Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Cleveland, Ohio (S.J.N., S.J.B., S.E.N.); Department of Cardiology, University Clinic Essen, Essen, Germany (R.E.); and Montreal Heart Institute, Montreal, Quebec, Canada (J.-C.T.). * To whom correspondence should be addressed. E-mail: cmb{at}bcm.tmc.edu.
Background—Previous studies using quantitative coronary angiography have demonstrated that statin therapy slows the progression of coronary stenoses in proportion to average low-density lipoprotein cholesterol levels during therapy. However, no major statin monotherapy study has demonstrated either halted progression or regression of angiographic disease. A Study to Evaluate the Effect of Rosuvastatin on Intravascular Ultrasound-Derived Coronary Atheroma Burden (ASTEROID) assessed whether rosuvastatin could regress coronary atherosclerosis by intravascular ultrasound and quantitative coronary angiography. Intravascular ultrasound showed atheroma volume regression in a single coronary artery with <50% angiographic luminal narrowing. Methods and Results—ASTEROID treated 507 coronary disease patients with rosuvastatin 40 mg/d for 24 months. Blinded quantitative coronary angiography analyses of percent diameter stenosis and minimum lumen diameter were performed for up to 10 segments of coronary arteries and major branches with >25% diameter stenosis at baseline. For each patient, the mean of all matched lesions at baseline and study end was calculated. There were 292 patients with 613 matched stenoses. Rosuvastatin reduced low-density lipoprotein cholesterol by 53.3% to 61.1±20.3 mg/dL and increased high-density lipoprotein cholesterol by 13.8% to 48.3±12.4 mg/dL. Mean±SD percent diameter stenosis decreased from 37.3±8.4% (median, 35.7%; range, 26% to 73%) to 36.0±10.1% (median, 34.5%; range, 8% to 74%; P<0.001). Minimum lumen diameter increased from 1.65±0.36 mm (median, 1.62 mm; range, 0.56 to 2.65 mm) to 1.68±0.38 mm (median, 1.67 mm; range, 0.76 to 2.77 mm; P<0.001). Conclusions—Rosuvastatin treatment for 24 months to average low-density lipoprotein cholesterol levels well below 70 mg/dL, accompanied by significant increases in high-density lipoprotein cholesterol, produced regression by decreasing percent diameter stenosis and improving minimum lumen diameter as measured by quantitative coronary angiography in coronary disease patients.
Accepted on March 19, 2008
Effect of Rosuvastatin Therapy on Coronary Artery Stenoses Assessed by Quantitative Coronary Angiography. A Study to Evaluate the Effect of Rosuvastatin on Intravascular Ultrasound-Derived Coronary Atheroma Burden
Christie M. Ballantyne MD*,
Key words: angiography • atherosclerosis • cholesterol • coronary disease • drugs
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Circulation 2008 117: 2425-2427.