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.
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.


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.
Ballantyne
Christie M
CM
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 77030, USA. cmb@bcm.tmc.edu
Raichlen
Joel S
JS
Nicholls
Stephen J
SJ
Erbel
Raimund
R
Tardif
Jean-Claude
JC
Brener
Sorin J
SJ
Cain
Valerie A
VA
Nissen
Steven E
SE
D000368:Aged; D008078:Cholesterol, LDL / Q000097:blood; D017023:Coronary Angiography / Q000379:methods*; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000188:drug therapy*; D023921:Coronary Stenosis / Q000175:diagnosis / Q000188:drug therapy*; D005260:Female; D005464:Fluorobenzenes / Q000008:administration & dosage* / Q000494:pharmacology; D006801:Humans; D008297:Male; D008875:Middle Aged; D011743:Pyrimidines / Q000008:administration & dosage* / Q000494:pharmacology; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000008:administration & dosage* / Q000494:pharmacology; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional
D008078:Cholesterol, LDL; D005464:Fluorobenzenes; D011743:Pyrimidines; D013449:Sulfonamides; D000068718:Rosuvastatin Calcium