The Effects of Rosuvastatin on Plaque Regression in Patients Who Have a Mild to Moderate Degree of Coronary Stenosis With Vulnerable Plaque.
10.4070/kcj.2008.38.7.366
- Author:
Young Joon HONG
1
;
Myung Ho JEONG
;
Jong Won CHUNG
;
Doo Sun SIM
;
Jung Sun CHO
;
Nam Sik YOON
;
Hyun Ju YOON
;
Jae Youn MOON
;
Kye Hun KIM
;
Hyung Wook PARK
;
Ju Han KIM
;
Youngkeun AHN
;
Jeong Gwan CHO
;
Jong Chun PARK
;
Jung Chaee KANG
Author Information
1. The Heart Center of Chonnam National University Hospital, Cardiovascular Research Institute of Chonnam National University, Gwangju, Korea. myungho@chollian.net
- Publication Type:Comparative Study ; Original Article ; Randomized Controlled Trial
- Keywords:
Atherosclerosis;
Lipids;
Statins, HMG-CoA;
Ultrasonics
- MeSH:
Atherosclerosis;
Coronary Angiography;
Coronary Artery Disease;
Coronary Stenosis;
Fluorobenzenes;
Follow-Up Studies;
Glycosaminoglycans;
Heptanoic Acids;
Humans;
Hydroxymethylglutaryl-CoA Reductase Inhibitors;
Lipoproteins;
Plaque, Atherosclerotic;
Prospective Studies;
Pyrimidines;
Pyrroles;
Sulfonamides;
Ultrasonics;
Atorvastatin Calcium
- From:Korean Circulation Journal
2008;38(7):366-373
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND AND OBJECTIVES: Intensive lipid-lowering therapy with statins improves the clinical outcomes and patient survival and it reduces the progression of atherosclerosis. Intravascular ultrasound (IVUS) has been used for calculating the plaque volumes to evaluate the mechanisms that may be involved in the progression or regression of coronary artery disease. We used serial IVUS exams to assess the efficacy of rosuvastatin on plaque regression in angina patients who had a mild to moderate degree of vulnerable plaque burden. SUBJECTS AND METHODS: This study was a prospective, randomized, comparative study for lipid lowering therapy with using rosuvastatin 20 mg or atorvastatin 40 mg. IVUS was performed during the baseline coronary angiography and it was repeated after 12 months of treatment. The efficacy parameters included the changes in the atheroma volume and the lipid pool size as determined by IVUS. A total of 45 lesions in 30 patients were analyzed (rosuvastatin: 24 lesions in 16 patients vs. atorvastatin: 21 lesions in 14 patients). RESULTS: The low density lipoprotein (LDL)-cholesterol level was reduced from 121+/-45 mg/dL to 65+/-25 mg/dL in the rosuvastatin group (a 46% decrease, p<0.001), and from 127+/-37 mg/dL to 72+/-26 mg/dL in the atorvastatin group (a 43% decrease, p<0.001). The total atheroma and vessel volumes were significantly decreased, whereas the lumen volume was significantly increased from baseline to follow-up in both groups (for the rosuvastatin group: the total atheroma volume, 252+/-80 to 246+/-79 mm3, p<0.001; the vessel volume, 555+/-158 to 553+/-130 mm3, p<0.001; the lumen volume, 303+/-91 to 307+/-92 mm3, p<0.001, and for the atorvastatin group: the total atheroma volume, 288+/-98 to 283+/-98 mm3, p<0.001; the vessel volume, 607+/-165 to 604+/-166 mm3, p<0.001; the lumen volume, 319+/-71 to 321+/-73 mm3, p<0.001). The follow-up LDL-cholesterol level was correlated with the change in the total atheroma volume (r=0.577, p<0.001), the change in the percent atheroma volume (r=0.558, p<0.001) and the change in the lipid pool size (r=0.470, p=0.001). CONCLUSION: Both rosuvastatin 20 mg and atorvastatin 40 mg could contribute to the regression of lipid-rich plaque. The follow-up LDL-cholesterol level is related to the regression and stabilization of vulnerable coronary plaque.
