Use of intravascular ultrasound to compare effects of different strategies of lipid-lowering therapy on plaque volume and composition in patients with coronary artery disease.
BACKGROUND
We studied whether lipid-lowering therapy with atorvastatin (target LDL cholesterol [LDL-C] <100 mg/dL) compared with a moderate treatment regimen that used other lipid-lowering drugs led to a lesser progression of atherosclerosis and to different changes in plaque echogenicity in patients with coronary artery disease.


RESULTS
This study was a 12-month, open-label, randomized, multicenter trial, which used serial 3D intracoronary ultrasound to calculate plaque volume and plaque echogenicity. After transcatheter therapy, 131 patients were randomized (atorvastatin n=65, usual care n=66). The target plaque had to be a minor lesion (ie, a diameter stenosis of <50% on angiography). After 12 months, mean LDL-C was reduced from 155 to 86 mg/dL in the atorvastatin group and from 166 to 140 mg/dL in the usual care group. Mean absolute plaque volume showed a larger increase in the usual care group compared with the atorvastatin group (usual care 9.6+/-28.1 mm(3), atorvastatin 1.2+/-30.4 mm(3); P=0.191). The hyperechogenicity index of the plaque increased to a larger extent for the atorvastatin group than for the usual care group, with a significant treatment effect for the percent change (atorvastatin 42.2%, usual care 10.1%; P=0.021).


CONCLUSIONS
One year of lipid-lowering therapy to <100 mg/dL LDL-C most likely led to a slowdown of plaque growth of minor lesions. The significantly larger increase in plaque hyperechogenicity is most likely due to a change in plaque composition.
Schartl
M
M
Universitaetsklinikum Charité, Campus Virchow, German Heart Institute Berlin, Germany. michael.schartl@charite.de
Bocksch
W
W
Koschyk
D H
DH
Voelker
W
W
Karsch
K R
KR
Kreuzer
J
J
Hausmann
D
D
Beckmann
S
S
Gross
M
M
D000924:Anticholesteremic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001161:Arteriosclerosis / Q000188:drug therapy* / Q000473:pathology; D018771:Arthralgia / Q000139:chemically induced; D000069059:Atorvastatin; D002087:Butyrates / Q000627:therapeutic use; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood / Q000187:drug effects; D002792:Cholestyramine Resin / Q000627:therapeutic use; D003327:Coronary Disease / Q000188:drug therapy* / Q000473:pathology; D003404:Creatinine / Q000097:blood; D005076:Exanthema / Q000139:chemically induced; D006538:Heptanoic Acids / Q000009:adverse effects / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D010352:Patient Dropouts; D011758:Pyrroles / Q000009:adverse effects / Q000627:therapeutic use*; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood; D018084:Ultrasonography, Interventional; D020246:Venous Thrombosis / Q000139:chemically induced
D000924:Anticholesteremic Agents; D002087:Butyrates; D008076:Cholesterol, HDL; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D014280:Triglycerides; D002792:Cholestyramine Resin; D002784:Cholesterol; D000069059:Atorvastatin; D003404:Creatinine