Statin-induced cholesterol lowering and plaque regression after 6 months of magnetic resonance imaging-monitored therapy.
BACKGROUND
Statin therapy reduces adverse outcomes, with a minimal decrease in vessel stenosis. Magnetic resonance imaging (MRI) noninvasively detects atherosclerotic plaque (AP) reduction. We hypothesized that statin-induced AP regression can be monitored by MRI and detected earlier than previously reported and is significantly associated with its lipid-lowering effect.


RESULTS
APs in thoracic aorta were measured by combined surface/transesophageal MRI in 27 patients (treated with simvastatin 20 to 80 mg daily) before and after 6 months of therapy. AP volume and luminal dimensions were measured from 6 cross sections used to construct a 2.4-cm 3D volume of the aorta that included plaque and lumen. Method reproducibility was studied in 10 patients imaged twice, 1 week apart. AP volume was reduced from 3.3+/-0.1.4 to 2.9+/-1.4 cm3 at 6 months (P<0.02), whereas luminal volume increase was less accentuated (from 12.0+/-3.9 to 12.2+/-3.7 cm3, P<0.06). LDL cholesterol decreased by 23% (from 125+/-32 to 97+/-27 mg/dL, P<0.05) in 6 months. AP regression (plaque volume/area reduction) was significantly related to LDL cholesterol reduction (P<0.02 and P<0.005, respectively), and luminal volume increase was inversely related to LDL cholesterol reduction (P<0.04). Plaque volume measurement was highly reproducible (intraclass correlation R=0.98 and variability=4.8%). Intraobserver (0.91) and interobserver (0.81) concordances were documented for plaque volume assessment.


CONCLUSIONS
AP regression and reverse remodeling can be detected accurately by MRI 6 months after statin therapy initiation, and it is strongly associated with LDL cholesterol reduction.
Cardiology Division of the Department of Medicine, Johns Hopkins University, Baltimore, Md, USA. jlima@jhmi.edu
João A C
JA
Lima
Milind Y
MY
Desai
Henning
H
Steen
William P
WP
Warren
Sandeep
S
Gautam
Shenghan
S
Lai
D000368:Aged; D001013:Aorta, Thoracic / Q000473:pathology; D001018:Aortic Diseases / Q000097:blood / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology; D001161:Arteriosclerosis / Q000097:blood / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology; D008078:Cholesterol, LDL / Q000097:blood*; D015897:Comorbidity; D003327:Coronary Disease / Q000453:epidemiology; D003920:Diabetes Mellitus / Q000453:epidemiology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D006937:Hypercholesterolemia / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D006973:Hypertension / Q000453:epidemiology; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D008875:Middle Aged; D015588:Observer Variation; D011446:Prospective Studies; D015203:Reproducibility of Results; D019821:Simvastatin / Q000008:administration & dosage / Q000627:therapeutic use*; D012907:Smoking / Q000453:epidemiology; D020521:Stroke / Q000453:epidemiology
D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D019821:Simvastatin