Comparison of intensive and low-dose atorvastatin therapy in the reduction of carotid intimal-medial thickness in patients with coronary heart disease.
BACKGROUND
Intensive statin therapy has been shown to improve prognosis in patients with coronary heart disease (CHD). It is unknown whether such benefit is mediated through the reduction of atherosclerotic plaque burden.


OBJECTIVE
To examine the efficacy of high-dose atorvastatin in the reduction of carotid intimal-medial thickness (IMT) and inflammatory markers in patients with CHD.


METHODS
Randomised trial.


METHODS
Single centre.


METHODS
112 patients with angiographic evidence of CHD.


METHODS
A high dose (80 mg daily) or low dose (10 mg daily) of atorvastatin was given for 26 weeks.


METHODS
Carotid IMT, C-reactive protein (CRP) and proinflammatory cytokine levels were assessed before and after therapy.


RESULTS
The carotid IMT was reduced significantly in the high-dose group (left: mean (SD), 1.24 (0.48) vs 1.15 (0.35) mm, p = 0.02; right: 1.12 (0.41) vs 1.01 (0.26) mm, p = 0.01), but was unchanged in the low-dose group (left: 1.25 (0.55) vs 1.20 (0.51) mm, p = NS; right: 1.18 (0.54) vs 1.15 (0.41) mm, p = NS). The CRP levels were reduced only in the high-dose group (from 3.92 (6.59) to 1.35 (1.83) mg/l, p = 0.01), but not in the low-dose group (from 2.25 (1.84) to 3.36 (6.15) mg/l, p = NS). A modest correlation was observed between the changes in carotid IMT and CRP (r = 0.21, p = 0.03).


CONCLUSIONS
In patients with CHD, intensive atorvastatin therapy results in regression of carotid atherosclerotic disease, which is associated with reduction in CRP levels. On the other hand, a low-dose regimen only prevents progression of the disease.
Yu
Cheuk-Man
CM
Division of Cardiology, SH Ho Cardiovascular and Stroke Centre, Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, NT, Hong Kong. cmyu@cuhk.edu.hk
Zhang
Qing
Q
Lam
Linda
L
Lin
Hong
H
Kong
Shun-Ling
SL
Chan
Wilson
W
Fung
Jeffrey Wing-Hong
JW
Cheng
Kenny K K
KK
Chan
Iris Hiu-Shuen
IH
Lee
Stephen Wai-Luen
SW
Sanderson
John E
JE
Lam
Christopher Wai-Kei
CW
D000368:Aged; D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000032:analysis; D002339:Carotid Arteries / Q000473:pathology; D002340:Carotid Artery Diseases / Q000188:drug therapy / Q000276:immunology / Q000473:pathology; D003327:Coronary Disease / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D004311:Double-Blind Method; D004334:Drug Administration Schedule; D005260:Female; D005500:Follow-Up Studies; D006538:Heptanoic Acids / Q000008:administration & dosage* / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage* / Q000627:therapeutic use; D020382:Interleukin-18 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000008:administration & dosage* / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D017539:Tunica Intima / Q000473:pathology; D017540:Tunica Media / Q000473:pathology
D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D020382:Interleukin-18; D015850:Interleukin-6; D016209:Interleukin-8; D008055:Lipids; D011758:Pyrroles; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D000069059:Atorvastatin