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Intensive lipid-lowering therapy for slowing progression as well as inducing regression of atherosclerosis in Japanese patients: subanalysis of the JART study.

Authors
  • Yamazaki, Tsutomu
  • Nohara, Ryuji
  • Daida, Hiroyuki
  • Hata, Mitsumasa
  • Kaku, Kohei
  • Kawamori, Ryuzo
  • Kishimoto, Junji
  • Kurabayashi, Masahiko
  • Masuda, Izuru
  • Sakuma, Ichiro
  • Yokoi, Hiroyoshi
  • Yoshida, Masayuki
Type
Published Article
Journal
International heart journal
Publication Date
Jan 01, 2013
Volume
54
Issue
1
Pages
33–39
Identifiers
PMID: 23428922
Source
Medline
License
Unknown

Abstract

This paper describes a subanalysis of the JART Study comparing rosuvastatin and pravastatin treatment. A total of 314 subjects were analyzed in this subanalysis, 282 of whom were eligible for evaluation of the relationship between LDL-C and carotid mean-IMT change. In the subanalysis, we evaluated the extent to which intensive lipid-lowering therapy slowed the mean-IMT progression by a correlation analysis between LDL-C and mean-IMT change after 12 months of statin treatment. Nearly half were male (49.4%) and elderly (49.7%). The majority (84.4%) were treated for primary prevention. Patients with hypertension and diabetes mellitus accounted for 65.3% and 44.0%, respectively. At the 12-month measurement point, mean-IMT change was correlated with LDL-C (R = 0.187; P = 0.0016), LDL-C/ HDL-C ratio (R = 0.152; P = 0.0105), and non-HDL-C (R = 0.132; P = 0.0259). Mean-IMT after 12 months was divided into 4 subgroups by LDL-C at 12 months; < 80, ≥ 80 to < 100, ≥ 100 to < 120, and ≥ 120 mg/dL. A trend analysis using the Jonckheere-Terpstra test showed statistical signifi cance (P = 0.0002). Even for prevention in Japanese patients who have lower risk of atherosclerotic disease than Western patients, lowering the LDL-C level to below the therapeutic target prevented mean-IMT progression after 12 months more strongly. These findings suggest that more intensive control of LDL-C to levels lower than those in current JAS guidelines should be required to achieve slowing of progression as well as induction of regression of atherosclerosis.

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