title: Lipoprotein(a) is associated with necrotic core progression of non-culprit coronary lesions in statin-treated patients with angina pectoris.
abstract: BACKGROUND
  Statin therapy results in regression and stabilization of coronary artery plaques, and reduces the incidence of coronary artery disease. However, statin therapy does not effectively halt the accumulation of necrotic core in all patients. The purpose of the present study was to identify the predictors associated with necrotic core progression during statin therapy.
  
  
  METHODS
  Coronary atherosclerosis in non-culprit lesions was evaluated using virtual histology intravascular ultrasound at baseline and 8 months after statin therapy. One hundred nineteen patients were divided into 2 groups based on necrotic core progression or regression during an 8-month follow-up period.
  
  
  RESULTS
  Patients with necrotic core progression had higher serum lipoprotein(a) [Lp(a)] levels than patients with regression at baseline (16 mg/dL vs. 12 mg/dL, p = 0.02) and at the 8-month follow-up (17 mg/dL vs. 10 mg/dL, p = 0.006). Patients with necrotic core progression had a higher fibro-fatty plaque volume (1.28 mm³/mm vs. 0.73 mm³/mm, p = 0.002), and less necrotic core (0.56 mm³/mm vs. 1.04 mm³/mm, p < 0.0001) and dense calcium (0.35 mm³/mm vs. 0.56 mm³/mm, p = 0.006) plaque volumes at baseline than patients with regression. Multivariate logistic regression analysis showed that Lp(a) was a significant independent predictor associated with necrotic core progression during statin therapy (odds ratio [OR]: 3.514; 95% confidence interval [CI]: 1.338-9.228; p = 0.01).
  
  
  CONCLUSIONS
  Serum Lp(a) is independently associated with necrotic core progression in statin-treated patients with angina pectoris.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, Yokohama Sakae Kyosai Hospital, 132 Katsura-cho, Sakae-ku, Yokohama 247-8581, Japan. nozue2493@yahoo.co.jp.
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Nozue
authors.forename: Shingo
authors.initials: S
authors.lastname: Yamamoto
authors.forename: Shinichi
authors.initials: S
authors.lastname: Tohyama
authors.forename: Kazuki
authors.initials: K
authors.lastname: Fukui
authors.forename: Shigeo
authors.initials: S
authors.lastname: Umezawa
authors.forename: Yuko
authors.initials: Y
authors.lastname: Onishi
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Kunishima
authors.forename: Akira
authors.initials: A
authors.lastname: Sato
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Nozato
authors.forename: Shogo
authors.initials: S
authors.lastname: Miyake
authors.forename: Youichi
authors.initials: Y
authors.lastname: Takeyama
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Morino
authors.forename: Takao
authors.initials: T
authors.lastname: Yamauchi
authors.forename: Toshiya
authors.initials: T
authors.lastname: Muramatsu
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Hibi
authors.forename: Mitsuyasu
authors.initials: M
authors.lastname: Terashima
authors.forename: Ichiro
authors.initials: I
authors.lastname: Michishita
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000097:blood* / Q000188:drug therapy* / Q000473:pathology; D003324:Coronary Artery Disease / Q000097:blood / Q000473:pathology; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D017270:Lipoprotein(a) / Q000097:blood*; D008297:Male; D008875:Middle Aged; D058226:Plaque, Atherosclerotic / Q000097:blood / Q000473:pathology
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D017270:Lipoprotein(a)