title: Lipoprotein(a) is an important factor to determine coronary artery plaque morphology in patients with acute myocardial infarction.
abstract: BACKGROUND
  Lipoprotein(a) [Lp(a)] can influence the development and disruption of atherosclerotic plaques through its effect on lipid accumulation. The purpose of this study was to evaluate the relationship between serum Lp(a) levels and plaque morphology of an infarct-related lesion and non-infarct-related lesion of the coronary artery in acute myocardial infarction (AMI).
  
  
  RESULTS
  Coronary plaque morphology was evaluated in 68 patients (age 62.1±12.1 years, mean±SD; men n=58, women n=10) with AMI by intravascular ultrasound with radiofrequency data analysis before coronary intervention and by 64-slice computed tomography angiography within 2 weeks. Patients were divided into a group with an Lp(a) level of 25 mg/dl or more (n=20) and a group with an Lp(a) level of less than 25 mg/dl (n=48). Intravascular ultrasound with radiofrequency data analysis identified four types of plaque components at the infarct-related lesion: fibrous, fibrofatty, dense calcium, and necrotic core. The necrotic core component was significantly larger in the group with an Lp(a) level of 25 mg/dl or more than in the group with an Lp(a) level of less than 25 mg/dl (27.6±8.0 vs. 15.7±10.0%, P=0.0001). Coronary plaques were classified as calcified plaques, noncalcified plaques, mixed plaques, and low-attenuation plaques on 64-slice computed tomography angiography. Computed tomography indicated that the group with an Lp(a) level of 25 mg/dl or more had a greater number of total plaques, noncalcified plaques, and low-attenuation plaques in whole coronary arteries than did the group with an Lp(a) level of less than 25 mg/dl (5.3±1.8 vs. 3.7±2.2, P=0.0061; 4.0±2.0 vs. 1.2±1.3, P=0.0001; 2.2±2.1 vs. 0.5±0.7, P=0.0001, respectively).
  
  
  CONCLUSIONS
  Elevated serum Lp(a) levels are associated with the number of plaques and plaque morphology. Patients with a high Lp(a) level during AMI require more intensive treatment for plaque stabilization.
authors: Cardiovascular Center, Yokosuka Kyosai Hospital, Yokosuka, Kanagawa, Japan. hihikita2000@yahoo.co.jp
authors: Hiroyuki
authors: H
authors: Hikita
authors: Takatoshi
authors: T
authors: Shigeta
authors: Keisuke
authors: K
authors: Kojima
authors: Yuki
authors: Y
authors: Oosaka
authors: Keiichi
authors: K
authors: Hishikari
authors: Naohiko
authors: N
authors: Kawaguchi
authors: Emiko
authors: E
authors: Nakashima
authors: Tomoyo
authors: T
authors: Sugiyama
authors: Daiki
authors: D
authors: Akiyama
authors: Tetsuo
authors: T
authors: Kamiishi
authors: Shigeki
authors: S
authors: Kimura
authors: Yoshihide
authors: Y
authors: Takahashi
authors: Taishi
authors: T
authors: Kuwahara
authors: Akira
authors: A
authors: Sato
authors: Atsushi
authors: A
authors: Takahashi
authors: Mitsuaki
authors: M
authors: Isobe
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D016009:Chi-Square Distribution; D017023:Coronary Angiography / Q000379:methods; D003324:Coronary Artery Disease / Q000097:blood* / Q000150:complications / Q000175:diagnosis*; D003331:Coronary Vessels / Q000000981:diagnostic imaging; D005260:Female; D005355:Fibrosis; D006801:Humans; D017270:Lipoprotein(a) / Q000097:blood*; D008297:Male; D008875:Middle Aged; D061330:Multidetector Computed Tomography; D009203:Myocardial Infarction / Q000097:blood* / Q000175:diagnosis* / Q000209:etiology; D009336:Necrosis; D058226:Plaque, Atherosclerotic; D011237:Predictive Value of Tests; D011379:Prognosis; D012720:Severity of Illness Index; D018084:Ultrasonography, Interventional; D015854:Up-Regulation; D061205:Vascular Calcification / Q000097:blood / Q000175:diagnosis
chemical_list: D015415:Biomarkers; D017270:Lipoprotein(a)