title: Increased lysophosphatidic acid levels in culprit coronary arteries of patients with acute coronary syndrome.
abstract: BACKGROUND
  Lysophosphatidic acid (LPA) is a platelet activator and highly thrombogenic lipid constituent of atherosclerotic plaque. However, whether or not LPA locally released from culprit lesions is associated with acute coronary syndrome (ACS) remains unclear.
  
  
  METHODS
  We studied 52 patients with ACS who were treated by emergency percutaneous coronary intervention and thrombectomy. Levels of LPA and other established biomarkers were enzymatically assayed in samples of culprit coronary arterial and systemic peripheral arterial blood. Levels of LPA and lysophosphatidylcholine (LPC) were measured in plasma, and those of autotaxin, soluble CD40 ligand (sCD40L), hs-CRP and Lp-PLA2 were measured in serum.
  
  
  RESULTS
  Median LPA levels were significantly higher in coronary (CB) than in peripheral (PB) arterial blood (p = 0.009). Levels of sCD40L were higher in CB than in PB, but the difference did not reach statistical significance (p = 0.177). In contrast, autotaxin and Lp-PLA2 levels were significantly higher in PB than in CB (p = 0.005 and p = 0.038, respectively). Levels of LPC and hs-CRP were also higher in PB than in CB (p = 0.129 and p = 0.121, respectively). Levels of LPA in both CB and PB were positively and significantly associated with those of LPC (r = 0.632, p < 0.01 and r = 0.465, p < 0.001).
  
  
  CONCLUSIONS
  Culprit coronary arteries of ACS contained significantly more LPA than the systemic arterial circulation. Higher LPA concentrations might be associated with the pathophysiology of ACS.
authors.affiliation: Department of Cardiovascular Medicine, Juntendo University School of Medicine, Japan. tdohi@juntendo.ac.jp
authors.forename: Tomotaka
authors.initials: T
authors.lastname: Dohi
authors.forename: Katsumi
authors.initials: K
authors.lastname: Miyauchi
authors.forename: Ryunosuke
authors.initials: R
authors.lastname: Ohkawa
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Nakamura
authors.forename: Makoto
authors.initials: M
authors.lastname: Kurano
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Kishimoto
authors.forename: Naotake
authors.initials: N
authors.lastname: Yanagisawa
authors.forename: Manabu
authors.initials: M
authors.lastname: Ogita
authors.forename: Tadashi
authors.initials: T
authors.lastname: Miyazaki
authors.forename: Akihisa
authors.initials: A
authors.lastname: Nishino
authors.forename: Kenji
authors.initials: K
authors.lastname: Yaginuma
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Tamura
authors.forename: Takahiko
authors.initials: T
authors.lastname: Kojima
authors.forename: Ken
authors.initials: K
authors.lastname: Yokoyama
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kurata
authors.forename: Kazunori
authors.initials: K
authors.lastname: Shimada
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Daida
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Yatomi
mesh_terms: D054058:Acute Coronary Syndrome / Q000378:metabolism*; D000368:Aged; D003324:Coronary Artery Disease / Q000378:metabolism*; D003326:Coronary Circulation / Q000502:physiology; D003328:Coronary Thrombosis / Q000378:metabolism; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D008055:Lipids / Q000097:blood; D008244:Lysophosphatidylcholines / Q000097:blood*; D008246:Lysophospholipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D015539:Platelet Activation / Q000502:physiology; D011446:Prospective Studies
chemical_list: D008055:Lipids; D008244:Lysophosphatidylcholines; D008246:Lysophospholipids; C032881:lysophosphatidic acid