title: Increased serum anandamide level at ruptured plaque site in patients with acute myocardial infarction.
abstract: Inflammation caused by activated macrophages and T lymphocytes may trigger plaque rapture in acute coronary syndrome (ACS). Anandamide and 2-arachidonylglycerol (2-AG) are macrophage-derived signal lipids and may be involved in the pathogenesis of ACS, but no clinical relevant data have been reported. In 43 acute myocardial infarction (AMI) patients (66 +/- 2 years), blood samples were obtained from the aortic root and the infarct-related coronary artery (IRA) using a PercuSurge system during primary percutaneous coronary intervention (PCI). In six patients with stable effort angina (SEA) (56 +/- 6 years), blood samples were obtained from the site of stenosis during elective PCI. In 25 of the 43 AMI patients, anandamide was detected in the serum. Serum anandamide level was 35 +/- 20 pmol/mL in the aorta and was significantly increased to 401 +/- 134 pmol/mL in the IRA (P < 0.01). 2-AG was undetectable in most of the patients. In patients with SEA, neither anandamide nor 2-AG was detected in the serum at the plaque site. In AMI patients with anandamide detected, left ventricular ejection fraction at 2 weeks after PCI was increased by 3.7 +/- 2.1% compared with that at the acute phase, while it was decreased by 3.0 +/- 1.8% in those without anandamide detected (P < 0.05). The serum anandamide level at the culprit lesion was elevated compared with the systemic level in a significant number of AMI patients, indicating the synthesis of anandamide at the IRA. Anandamide was suggested to be derived from ruptured plaque and may exert beneficial effects in humans.
authors.affiliation: Department of Cardiology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
authors.forename: Naotaka
authors.initials: N
authors.lastname: Maeda
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Osanai
authors.forename: Motoi
authors.initials: M
authors.lastname: Kushibiki
authors.forename: Takayuki
authors.initials: T
authors.lastname: Fujiwara
authors.forename: Yujin
authors.initials: Y
authors.lastname: Tamura
authors.forename: Shingen
authors.initials: S
authors.lastname: Oowada
authors.forename: Takumi
authors.initials: T
authors.lastname: Higuma
authors.forename: Shingo
authors.initials: S
authors.lastname: Sasaki
authors.forename: Jin
authors.initials: J
authors.lastname: Yokoyama
authors.forename: Fuminobu
authors.initials: F
authors.lastname: Yoshimachi
authors.forename: Toshiro
authors.initials: T
authors.lastname: Matsunaga
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Hanada
authors.forename: Ken
authors.initials: K
authors.lastname: Okumura
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000503:physiopathology; D015906:Angioplasty, Balloon, Coronary; D001011:Aorta / Q000503:physiopathology; D001095:Arachidonic Acids / Q000096:biosynthesis / Q000097:blood*; D003331:Coronary Vessels / Q000503:physiopathology*; D063388:Endocannabinoids; D005260:Female; D005989:Glycerides / Q000097:blood; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology*; D053284:Polyunsaturated Alkamides / Q000097:blood*; D012422:Rupture, Spontaneous
chemical_list: D001095:Arachidonic Acids; D063388:Endocannabinoids; D005989:Glycerides; D053284:Polyunsaturated Alkamides; C094503:glyceryl 2-arachidonate; C078814:anandamide