title: Increase in plasma levels of secretory type II phospholipase A(2) in patients with coronary spastic angina.
abstract: OBJECTIVE
  Plasma levels of sPLA(2) were increased in various chronic inflammatory diseases including coronary artery disease. Lipid products mediated through PLA(2) have been shown to induce impairment of endothelium-dependent dilation, contraction of smooth muscle and proliferation of smooth muscle cells, all of which might lead to coronary spasm. Thus, this study investigated whether plasma levels of secretory non-pancreatic type II phospholipase A(2) (sPLA(2)) may be increased in patients with coronary spastic angina, considering the possible link of sPLA(2) with pathogenesis of coronary artery spasm.
  
  
  METHODS
  Plasma levels of sPLA(2) in peripheral circulation, in coronary sinus and in aortic root were measured in 57 patients with coronary spastic angina, 46 patients with stable effort angina and 53 control patients by radioimmunoassay.
  
  
  RESULTS
  The peripheral plasma levels of sPLA(2) were increased in patients with coronary spastic angina compared with control patients. In multivariate statistical analysis, the increase in sPLA(2) levels was a significant risk for the presence of coronary spasm independent of other risk factors including C-reactive protein levels. The coronary sinus-arterial difference of plasma sPLA(2) levels, reflecting sPLA(2) released into the coronary circulation, was increased during coronary spasm induced by the intracoronary infusion of acetylcholine in patients with coronary spastic angina, but it remained unchanged both during the acetylcholine infusion and during myocardial ischemia provoked by rapid atrial pacing in patients with stable effort angina and in control patients.
  
  
  CONCLUSIONS
  The increase in peripheral plasma levels of sPLA(2) is a significant risk factor for the presence of coronary spasm and it may possibly reflect inflammatory activity in spasm coronary arteries.
authors.affiliation: Department of Cardiovascular Medicine, Kumamoto University School of Medicine, Kumamoto, Japan. kiyo@gpo.kumamoto-u.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Kugiyama
authors.forename: Y
authors.initials: Y
authors.lastname: Ota
authors.forename: H
authors.initials: H
authors.lastname: Kawano
authors.forename: H
authors.initials: H
authors.lastname: Soejima
authors.forename: H
authors.initials: H
authors.lastname: Ogawa
authors.forename: S
authors.initials: S
authors.lastname: Sugiyama
authors.forename: H
authors.initials: H
authors.lastname: Doi
authors.forename: H
authors.initials: H
authors.lastname: Yasue
mesh_terms: D000109:Acetylcholine; D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D000787:Angina Pectoris / Q000000981:diagnostic imaging / Q000201:enzymology*; D016022:Case-Control Studies; D017023:Coronary Angiography; D003329:Coronary Vasospasm / Q000000981:diagnostic imaging / Q000201:enzymology*; D005260:Female; D006801:Humans; D008297:Male; D010741:Phospholipases A / Q000097:blood*; D012307:Risk Factors; D014665:Vasodilator Agents
chemical_list: D014665:Vasodilator Agents; D010741:Phospholipases A; D000109:Acetylcholine