title: Elevation of ceramide and activation of secretory acid sphingomyelinase in patients with acute coronary syndromes.
abstract: BACKGROUND
  Although there are several reported evidences for a pathogenic role of sphingolipid signaling in atherosclerosis, peripheral blood levels of ceramide and secretory acid sphingomyelinase (S-SMase) activity in patients with acute coronary syndromes (ACS) have not been evaluated.
  
  
  RESULTS
  A total of 304 CAD patients and 52 healthy individuals were divided into four groups: control group (n=52), stable angina pectoris (SAP) group (n=98), unstable angina pectoris (UAP) group (n=92), and acute myocardial infarction (AMI) group (n=114). Plasma levels of sphingomyelin (SPM) were elevated in patients with UAP and AMI compared with those in the control and SAP participants. Plasma ceramide levels and S-SMase activity in patients with ACS (including UAP and AMI) on day 0 were significantly higher than those in the control and SAP participants. Elevation in plasma ceramide levels in patients with UAP and AMI was sustained until a day after percutaneous coronary intervention or day 7, respectively. Moreover, in patients with UAP, S-SMase activity elevation on day 0 was followed by a gradual decrease toward the SAP range up to a day after percutaneous coronary intervention. In patients with AMI, elevation in S-SMase activity showed a peak on day 3.
  
  
  CONCLUSIONS
  Serial changes in plasma ceramide and S-SMase activity were documented in patients with ACS. These findings provide an insight into the molecular mechanism of plaque destabilization.
authors.affiliation: aDepartment of Cardiovascular Medicine, Xiangya Hospital, Central South University, Changsha bThe State Key Laboratory of Medical Genetics, Xiangya Medical School, Central South University cDepartment of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha, China dDepartment of Genetics and Genomic Sciences, Mount Sinai School of Medicine, New York, New York, USA.
authors.forename: Wei
authors.initials: W
authors.lastname: Pan
authors.forename: Jingjia
authors.initials: J
authors.lastname: Yu
authors.forename: Ruizheng
authors.initials: R
authors.lastname: Shi
authors.forename: Lei
authors.initials: L
authors.lastname: Yan
authors.forename: Tianlun
authors.initials: T
authors.lastname: Yang
authors.forename: Yuanjian
authors.initials: Y
authors.lastname: Li
authors.forename: Zhuohua
authors.initials: Z
authors.lastname: Zhang
authors.forename: Guolong
authors.initials: G
authors.lastname: Yu
authors.forename: Yongping
authors.initials: Y
authors.lastname: Bai
authors.forename: Edward H
authors.initials: EH
authors.lastname: Schuchman
authors.forename: Xingxuan
authors.initials: X
authors.lastname: He
authors.forename: Guogang
authors.initials: G
authors.lastname: Zhang
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000097:blood* / Q000503:physiopathology; D002518:Ceramides / Q000097:blood*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic; D009203:Myocardial Infarction / Q000097:blood* / Q000503:physiopathology; D062645:Percutaneous Coronary Intervention / Q000379:methods; D058226:Plaque, Atherosclerotic / Q000378:metabolism / Q000503:physiopathology; D013108:Sphingomyelin Phosphodiesterase / Q000378:metabolism*; D013109:Sphingomyelins / Q000097:blood; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D002518:Ceramides; D013109:Sphingomyelins; D013108:Sphingomyelin Phosphodiesterase