title: Release of cardiac biochemical markers after percutaneous myocardial laser or sham procedures.
abstract: BACKGROUND
  Percutaneous myocardial laser (PML) reduces symptoms in patients with intractable angina. PML leads to a certain loss of viable myocardium, we therefore assessed if troponin or cardiac markers release may explain the clinical effect, and furthermore assessed the markers release during percutaneous sham procedures.
  
  
  METHODS
  Eighty-two patients with chronic refractory angina were randomized to either percutaneous myocardial laser or a true sham procedure. Cardiac markers were assessed before the procedure, and (1/2), 2, 4, 6, and 10-12 h postprocedure.
  
  
  RESULTS
  Troponin I increased to median peak levels (range) of 4 (0.6-43) microg/L in the laser group vs. 1.5 (0.1-5.9) microg/L, p=0.001, and creatine kinase MB to 14 (6-357) microg/L vs. 11 (3-40) microg/L, p<0.05, within and between-group comparison, the rise of CK-MB occurred significantly earlier in the sham group, 3.8 vs. 2.5 h. A time-dependent between-group difference was only detected for troponin. 88% of sham and 100% of laser patients had marker levels above reference limits. There was no correlation between the number of laser/sham created channels, biomarker levels postprocedure, and changes in left ventricular ejection fraction or angina improvement during 12 months of follow-up.
  
  
  CONCLUSIONS
  The release of cardiac markers is not related to relief of angina after myocardial laser. The use of intracardiac catheters induces a considerable marker release, which is not caused by acute ischemia.
authors.affiliation: Department of Heart Disease, Haukeland University Hospital, N-5021 Bergen, Norway.
authors.forename: Mohammed
authors.initials: M
authors.lastname: Salem
authors.forename: Svein
authors.initials: S
authors.lastname: Rotevatn
authors.forename: Sindre
authors.initials: S
authors.lastname: Stavnes
authors.forename: Magne
authors.initials: M
authors.lastname: Brekke
authors.forename: Reidar
authors.initials: R
authors.lastname: Pettersen
authors.forename: Karel
authors.initials: K
authors.lastname: Kuiper
authors.forename: Rune
authors.initials: R
authors.lastname: Ulvik
authors.forename: Jan Erik
authors.initials: JE
authors.lastname: Nordrehaug
mesh_terms: D000787:Angina Pectoris / Q000378:metabolism / Q000503:physiopathology / Q000601:surgery; D015906:Angioplasty, Balloon, Coronary / Q000379:methods; D017222:Angioplasty, Balloon, Laser-Assisted; D001219:Aspartate Aminotransferases / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D003324:Coronary Artery Disease / Q000378:metabolism / Q000503:physiopathology / Q000601:surgery; D052279:Creatine Kinase, MB Form / Q000097:blood* / Q000378:metabolism; D004311:Double-Blind Method; D005500:Follow-Up Studies; D006801:Humans; D009211:Myoglobin / Q000097:blood*; D011446:Prospective Studies; D013318:Stroke Volume; D013997:Time Factors; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood* / Q000378:metabolism
chemical_list: D015415:Biomarkers; D009211:Myoglobin; D019210:Troponin I; D001219:Aspartate Aminotransferases; D052279:Creatine Kinase, MB Form