title: Biochemical evidence of cardiac damage following transvenous implantation of a permanent antibradycardia pacemaker lead.
abstract: OBJECTIVE
  We tested the hypothesis that transvenous permanent pacemaker lead implantation causes clinically detectable myocardial damage.
  
  
  BACKGROUND
  Histological evidence of myocardial damage has been reported after antibradycardia pacemaker lead implantation.
  
  
  METHODS
  We studied 30 patients undergoing implantation of a full antibradycardia pacemaker system (pulse generator plus leads) and 10 patients in whom only a generator was implanted. Blood samples for cardiac troponin-I (CTNI), CK-MB mass, and myoglobin measurement were drawn at baseline, at the end of the procedure, and at 2, 6, 12, 24, 48, and 72 hours thereafter.
  
  
  RESULTS
  Abnormal CTNI levels were noted only in 24 of the 30 patients undergoing a full system implantation. CTNI levels were already abnormal at the end of the procedure in 16 and became so in all 24 during the next 6 hours. Peak levels were reached within 6 hours in 21 patients and were compatible with "minimal" necrosis (CTNI < 1.5 pg/mL) in 20. Maximum ventricular lead diameter and number of implanted leads were independent predictors of peak CTNI levels. CK-MB mass also increased after the procedure, but exceeded the normal range in only 10 patients. Myoglobin levels increased significantly both in patients undergoing a complete system implantation and in those where only a pulse generator was implanted.
  
  
  CONCLUSIONS
  Transvenous insertion of endocardial leads for permanent pacing is accompanied in most patients by "minimal" myocardial damage. In this setting CTNI level kinetics are fast, characterized by early elevation and peak.
authors.affiliation: Department of Cardiology, Konstantopoulio-Agia Olga General Hospital, Athens, Greece. nikosnik@otenet.gr
authors.forename: Nikolaos I
authors.initials: NI
authors.lastname: Nikolaou
authors.forename: Stavros G
authors.initials: SG
authors.lastname: Spanodimos
authors.forename: Elias P
authors.initials: EP
authors.lastname: Tsaglis
authors.forename: Dionysios G
authors.initials: DG
authors.lastname: Antonatos
authors.forename: Sotiris P
authors.initials: SP
authors.lastname: Patsilinakos
authors.forename: Georgios M
authors.initials: GM
authors.lastname: Fournarakis
authors.forename: Dimitrios L
authors.initials: DL
authors.lastname: Tsigas
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001671:Biochemistry / Q000379:methods; D001919:Bradycardia / Q000097:blood / Q000150:complications / Q000517:prevention & control; D009202:Cardiomyopathies / Q000097:blood* / Q000209:etiology*; D052281:Creatine Kinase, Mitochondrial Form / Q000097:blood; D004567:Electrodes, Implanted / Q000009:adverse effects*; D019317:Evidence-Based Medicine / Q000379:methods; D005260:Female; D005549:Foreign-Body Reaction / Q000097:blood* / Q000209:etiology*; D006801:Humans; D008297:Male; D009211:Myoglobin / Q000097:blood*; D010138:Pacemaker, Artificial / Q000009:adverse effects; D018570:Risk Assessment / Q000379:methods; D012307:Risk Factors; D019210:Troponin I / Q000097:blood*; D014680:Veins / Q000601:surgery
chemical_list: D009211:Myoglobin; D019210:Troponin I; D052281:Creatine Kinase, Mitochondrial Form