title: Bioprosthetic tricuspid valve regurgitation associated with pacemaker or defibrillator lead implantation.
abstract: OBJECTIVE
  The goal of this study was to determine the impact of transvenous pacemaker and defibrillator leads on the incidence of bioprosthetic tricuspid valve (BTV) regurgitation compared with BTV patients without a transvalvular lead.
  
  
  BACKGROUND
  Although concern has been raised regarding the potential deleterious effect of permanent transvenous device leads on BTV function, little is known about the incidence of prosthetic tricuspid regurgitation (TR) after lead placement.
  
  
  METHODS
  A retrospective review of 58 patients who underwent BTV implantation and subsequently required endocardial pacemaker (n = 52) or defibrillator (n = 6) lead implantation across the BTV was conducted. Patient and prosthesis characteristics, lead type, and clinical events were collected. The incidence and severity of prosthetic TR, determined by Doppler echocardiography, was compared with 265 consecutive patients who underwent BTV implantation without undergoing subsequent transvalvular device lead implantation.
  
  
  RESULTS
  Over a mean follow-up of 25 months, in 5 patients (9%) with a transvalvular lead significant (moderate or greater) prosthetic TR developed compared with 12 patients (5%) in the control group (p = 0.20). Kaplan-Meier analysis revealed no significant difference in the incidence of TR in BTV patients with and without transvalvular leads (p = 0.45). Significant prosthetic TR in patients with and without a transvalvular lead more commonly occurred 2 years or later after lead or BTV implantation (4 of 5, 80% and 10 of 12, 83%, respectively).
  
  
  CONCLUSIONS
  Transvalvular device lead implantation in BTV patients was not associated with an increased incidence of significant prosthetic TR (p = 0.45). Based on these data, transvalvular lead implantation appears to be an acceptable approach for patients with a BTV who require permanent pacemaker or defibrillator placement.
authors.affiliation: Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA. eleid.mackram@mayo.edu
authors.forename: Mackram F
authors.initials: MF
authors.lastname: Eleid
authors.forename: Lori A
authors.initials: LA
authors.lastname: Blauwet
authors.forename: Yong-Mei
authors.initials: YM
authors.lastname: Cha
authors.forename: Heidi M
authors.initials: HM
authors.lastname: Connolly
authors.forename: Peter A
authors.initials: PA
authors.lastname: Brady
authors.forename: Joseph A
authors.initials: JA
authors.lastname: Dearani
authors.forename: Raúl E
authors.initials: RE
authors.lastname: Espinosa
mesh_terms: D000368:Aged; D001705:Bioprosthesis; D015150:Echocardiography, Doppler; D004567:Electrodes, Implanted / Q000009:adverse effects*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D008910:Minnesota / Q000453:epidemiology; D010138:Pacemaker, Artificial / Q000009:adverse effects*; D011379:Prognosis; D011475:Prosthesis Failure; D012189:Retrospective Studies; D012307:Risk Factors; D017180:Tachycardia, Ventricular / Q000628:therapy*; D013997:Time Factors; D014262:Tricuspid Valve Insufficiency / Q000175:diagnosis / Q000453:epidemiology / Q000209:etiology*