title: Carcinoid Heart Valve Disease: Transcatheter Pulmonary Valve-In-Valve Implantation in Failing Biological Xenografts.
abstract: OBJECTIVE
  Carcinoid heart valve disease (CHVD) occurs as the cardiac manifestation of carcinoid syndrome (also known as Hedinger's syndrome), which develops secondary to neuroendocrine tumor activity. CHVD almost exclusively affects right-sided heart valves, since circulating serotonin is metabolized by pulmonary endothelial cells, thus sparing left-sided valves. Replacement of the tricuspid and pulmonary valve is a well-established and feasible therapeutic option for these patients. Whether biological valve substitutes are subject to a continuous degenerative process is not entirely clear at present due to the rarity of the disease and inconclusive findings in the current literature.
  
  
  METHODS
  Herein are presented the details of two patients suffering from advanced CHVD who had undergone previous combined tricuspid valve replacement (TVR) and pulmonary valve replacement (PVR) using biological xenografts, and had subsequently been readmitted with failure of the pulmonary valve substitute.
  
  
  RESULTS
  Due to the increased risk for repeat surgical valve replacement, the patients were treated by percutaneous stent implantation into the pulmonary artery, followed by the implantation of a balloon- expandable transcatheter heart valve (THV). The procedures were feasible and safe through the intact TVR.
  
  
  CONCLUSIONS
  This strategy resulted in a favorable acute outcome in both patients, with adequate valve function and no PVL as documented by TTE, although the transvalvular gradients were elevated in both cases. The patients had an uneventful postoperative course and were discharged home in timely fashion. Whether the residual elevated transvalvular gradients following the valve-in-valve procedures, or an early degeneration of the implanted bioprostheses, will have a negative impact on the patients' further course will become clear in the future.
authors.forename: Lenard
authors.initials: L
authors.lastname: Conradi
authors.forename: Andreas
authors.initials: A
authors.lastname: Schaefer
authors.forename: Goetz C
authors.initials: GC
authors.lastname: Mueller
authors.forename: Moritz
authors.initials: M
authors.lastname: Seiffert
authors.forename: Helmut
authors.initials: H
authors.lastname: Gulbins
authors.forename: Stefan
authors.initials: S
authors.lastname: Blankenberg
authors.forename: Hermann
authors.initials: H
authors.lastname: Reichenspurner
authors.forename: Hendrik
authors.initials: H
authors.lastname: Treede
authors.forename: Patrick
authors.initials: P
authors.lastname: Diemert
mesh_terms: D000328:Adult; D002275:Carcinoid Heart Disease / Q000175:diagnosis / Q000503:physiopathology / Q000601:surgery*; D006328:Cardiac Catheterization / Q000379:methods*; D005260:Female; D006349:Heart Valve Diseases / Q000175:diagnosis / Q000503:physiopathology / Q000601:surgery*; D006350:Heart Valve Prosthesis; D019918:Heart Valve Prosthesis Implantation / Q000009:adverse effects / Q000295:instrumentation*; D006439:Hemodynamics; D064593:Heterografts; D006801:Humans; D008297:Male; D008875:Middle Aged; D011474:Prosthesis Design; D011475:Prosthesis Failure; D011664:Pulmonary Valve / Q000503:physiopathology / Q000601:surgery*; D015641:Radiography, Interventional; D020127:Recovery of Function; D013997:Time Factors; D016896:Treatment Outcome; D014261:Tricuspid Valve / Q000503:physiopathology / Q000601:surgery