title: Reversible pulmonary trunk banding. II. An experimental model for rapid pulmonary ventricular hypertrophy.
abstract: OBJECTIVE
  An experimental model with a reversible pulmonary trunk banding device was developed with the aim of inducing rapid ventricular hypertrophy. The device consists of an insufflatable cuff connected to a self-sealing button.
  
  
  METHODS
  The right ventricles of 7 young goats (average weight, 8.7 kg) were submitted to systolic overload and evaluated according to the hemodynamic, echocardiographic, and morphologic aspects. Baseline biopsy specimens were taken from the myocardium for microscopic analysis. The device was implanted on the pulmonary trunk and inflated so that a 0.7 right ventricular/left ventricular pressure ratio was achieved. Echocardiographic and hemodynamic evaluations were performed every 24 hours. Systolic overload was maintained for 96 hours. The animals were then killed for morphologic study. Another 9 goats (average weight, 7.7 kg) were used for control right ventricular weight.
  
  
  RESULTS
  The systolic right ventricular/pulmonary trunk pressure gradient varied from 10.1 +/- 4.3 mm Hg (baseline) to 60.0 +/- 11.0 mm Hg (final). Consequently, the right ventricular/left ventricular pressure ratio increased from 0.29 +/- 0.06 to 1.04 +/- 0.14. The protocol group showed a 74% increase in right ventricular mass when compared with the control group. Serial 2-dimensional echocardiography showed a 66% increase in right ventricular wall thickness. There was a 24% increase in the mean myocyte perimeter, and the myocyte area increased 61%.
  
  
  CONCLUSIONS
  The device is easily adjustable percutaneously, enabling right ventricular hypertrophy in 96 hours of gradual systolic overload. This study suggests that the adjustable pulmonary trunk banding might provide better results for the 2-stage Jatene operation and for the failed atrial switch operations to convert to the double-switch operation.
authors.affiliation: Heart Institute University of São Paulo Medical School, São Paulo, Brazil.
authors.forename: Carlos A
authors.initials: CA
authors.lastname: Dias
authors.forename: Renato S
authors.initials: RS
authors.lastname: Assad
authors.forename: Luiz F
authors.initials: LF
authors.lastname: Caneo
authors.forename: Maria Cristina D
authors.initials: MC
authors.lastname: Abduch
authors.forename: Vera D
authors.initials: VD
authors.lastname: Aiello
authors.forename: Altamiro R
authors.initials: AR
authors.lastname: Dias
authors.forename: Miguel Barbero
authors.initials: MB
authors.lastname: Marcial
authors.forename: Sérgio A
authors.initials: SA
authors.lastname: Oliveira
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D004195:Disease Models, Animal; D015150:Echocardiography, Doppler; D004867:Equipment Design / Q000009:adverse effects; D006041:Goats; D006352:Heart Ventricles / Q000166:cytology / Q000473:pathology* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000209:etiology* / Q000503:physiopathology; D017380:Hypertrophy, Right Ventricular / Q000209:etiology* / Q000503:physiopathology; D008853:Microscopy; D008955:Models, Cardiovascular; D032383:Myocytes, Cardiac / Q000378:metabolism; D009929:Organ Size / Q000502:physiology; D011664:Pulmonary Valve / Q000473:pathology* / Q000503:physiopathology; D013318:Stroke Volume / Q000502:physiology; D013599:Systole / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology; D017725:Ventricular Pressure / Q000502:physiology