Pulmonary Trunk Banding Research Articles

Reversible pulmonary trunk banding. II. An experimental model for rapid pulmonary ventricular hypertrophy

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.J Thorac Cardiovasc Surg 2002;124:999-1006

Análise da atividade da enzima conversora da angiotensina na hipertrofia aguda do ventrículo direito em modelo experimental de estenose endovascular ajustável do tronco pulmonar

INTRODUCAO: A bandagem do tronco pulmonar (TP) tem sido aplicada para treinamento do ventriculo esquerdo (VE) em pacientes portadores de transposicao das grandes arterias (TGA) com septo integro. Este procedimento, alem de apresentar alta morbi-mortalidade, pode ocasionar alteracoes da funcao ventricular a longo prazo. Com o objetivo de analisar a hipertrofia aguda do ventriculo direito (VD), foi implantado um cateter balao no TP de seis cabritos jovens. MATERIAL E METODOS: A sobrecarga sistolica foi aplicada atraves de insuflacoes progressivas do balao, durante 96 horas. Esta hipertrofia foi acompanhada por medidas hemodinâmicas diarias, atraves de cateteres implantados na aorta, VD e TP, alem de ecocardiogramas seriados a cada 24 horas, com medidas das espessuras do septo interventricular e dos ventriculos. Ao final das 96 horas, os animais foram mortos para remocao dos coracoes. Os ventriculos e o septo foram pesados separadamente. Foram colhidas biopsias musculares de cada câmara para analise da atividade da enzima conversora da angiotensina (ECA). Oito cabritos (idade e peso semelhantes) foram utilizados como controle para os pesos dos ventriculos e para a atividade da ECA. RESULTADOS: Observou-se um aumento do gradiente VD/TP (p=0,001), com consequente aumento da razao VD/VE (p=0,005) durante o tempo de sobrecarga sistolica. Ao fim do protocolo, a parede livre do VD apresentou aumento de espessura (p=0,002) e, consequentemente, um aumento do peso indexado (p=0,002). A analise da atividade da ECA revelou aumento somente no musculo do VD hipertrofiado (p=0,002). CONCLUSAO: O cateter balao foi eficiente em induzir a hipertrofia aguda do VD atraves do protocolo utilizado. Consequentemente, um aumento expressivo da atividade da ECA esta associado ao processo de hipertrofia miocardica induzida por sobrecarga pressorica.

Modelo experimental de bandagem ajustável do tronco pulmonar para preparo rápido do ventrículo

OBJETIVO: Um dispositivo de bandagem do tronco pulmonar (TP) com ajuste percutâneo foi desenvolvido com o objetivo de induzir a hipertrofia rápida do ventrículo subpulmonar. MATERIAL E MÉTODOS: Consiste de um manguito de silicone insuflável percutaneamente, através de um botão de silicone auto-selante. Os corações de 7 cabritos jovens (peso médio: 8,7 kg) foram submetidos à sobrecarga sistólica imposta pelo dispositivo e avaliados sob os aspectos hemodinâmicos, ecocardiográficos e morfológicos. Foram extraídas biópsias basais do miocárdio do ventrículo direito (VD) para análise microscópica (perímetro e área do miócito). O dispositivo foi implantado no TP. As pressões do VD, TP e aorta foram monitorizadas. Após convalescença, foi iniciado o protocolo de insuflação do dispositivo de bandagem do TP. Foi injetada água destilada no botão auto-selante (via percutânea), até que a pressão sistólica do VD atingisse 70% da pressão sistólica do VE. As avaliações ecocardiográfica e hemodinâmica foram realizadas a cada 24 horas. A sobrecarga sistólica do VD foi mantida por um período de 96 horas, com insuflações progressivas no limite máximo tolerado, a cada 24 horas. Após esse período, os animais foram sacrificados para análise morfológica dos corações. Outros 9 cabritos (peso médio: 7,7 kg) foram utilizados como grupo controle, para análise do peso do VD. RESULTADOS: Após 96 horas de sobrecarga sistólica do VD, foi observado um aumento do gradiente sistólico VD/TP de 10,1±4,3 mmHg para 60,0±11,0 mmHg e da pressão sistólica no VD de 22,4±4,1 mmHg para 71,0±10,0 mmHg (p<0,0001). O ecocardiograma revelou aumento da espessura muscular do VD, de 4,4±0,5 mm para 7,3±1,7 mm (p=0,001). Quando comparado ao grupo controle, houve um ganho de peso de 74% do VD submetido à sobrecarga sistólica (p<0,0001). À microscopia óptica, foi observado aumento de 27% no perímetro e de 69% na área dos miócitos (p=0,0001). CONCLUSÕES: O dispositivo proposto neste trabalho é efetivo e facilmente ajustável por via percutânea, possibilitando a hipertrofia do ventrículo subpulmonar em 96 horas de sobrecarga sistólica. A melhora na ajustabilidade da bandagem do TP poderá permitir melhores resultados da operação de Jatene em dois estágios, nos pacientes com transposição das grandes artérias.

Reversible pulmonary trunk banding with a balloon catheter: Assessment of rapid pulmonary ventricular hypertrophy

Objective: We sought to assess the rapid hypertrophy of the right ventricle of young goats submitted to progressive pressure load by a balloon catheter. Methods: The hearts of 6 young goats were assessed by means of echocardiography and cell morphology during and after right ventricular hypertrophy had been produced by a balloon catheter. Myocardial samples of the right ventricular outflow tract were harvested for microscopic studies. The external diameter of longitudinally sectioned myocytes was measured at the nucleus level. The volume density of mitochondria was also determined. A balloon catheter was then placed through the right ventricular outflow tract in the pulmonary trunk and progressively inflated every 2 days. Postoperative serial echocardiography was performed at intervals of 1 to 2 days. The animals were killed after 2 to 3 weeks of right ventricular training for morphologic analysis. Results: Under optical microscopy, there was a 20.5% increase in the mean diameter of the myocyte of the trained right ventricle. However, under electron microscopy, there was no significant change in the mean volume density of mitochondria from the trained right ventricle. Serial echocardiography showed equalization of the ventricular thickness over a short interval of 6 to 10 days of progressive balloon inflation. Conclusions: The balloon catheter permits the manipulation of the pressure load over the right ventricle, causing rapid hypertrophy in a 6- to 10-day period. This study suggests that nonsurgical preparation of the “pulmonary ventricle” in patients with transposition of great arteries with intact ventricular septum beyond the neonatal period could probably be accomplished within a very few days. (J Thorac Cardiovasc Surg 2000;120:66-72)

Modified arterial switch operation by spiral reconstruction of the great arteries in transposition

Background. Spiral relationship of the normally related great arteries (SRGA) has never been reconstructed in an arterial switch operation. Methods. From March 1998 to April 1999, 9 consecutive cases of transposition of the great arteries (TGA) family (from 2 days to 1.6 years old) underwent arterial switch operations with SRGA at our hospital. Two had a congenitally corrected TGA (plus atrial redirection). Lecompte maneuver was not used in all. The posterior wall of pulmonary trunk was not divided but three were reattached, two of whom had had previous pulmonary trunk banding. Thus the wall was shared between the great arteries facing each other. Results. All survived the operation. Supraaortic stenosis was balloon-dilated in 2 cases of early series, but technical modifications later were able to avoid it. Angiogram showed smooth flow into SRGA without upward and anterior tilting of the pulmonary bifurcation. All great and coronary arteries were patent. All were doing well on follow-up (16.5 ± 4.2 months). Conclusions. We concluded that the techniques to relocate the coronary arteries using common wall and in situ switch could also be applied to pulmonary arterial reconstruction, so that SRGA can be resumed in TGA.

Changing Patterns of Gene Expression in the Pulmonary Trunk-banded Rat Heart

A pressure-overload model in the rat by banding the pulmonary trunk (PT) was developed to investigate alterations in gene expression in left- and right-ventricular compartments during the transition from compensated right-ventricular (RV) hypertrophy to right heart failure. Right heart failure in rat is characterized by liver cirrhosis, hydrothorax and ascites. The diameter of constriction was found to determine the time course of heart failure development. Only the RV free wall and the right atrium increased in weight, without a difference between compensated and failing RV. An increase in circulating ANP revealed a hypertrophic response of the myocardium, while increased circulating ammonia levels discriminated between compensated hypertrophy and failure. As parameters for stress, fibrosis and Ca2+-handling, changes in the pattern and level of the mRNAs encoding atrial natriuretic peptide (ANP), collagenIIIα1, and sarcoplasmic endoplasmic reticular calcium ATPase 2 (SERCA2), phospholamban (PLB) and calsequestrin (CSQ) were studied by Northern blot andin situhybridization analyses. Pulmonary trunk banding resulted in an induction of ANP mRNA, a moderate increase in collagenIIIα1mRNA and a decrease in SERCA2 and PLB mRNA levels in both the left and right ventricles, but changes were most pronounced in the myocardium surrounding the RV cavity. Increased ammonia blood levels are a promising prognostic marker to detect the development of right heart failure.

Outcomes in seriously ill neonates with coarctation of the aorta

Among 326 severely symptomatic neonates with coarctation with or without ventricular septal defect, four died before an initial procedure was performed. Among the 322 undergoing an initial procedure, survival for at least 24 months was 84%; the hazard function for death was lower initially but more prolonged in patients without than in those with ventricular septal defect. Important mitral valve anomalies coexisted in 5% of patients, left ventricular hypoplasia in 5% (more commonly in patients without ventricular septal defect), narrowing of the left ventricular outflow tract in 9% (more common in patients without ventricular septal defect), and narrowing of the proximal arch in 1%; one or more of these anomalies was present in most patients without ventricular septal defect who died. Five percent of the 322 patients had more than one of these coexisting anomalies, and 8% had just one. The most commonly used technique of repair of the coarctation was resection and end-to-end anastomosis, but no technique was a risk factor for death by multivariable analysis. Extension of the area of resection so that the end-to-end anastomosis was proximal to the left subclavian artery but distal to the left common carotid artery did not increase risk; extensions beyond this, and in the case of patch graft repair, extensions proximal to the left subclavian artery, did increase risk. Patch graft repair was associated with the highest prevalence (21%) of reintervention to the coarctation repair. Among patients with coexisting moderate-sized or large ventricular septal defects, repair of the coarctation, pulmonary trunk banding, and subsequent repair of the defect were associated with the highest 2-year survival, 97% in those with single ventricular septal defect. The risk-adjusted outcomes in two institutions were less good than in all others.

Operative repair of coarctation of the aorta in infancy: Results with and without ventricular septal defect

Coarctation of the aorta (CA) presenting in infancy is a life-threatening condition, especially it associated with intracardlac left-to-right shunts. Between 1971 and 1980, 51 infants with symptomatic CA have been, diagnosed and treated. Ventricular septal defect (VD) was present in 18 patients and patent ductus arteriosus in 24. End-to-end repair was performed in 20 patients, 17 (85%) of whom were long-term survivors. Subclavian flap angioplasty repair was used in 28 patients, of whom 25 (89%) were long-term survivors. During long-term follow-up 6 patients (35%) who underwent end-to-end repair had recurrent CA, whereas only 3 patients (12%) who underwent subclavian flap angioplasty had recurrent CA (p <0.05). The mortality rate In patients with associated VSD was higher (4 of 18, 22%). Pulmonary trunk banding with subsequent VSD repair was associated with a better survival (13 of 14 patients, 90%) than when banding was not performed (2 of 5 patients) (p <0.05). These results suggest subclavian flap angioplasty is the preferred treatment for symptomatic CA occurring in infancy. Concomitant pulmonary trunk banding in patients with VSD can be performed with the expectation of a lower mortality at subsequent VSD repair.

High takeoff of the left main coronary artery from the pulmonary trunk: Potentially fatal combination with pulmonary trunk banding

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Production of externally controlled progressive pulmonic stenosis in the dog.

ARTICLESProduction of externally controlled progressive pulmonic stenosis in the dogS. P. Bishop, and C. R. ColeS. P. Bishop, and C. R. ColePublished Online:01 May 1969https://doi.org/10.1152/jappl.1969.26.5.659MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByMechanics of the left ventricular myocardial interstitium: effects of acute and chronic myocardial edemaKetaki V. Desai, Glen A. Laine, Randolph H. Stewart, Charles S. Cox, Christopher M. Quick, Steven J. Allen, and Uwe M. Fischer1 June 2008 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 294, No. 6Reversible pulmonary trunk banding. II. An experimental model for rapid pulmonary ventricular hypertrophyThe Journal of Thoracic and Cardiovascular Surgery, Vol. 124, No. 5Left ventricular dimensions and function during exercise in dogs with chronic right ventricular pressure overloadThe American Journal of Cardiology, Vol. 53, No. 8A model of delayed aortic coarctation employing arterial and venous catheters for chronic blood sampling in conscious dogsJournal of Pharmacological Methods, Vol. 8, No. 2Adrenal medulla denervation prevents stress-induced epinephrine plasma elevation and cardiac hypertrophyLife Sciences, Vol. 27, No. 24Epinephrine elevation in plasma parallels canine cardiac hypertrophyLife Sciences, Vol. 23, No. 19The amino acid composition of actin and myosin and Ca2+-activated myosin adenosine triphosphatase in chronic canine congestive heart failure.Circulation Research, Vol. 40, No. 2Myocardial necrosis, fibrosis, and DNA synthesis in experimental cardiac hypertrophy induced by sudden pressure overload.Circulation Research, Vol. 39, No. 2Comparison of mild vs severe pressure overload on the enzymatic activity of myosin in the canine ventriclesBiochemical Medicine, Vol. 14, No. 2Sarcolemmal and Sarcoplasmic Reticular ATPase Activities in the Falling Canine HeartCirculation Research, Vol. 29, No. 1 More from this issue > Volume 26Issue 5May 1969Pages 659-663 Copyright & PermissionsCopyright © 1969 the American Physiological Societyhttps://doi.org/10.1152/jappl.1969.26.5.659PubMed5781623History Published online 1 May 1969 Published in print 1 May 1969 Metrics