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Right ventricular failure secondary to chronic overload in congenital heart disease: an experimental model for therapeutic innovation.
J Thorac Cardiovasc Surg. 2010 May; 139(5):1197-204, 1204.e1.JT

Abstract

OBJECTIVE

Mortality and morbidity related to right ventricular failure remain a problem for the long-term outcome of congenital heart diseases. Therapeutic innovation requires establishing an animal model reproducing right ventricular dysfunction secondary to chronic pressure-volume overload.

METHODS

Right ventricular tract enlargement by transvalvular patch and pulmonary artery banding were created in 2-month-old piglets (n = 6) to mimic repaired tetralogy of Fallot. Age-matched piglets were used as controls (n = 5). Right ventricular function was evaluated at baseline and 3 and 4 months of follow-up by hemodynamic parameters and electrocardiography. Right ventricular tissue remodeling was characterized using cellular electrophysiologic and histologic analyses.

RESULTS

Four months after surgery, right ventricular peak pressure increased to 75% of systemic pressure and pulmonary regurgitation significantly progressed, end-systolic and end-diastolic volumes significantly increased, and efficient ejection fraction significantly decreased compared with controls. At 3 months, the slope of the end-systolic pressure-volume relationship was significantly elevated compared with baseline and controls; a significant rightward shift of the slope, returning to the baseline value, was observed at 4 months, whereas stroke work progressed at each step and was significantly higher than in controls. Four months after surgery, QRS duration was significantly prolonged as action potential duration. Significant fibrosis and myocyte hypertrophy without myolysis and inflammation were observed in the operated group at 4 months.

CONCLUSION

Various aspects of early right ventricular remodeling were analyzed in this model. This model reproduced evolving right ventricular alterations secondary to chronic volumetric and barometric overload, as observed in repaired tetralogy of Fallot with usual sequelae, and can be used for therapeutic innovation.

Authors+Show Affiliations

Département de Recherche Médicale, CNRS UMR 8162, Centre Chirurgical Marie Lannelongue, Le Plessis Robinson, France. v.lambert@ccml.frNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20412956

Citation

Lambert, Virginie, et al. "Right Ventricular Failure Secondary to Chronic Overload in Congenital Heart Disease: an Experimental Model for Therapeutic Innovation." The Journal of Thoracic and Cardiovascular Surgery, vol. 139, no. 5, 2010, pp. 1197-204, 1204.e1.
Lambert V, Capderou A, Le Bret E, et al. Right ventricular failure secondary to chronic overload in congenital heart disease: an experimental model for therapeutic innovation. J Thorac Cardiovasc Surg. 2010;139(5):1197-204, 1204.e1.
Lambert, V., Capderou, A., Le Bret, E., Rücker-Martin, C., Deroubaix, E., Gouadon, E., Raymond, N., Stos, B., Serraf, A., & Renaud, J. F. (2010). Right ventricular failure secondary to chronic overload in congenital heart disease: an experimental model for therapeutic innovation. The Journal of Thoracic and Cardiovascular Surgery, 139(5), 1197-204, e1. https://doi.org/10.1016/j.jtcvs.2009.11.028
Lambert V, et al. Right Ventricular Failure Secondary to Chronic Overload in Congenital Heart Disease: an Experimental Model for Therapeutic Innovation. J Thorac Cardiovasc Surg. 2010;139(5):1197-204, 1204.e1. PubMed PMID: 20412956.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Right ventricular failure secondary to chronic overload in congenital heart disease: an experimental model for therapeutic innovation. AU - Lambert,Virginie, AU - Capderou,André, AU - Le Bret,Emmanuel, AU - Rücker-Martin,Catherine, AU - Deroubaix,Edith, AU - Gouadon,Elodie, AU - Raymond,Nicolas, AU - Stos,Bertrand, AU - Serraf,Alain, AU - Renaud,Jean-François, PY - 2009/06/19/received PY - 2009/10/07/revised PY - 2009/11/14/accepted PY - 2010/4/24/entrez PY - 2010/4/24/pubmed PY - 2010/5/7/medline SP - 1197-204, 1204.e1 JF - The Journal of thoracic and cardiovascular surgery JO - J Thorac Cardiovasc Surg VL - 139 IS - 5 N2 - OBJECTIVE: Mortality and morbidity related to right ventricular failure remain a problem for the long-term outcome of congenital heart diseases. Therapeutic innovation requires establishing an animal model reproducing right ventricular dysfunction secondary to chronic pressure-volume overload. METHODS: Right ventricular tract enlargement by transvalvular patch and pulmonary artery banding were created in 2-month-old piglets (n = 6) to mimic repaired tetralogy of Fallot. Age-matched piglets were used as controls (n = 5). Right ventricular function was evaluated at baseline and 3 and 4 months of follow-up by hemodynamic parameters and electrocardiography. Right ventricular tissue remodeling was characterized using cellular electrophysiologic and histologic analyses. RESULTS: Four months after surgery, right ventricular peak pressure increased to 75% of systemic pressure and pulmonary regurgitation significantly progressed, end-systolic and end-diastolic volumes significantly increased, and efficient ejection fraction significantly decreased compared with controls. At 3 months, the slope of the end-systolic pressure-volume relationship was significantly elevated compared with baseline and controls; a significant rightward shift of the slope, returning to the baseline value, was observed at 4 months, whereas stroke work progressed at each step and was significantly higher than in controls. Four months after surgery, QRS duration was significantly prolonged as action potential duration. Significant fibrosis and myocyte hypertrophy without myolysis and inflammation were observed in the operated group at 4 months. CONCLUSION: Various aspects of early right ventricular remodeling were analyzed in this model. This model reproduced evolving right ventricular alterations secondary to chronic volumetric and barometric overload, as observed in repaired tetralogy of Fallot with usual sequelae, and can be used for therapeutic innovation. SN - 1097-685X UR - https://www.unboundmedicine.com/medline/citation/20412956/Right_ventricular_failure_secondary_to_chronic_overload_in_congenital_heart_disease:_an_experimental_model_for_therapeutic_innovation_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-5223(09)01484-6 DB - PRIME DP - Unbound Medicine ER -