• Renato S Assad, Fernando A Atik, Fernanda S Oliveira, Miriam H Fonseca-Alaniz, Maria C D Abduch, Gustavo J J Silva, Gustavo G Favaro, Jose E Krieger, and Noedir A G Stolf.
• Heart Institute, University of São Paulo Medical School, São Paulo, Brazil. rsassad@cardiol.br
• J. Thorac. Cardiovasc. Surg. 2011 Nov 1;142(5):1108-13, 1113.e1.

ObjectiveIncreased myocardial glucose-6-phosphate dehydrogenase (G6PD) activity occurs in heart failure. This study compared G6PD activity in 2 protocols of right ventricle (RV) systolic overload in young goats.MethodsTwenty-seven goats were separated into 3 groups: sham (no overload), continuous (continuous systolic overload), and intermittent (four 12-hour periods of systolic overload paired with a 12-hour resting period). During a 96-hour protocol, systolic overload was adjusted to achieve a 0.7 RV/aortic pressure ratio. Echocardiographic and hemodynamic evaluations were performed before and after systolic overload every day postoperatively. After the study period, the animals were humanely killed for morphologic and G6PD tissue activity assessment.ResultsA 92.1% and 46.5% increase occurred in RV and septal mass, respectively, in the intermittent group compared with the sham group; continuous systolic overload resulted in a 37.2% increase in septal mass. A worsening RV myocardial performance index occurred in the continuous group at 72 hours and 96 hours, compared with the sham (P < .039) and intermittent groups at the end of the protocol (P < .001). Compared with the sham group, RV G6PD activity was elevated 130.1% in the continuous group (P = .012) and 39.8% in the intermittent group (P = .764).ConclusionsContinuous systolic overload for ventricle retraining causes RV dysfunction and upregulation of myocardial G6PD activity, which can elevate levels of free radicals by NADPH oxidase, an important mechanism in the pathophysiology of heart failure. Intermittent systolic overload promotes a more efficient RV hypertrophy, with better preservation of myocardial performance and and less exposure to hypertrophic triggers.Copyright © 2011 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.

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