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Ann Thorac Surg 2003;76:141-147
© 2003 The Society of Thoracic Surgeons

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Original article: cardiovascular

Ventricular constraint in severe heart failure halts decline in cardiovascular function associated with experimental dilated cardiomyopathy

^a Department of Cardiac Surgery, Austin and Repatriation Medical Centre, Heidelberg, Melbourne, Victoria, Australia
^b Baker Medical Research Institute, Prahran, Melbourne, Victoria, Australia
^c Acorn Cardiovascular, Inc, St. Paul, Minnesota, USA

Accepted for publication January 18, 2003.

^* Address reprint requests to Dr Raman, University of Chicago Hospital, Section of Cardiothoracic Surgery, 5841 S Maryland, Suite E-500, MC 5040, Chicago, IL 60637, USA.
e-mail: jraman{at}surgery.bsd.uchicago.edu

BACKGROUND: We have shown that passive ventricular constraint during moderate heart failure can halt progressive deterioration in cardiac function in an experimental model of ovine pacing induced heart failure (HF). We report on ventricular constraint in severe heart failure.

METHODS: Eighteen adult merino sheep were used. Severe heart failure was induced in two stages, ie, high rate ventricular pacing for 21 days to produce moderate HF and then for 42 days to induce severe HF. A custom-made polyester mesh cardiac support device ([CSD] Acorn Cardiovascular, St Paul, MN) was implanted snugly around both ventricles through a lower partial sternotomy in 9 sheep (group 1). Rapid ventricular pacing was continued for a further 28 days in all animals to induce advanced HF. Cardiovascular functional indicators were determined using echocardiography and a submaximal treadmill exercise protocol at base line, moderate, severe, and advanced stages. The 9 sheep in group 2 were used as controls.

RESULTS: Cardiovascular function was significantly depressed in all animals in advanced heart failure compared with base line, with left ventricular ejection fraction (LVEF) falling from 50% to 25% (p < 0.05) and LV +dp/dt_(max) declining from 1,777 to 1,243 (p < 0.05). However after CSD implantation cardiovascular function during exercise improved significantly despite ongoing rapid pacing, with LVEF increasing to 30% and LV +dp/dt to 1,499 (p < 0.05) in group 1. There were no significant changes in left ventricular long axis area (157 to 151 cm²) and short axis (6.8 to 6.1 cm) dimensions at the termination of pacing compared with those at time of CSD implant. Mitral regurgitation improved slightly from 2.5 to 2.19 after containment (p < 0.05) in group 1 but increased to 2.83 in group 2.

CONCLUSIONS: Ventricular constraint in advanced heart failure with a custom-made polyester mesh device halted the decline in cardiac function seen in untreated animals with this pacing-induced animal model of heart failure. These results indicate potential clinical implications for ventricular containment in the treatment of end-stage heart failure.

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