Efficacy of the Acorn Cardiac Support Device in animals with heart failure secondary to high rate pacing.

AIM: To utilise an ovine model of tachycardia induced progressive dilated cardiomyopathy and heart failure to investigate the efficacy of passive ventricular constraint with the Acorn cardiac support device as a heart failure treatment. METHODS: (a) Moderate heart failure was produced in 16 sheep by pacing for 3 weeks. Half were implanted and half sham implanted with the CSD. Pacing continued at a higher rate for an additional 3 weeks. Cardiac function was assessed by echocardiography and manometry. (b) Moderate heart failure was produced (as above) in 27 sheep, 9 were implanted with CSD, pacing was restarted for 4 weeks, the initial CSD implants were terminated and another 9 animals were CSD implanted (severe heart failure), pacing was restarted in the remaining 18 animals for an additional 4 weeks (total 12 weeks) and then all animals were terminated. Cardiac function was assessed using echocardiography and treadmill exercise testing. RESULTS: (a) After 6 weeks of rapid pacing CSD implant animals had significantly better cardiac function both when compared with pre implant values and with non-implanted animals at termination. (b) CSD implantation at both moderate and severe failure resulted in significant improvements in cardiac function both when compared with pre implant values and with non-implanted animals at termination. When compared to pre implant values the improvement was greatest in severe implant animals. CONCLUSION: In this ovine model of tachycardia induced progressive heart failure, CSD implantation in either moderate or severe heart failure resulted in improved cardiac function, reduced left ventricular volume and mitral regurgitation both when compared with function at time of implant and with non implanted control animals.

Percutaneous mitral annular reduction provides continued benefit in an ovine model of dilated cardiomyopathy.

BACKGROUND: Functional mitral valve regurgitation plays a key role in the symptomatic severity and progression of heart failure. In an ovine model of dilated cardiomyopathy, we examined the chronic functional consequences of mitral regurgitation reduction using a recently developed novel percutaneous mitral annular reduction (PMAR) device. METHODS AND RESULTS: Fourteen adult sheep were paced right ventricularly at 180 to 190 bpm for 5 weeks, leading to the development of moderate mitral valve regurgitation. After echocardiographic, hemodynamic, and neurohormonal analysis, 9 animals underwent PMAR. All animals were subsequently paced for another 28 days, and a final echocardiographic and hemodynamic study was conducted. Animals that had undergone PMAR showed significantly increased negative and positive dP/dt, whereas pulmonary capillary wedge pressure and mitral valve regurgitation were significantly reduced compared with those at device implant despite continued pacing. In conjunction, significant improvements in plasma norepinephrine and brain natriuretic peptide were apparent. CONCLUSIONS: The application of PMAR in animals with pacing-induced dilated cardiomyopathy and functional mitral valve regurgitation resulted in continued improvements in hemodynamic and neurohormonal parameters.

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

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 cm(2)) 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.

An ovine model of tachycardia-induced degenerative dilated cardiomyopathy and heart failure with prolonged onset.

BACKGROUND: The aim of this study was to develop a model of long-term progressive heart failure (HF). METHODS AND RESULTS: A cardiac output flowprobe was implanted on the pulmonary artery of 9 adult sheep weighing 40 to 50 kg. Rapid ventricular pacing for 21 days at 160 to 190 bpm (rate A) resulted in moderate HF. Animals were then paced at 205 to 215 bpm (rate B) for 42 days (severe HF) and for 28 days at rate B (advanced HF). Data were collected at baseline and moderate, severe, and advanced HF during submaximal exercise testing and by transthoracic echocardiography in sinus rhythm. There were marked increases in left ventricular (LV) area, mitral valve regurgitation, and LV end-diastolic pressure and decreases in LV wall thickness, LV ejection fraction, positive and negative dP/dt(max), and positive (dP/dt(max))/P throughout the pacing protocol. CONCLUSIONS: This ovine HF model incorporates the progressive nature of human HF and allows examination of both structural changes and hemodynamic parameters of HF during and after exercise challenge.