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J Thorac Cardiovasc Surg 2002;123:544-549
© 2002 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology (CSP)

Induction and maintenance of an experimental model of severe cardiomyopathy with a novel protocol of rapid ventricular pacing

From the Department of Biomedical Engineering,^a Lerner Research Institute, the Departments of Thoracic and Cardiovascular Surgery,^b and Cardiology,^c George M. and Linda H. Kaufman Center for Heart Failure, and the Department of Biostatistics and Epidemiology,^d The Cleveland Clinic Foundation, Cleveland, Ohio.

This study was funded by The Kaufman Center for Heart Failure and Myocor, Inc (Maple Grove, Minn).

Received for publication March 9, 2001; revisions requested April 30, 2001; revisions received June 20, 2001; accepted for publication June 26, 2001. Address for reprints: Patrick M. McCarthy, MD, Department of Thoracic and Cardiovascular Surgery/F25, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195 (E-mail: mccartp{at}ccf.org).

Objective: An animal model of chronic severe heart failure is needed to evaluate new mechanical devices, surgical procedures, and medical therapies. The purpose of this study was to evaluate a unique new model of severe heart failure developed by means of a novel protocol of rapid ventricular pacing.
Methods: Heart failure was induced in 8 mongrel dogs by means of rapid ventricular pacing (230 beats/min) for 4 weeks. After a sham operation, maintenance pacing at a reduced rate (190 beats/min) was continued for another 4 weeks.
Results: Left ventricular systolic function was significantly reduced at week 4 and remained low at week 8, including the slope of the end-systolic pressure-volume relationship (2.4 ± 1.0 vs 0.7 ± 0.2 vs 0.8 ± 0.3 mm Hg/mL [baseline vs week 4 vs week 8, respectively]), ejection fraction (63% ± 5% vs 28% ± 7% vs 33% ± 5%), and cardiac output (3.1 ± 0.7 vs 2.0 ± 0.3 vs 2.2 ± 0.7 L/min). Significant ventricular remodeling changes took place with increased ventricular volumes and circumferential wall stress, which were stable between weeks 4 and 8. Serum catecholamine and atrial natriuretic polypeptide levels also increased from baseline but stabilized between weeks 4 and 8. The end-diastolic pressure-volume relationship also showed stable diastolic function between weeks 4 and 8.
Conclusions: Induction pacing at 230 beats/min readily created severe heart failure in all animals, and a new technique of maintenance pacing provided a consistent model of severe heart failure. This model can be used to study a variety of new interventions for heart failure.

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