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.
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.
Authors: Pavel Hála; Mikuláš Mlček; Petr Ošťádal; David Janák; Michaela Popková; Tomáš Bouček; Stanislav Lacko; Jaroslav Kudlička; Petr Neužil; Otomar Kittnar Journal: J Vis Exp Date: 2018-02-17 Impact factor: 1.355
Authors: Pavel Hála; Mikuláš Mlček; Petr Ošťádal; Michaela Popková; David Janák; Tomáš Bouček; Stanislav Lacko; Jaroslav Kudlička; Petr Neužil; Otomar Kittnar Journal: J Transl Med Date: 2020-02-13 Impact factor: 5.531