Key result
Dynamic cardiomyoplasty increases LVEF by ~13% absolute in a canine heart failure model.
Why the study?
The effects of dynamic cardiomyoplasty on left ventricular systolic and diastolic function in chronic heart failure were evaluated to understand its potential benefits.
Does dynamic cardiomyoplasty improve indices of left ventricular systolic and diastolic function in a canine model of chronic heart failure?
Does dynamic cardiomyoplasty improve indices of left ventricular systolic and diastolic function in a canine model of chronic heart failure?
Absolute Event Rate: 31% vs 18.4%
p-value: p=<0.05
Dynamic cardiomyoplasty significantly improves indices of systolic and diastolic function in a doxorubicin-induced canine model of chronic heart failure.
May improve experimental HF models; leaves open clinical translation of dynamic cardiomyoplasty.
The effects of cardiomyoplasty were evaluated with multiple-gated equilibrium radionuclide angiocardiography and catheterization in a canine model of chronic heart failure. Doxorubicin was administered to 12 dogs at a dose of 1 mg/kg/wk intravenously for 10 weeks. Left ventricular ejection fraction was reduced from a mean of 53.6% +/- 3.4% to 33.5% +/- 2.3% preoperatively. Two dogs died of presumed arrhythmia during this period. Cardiomyoplasty with the left latissimus dorsi muscle was performed on 10 dogs. The muscle was wrapped around both the left and right ventricles. Five dogs died of infection or arrhythmia after the operation. Postoperatively the muscle remained unstimulated for 2 weeks to allow adhesion to the heart. After this period, the latissimus dorsi muscle was conditioned by a progressive stimulation protocol. After the muscle was conditioned, multiple-gated equilibrium radionuclide angiocardiography studies showed that left ventricular global ejection fraction was 18.4% +/- 7.2% at 0 volts (nonstimulation), 26.2% +/- 3.7% at 5-volt stimulation (p less than 0.05), and 31.0% +/- 5.4% at 10-volt stimulation (p less than 0.05). Regional ejection fractions in low lateral, apical, and low septal regions at 5 volts and 10 volts were higher than those at 0 volts (p less than 0.05). Regional wall motion (percent radial shortening) of the low lateral region was higher than that during nonstimulation (p less than 0.05). Peak emptying rate was 2.07 +/- 0.95 end-diastolic counts per second at 0-volt, 3.10 +/- 0.67 at 5-volt, and 3.34 +/- 0.89 at 10-volt stimulation (p less than 0.05). Peak filling rate was 1.81 +/- 0.52 end-diastolic counts per second at 0-volt, 2.67 +/- 1.18 at 5-volt, and 3.11 +/- 0.65 at 10-volt stimulation (p less than 0.05). Cardiac catheterization data showed a nonsignificant increase in left ventricular rate of pressure rise with increasing voltage (1302 +/- 355 mm Hg/sec at 0 volts, 1450 +/- 413 mm Hg/sec at 5 volts, and 1568 +/- 455 mm Hg/sec at 10 volts). Left ventricular systolic pressures were unchanged. End-diastolic pressures decreased (11.2 +/- 1.48 mm Hg at 0 volts, 10.4 +/- 2.30 mm Hg at 5 volts, and 9.6 +/- 1.52 at 10 volts; p less than 0.05). These data show that cardiomyoplasty can improve indices of systolic and diastolic function in a canine model of chronic heart failure.
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Justicz et al. (1992) studied Chronic heart failure (n=12). Dynamic cardiomyoplasty vs. 0 volts (nonstimulation) was evaluated on Left ventricular global ejection fraction (p=<0.05). In a canine model of chronic heart failure, dynamic cardiomyoplasty with 10-volt stimulation increased left ventricular global ejection fraction from 18.4% to 31.0% (p<0.05).
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