Key result
In pacing-induced heart failure, beta-adrenergic stimulation showed a blunted ability to augment contractility but maintained its ability to shorten relaxation.
Why the study?
Does beta adrenergic stimulation augment contractility and shorten relaxation in a canine model of pacing-induced heart failure and recovery?
Population
8 dogs with pacing-induced severe heart failure (paced at 250 beats/min for 3 weeks)
Comparison
Beta adrenergic stimulation during heart failure… vs Baseline measurements without beta adrenergic…
Design
Preclinical
Follow-up
3 weeks of pacing followed by 4 weeks of recovery
Authors
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Should not yet alter beta-adrenergic management in HF; leaves open whether contractility-relaxation dissociation persists in patients.
Does beta adrenergic stimulation augment contractility and shorten relaxation in a canine model of pacing-induced heart failure and recovery?
p-value: p=<0.01
In pacing-induced heart failure, there is a dissociation between the recovery of contractility (which normalizes) and relaxation (which remains abnormal), as well as a differential response to beta-adrenergic stimulation.
Moe et al. (1994) studied Pacing induced heart failure (n=8). Beta adrenergic stimulation (dobutamine) vs. Without beta adrenergic stimulation was evaluated on Left ventricular contractility (dP/dt) and relaxation (tau) (p=<0.01). In pacing-induced heart failure, beta-adrenergic stimulation showed a blunted ability to augment contractility but maintained its ability to shorten relaxation.
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