Why the study?
Does phospholamban inhibition via rAAV-S16EPLN gene transfer improve cardiac function and prevent remodeling in rats with established post-myocardial infarction heart failure?
Population
34 adult male Sprague-Dawley rats with established heart failure 5 weeks after myocardial infarction
Comparison
S16EPLN delivered by transcoronary gene transfer… vs Saline injection delivered by the same…
Design
Preclinical, Animals with an infarct size between 30% and 40% were randomized…
Follow-up
6 months
Key result
In rats with established heart failure after myocardial infarction, rAAV-mediated gene transfer of S16EPLN significantly improved left ventricular ejection fraction (36.4% vs 25.8%) and suppressed ventricular dilation at 6 months compared to saline.
Authors
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May support phospholamban-targeted gene therapy development; leaves open translation from rodent models to clinical use.
Does phospholamban inhibition via rAAV-S16EPLN gene transfer improve cardiac function and prevent remodeling in rats with established post-myocardial infarction heart failure?
Absolute Event Rate: 36.4% vs 25.8%
p-value: p=<0.05
Phospholamban inhibition via rAAV-mediated S16EPLN gene transfer improves cardiac function and attenuates pathological remodeling in a rat model of established post-MI heart failure.
Iwanaga et al. (2004) studied Heart failure after myocardial infarction (n=34). rAAV-S16EPLN gene transfer vs. Saline injection was evaluated on Left ventricular ejection fraction (LVEF) at 6 months (p=<0.05). In rats with established heart failure after myocardial infarction, rAAV-mediated gene transfer of S16EPLN significantly improved left ventricular ejection fraction (36.4% vs 25.8%) and suppressed ventricular dilation at 6 months compared to saline.
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