Key result
Upregulating SERCA2a via gene delivery in a sheep model of ischemic mitral regurgitation maintained preload-recruitable stroke work (8% vs 42% decrease; P<0.001) and reduced left ventricular volume.
Why the study?
Does percutaneous gene delivery of SERCA2a inhibit ventricular remodeling in a sheep model of ischemic mitral regurgitation?
Population
12 sheep with a surgical model of apical myocardial infarction and a shunt between the left ventricle and…
Comparison
Percutaneous gene delivery of adeno-associated… vs Percutaneous gene delivery of a reporter gene
Design
Preclinical
Follow-up
3 months
Authors
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Should not alter clinical management; leaves open translation of SERCA2a gene therapy to human ischemic mitral regurgitation.
Does percutaneous gene delivery of SERCA2a inhibit ventricular remodeling in a sheep model of ischemic mitral regurgitation?
Absolute Event Rate: 8% vs 42%
p-value: p=<0.001
In a sheep model of ischemic mitral regurgitation, upregulating SERCA2a via gene delivery improved contractility and reduced ventricular remodeling.
Beeri et al. (2010) studied Ischemic mitral regurgitation (n=12). Adeno-associated virus 6 (AAV6) carrying SERCA2a vs. Reporter gene was evaluated on Decrease in preload-recruitable stroke work at 3 months (p=<0.001). Upregulating SERCA2a via gene delivery in a sheep model of ischemic mitral regurgitation maintained preload-recruitable stroke work (8% vs 42% decrease; P<0.001) and reduced left ventricular volume.
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