Key result
Aged Pgc1β−/− murine hearts showed greater atrial arrhythmogenicity, reduced maximal rates of AP depolarization, increased AP latencies, and reduced AP wavelengths compared to wild-type.
Population
Langendorff-perfused murine hearts from young and aged wild-type and peroxisome proliferative activated…
Comparison
Pgc1β−/− genotype and aging, subjected to S1S2… vs Wild-type (WT) genotype and young age
Design
Preclinical
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Establishes experimental models for metabolic atrial arrhythmogenesis; leaves open translation to human risk or therapy.
Aged Pgc1β−/− murine hearts exhibit increased atrial arrhythmogenicity driven by compromised action potential conduction and reduced wavelengths, providing an experimental model for pro-arrhythmic changes in chronic metabolic disease.
A 2017 study studied Atrial arrhythmias. Pgc1β−/− genotype and aging vs. Wild-type (WT) and young hearts was evaluated on Atrial arrhythmogenicity and electrophysiological properties (AP depolarization, latencies, APD90, wavelengths). Aged Pgc1β−/− murine hearts showed greater atrial arrhythmogenicity, reduced maximal rates of AP depolarization, increased AP latencies, and reduced AP wavelengths compared to wild-type.
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