Abstract
Frequent premature ventricular contractions (PVCs) are prevalent in adult patients and commonly associated with left ventricular (LV) systolic dysfunction. Animal translational models of PVC- induced cardiomyopathy (PVC-CM) are reproducible and allow for study of specific adaptations resulting from frequent PVCs. Our PVC-CM canine model has shown LV eccentric hypertrophy and downregulation of key Ca2+ handling proteins. We performed subsequent studies to understand cellular and chemical mediators involved in LV remodeling observed in PVC-CM.
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