Key result
Ventricular tachypacing-induced congestive heart failure caused substantially more fibrosis in the left atrium (10%) than in the left ventricle (0.4%, P<0.01) at 5 weeks.
Population
Dogs with congestive heart failure induced by ventricular tachypacing (220-240/min)
Comparison
Ventricular tachypacing for 24 h, 1, 2 or 5 weeks vs 0 h (control)
Design
Preclinical
Follow-up
up to 5 weeks
Authors
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Greater atrial fibrosis and signaling in experimental CHF cautions against uniform remodeling assumptions; leaves open targeted atrial therapies in patients.
Absolute Event Rate: 10% vs 0.4%
p-value: p=<0.01
In a canine model of tachypacing-induced CHF, atrial remodeling (fibrosis, apoptosis, inflammation) occurs faster and more extensively than ventricular remodeling.
Nader Hanna (2004) studied Congestive heart failure. Ventricular tachypacing vs. Control (0 h) or left ventricle was evaluated on Fibrosis (p=<0.01). Ventricular tachypacing-induced congestive heart failure caused substantially more fibrosis in the left atrium (10%) than in the left ventricle (0.4%, P<0.01) at 5 weeks.
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