Key result
Adaptation of the rat heart to hypertension-induced mechanical overload results in maladaptive gap junction connexin-43 remodeling and a significantly higher incidence of fatal arrhythmias.
Why the study?
Does hypertension-induced myocardial remodeling increase susceptibility to ventricular fibrillation via gap junction connexin-43 alterations in rat models?
Population
Rat heart tissues from spontaneous (SHR) and L-NAME models of hypertension
Comparison
Hypertension (spontaneous or L-NAME-induced) vs Normotensive rat hearts
Design
Preclinical
Authors
Loading...
May implicate connexin-43 remodeling in hypertensive arrhythmia risk; leaves open human translation and therapeutic targeting.
Does hypertension-induced myocardial remodeling increase susceptibility to ventricular fibrillation via gap junction connexin-43 alterations in rat models?
p-value: p=<0.05
Hypertension-induced mechanical overload in rat models leads to maladaptive gap junction connexin-43 remodeling, which promotes the development of fatal ventricular arrhythmias.
Fialová et al. (2008) studied Hypertension (n=56). Hypertension (Spontaneous or L-NAME induced) vs. Normotensive controls (WKY and Wistar rats) was evaluated on Incidence of sustained ventricular fibrillation (SVF) induced by low potassium perfusion (p=<0.05). Adaptation of the rat heart to hypertension-induced mechanical overload results in maladaptive gap junction connexin-43 remodeling and a significantly higher incidence of fatal arrhythmias.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: