Key result
Advanced heart failure in cardiomyopathic hamsters is associated with a decline in junctional conductance and impulse propagation, contributing to anisotropic conduction and cardiac arrhythmias.
Extends preclinical insights on conduction defects in HF models; leaves open relevance to human arrhythmia therapies.
Cell coupling and impulse propagation were investigated in the ventricle of cardiomyopathic hamsters at an advanced stage of heart failure. An appreciable decline in junctional conductance was found, a phenomenon in part related to activation of the plasma and cardiac renin-angiotensin systems. Decreased expression of connexin43 or an alteration of junctional proteins also might be implicated in the decreased cell coupling. Morphologic abnormalities such as fibrosis, necrosis, and rupture of cell contacts contribute to the decline of conduction velocity or to the blockade of impulse propagation in some areas of the ventricle, creating the conditions for anisotropic conduction and cardiac arrhythmias. The decrease in membrane potential found in myopathic cells is related in part to depression of Na-KATPase activity, and the lack of action of beta-adrenergic agonists on junctional conductance is explained by down-regulation of beta receptors and an abnormality of adenyl cyclase.
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Walmor C. De Mello (1999) studied Heart failure. Advanced stage of heart failure was evaluated on Cell coupling and impulse propagation. Advanced heart failure in cardiomyopathic hamsters is associated with a decline in junctional conductance and impulse propagation, contributing to anisotropic conduction and cardiac arrhythmias.
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