Cell coupling and impulse propagation in the failing heart

Cell coupling and impulse propagation were investigated in the ventricle of cardiomyopathic hamsters at an advanced stage of heart failure. An appreci able decline in junctional conductance was found, a phenomenon in part rela ted to activation of the plasma and cardiac renin-angiotensin systems. Decr eased expression of connexin43 or an alteration of junctional proteins also might be implicated in the decreased cell coupling, Morphologic abnormalit ies such as fibrosis, necrosis, and rupture of cell contacts contribute to the decline of conduction velocity or to the blockade of impulse propagatio n in some areas of the ventricle, creating the conditions for anisotropic c onduction 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 conducta nce is explained by down-regulation of beta receptors and an abnormality of adenyl cyclase.