title: [Electrophysiological changes in the failing myocardium].
abstract: Contraction-excitation feedback is defined as a change in the mechanical state that precedes or alters the transmembrane electrical potential. The latter could be an important electrophysiologic disorder in patients with cardiac failure since the electrophysiological changes may be induced by alterations in ventricular size, pressure or factors common to all types of congestive heart failure, regardless of aetiology. A stretch of the ventricular myocardium caused (1) a shortening of the action potential duration (APD), (2) a decrease in the resting potential (RP) and (3) the early or delayed after-depolarization that culminated in the triggered activity. Failing myocardium without ventricular hypertrophy also showed (1) a reduction in the RP and the action potential upstroke velocity and (2) APD shortening. In contrast, the majority of investigators have found a significant lengthening of the APD in the hypertrophied myocardium. These electrophysiologic changes shown in the failing myocardium with or without hypertrophy and in the mechanically stretched myocardium may be a possible substrate for the genesis of the reentrant circuit and the early or delayed afterdepolarizations, leading to ventricular arrhythmia.
authors.affiliation: Department of Physiology, Kanazawa Medical University.
authors.forename: S
authors.initials: S
authors.lastname: Imanishi
authors.forename: M
authors.initials: M
authors.lastname: Arita
mesh_terms: D000200:Action Potentials; D000818:Animals; D002118:Calcium / Q000378:metabolism / Q000502:physiology; D004594:Electrophysiology; D005246:Feedback; D006325:Heart Atria / Q000503:physiopathology; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D066298:In Vitro Techniques; D007473:Ion Channels / Q000378:metabolism / Q000502:physiology; D009200:Myocardial Contraction
chemical_list: D007473:Ion Channels; D002118:Calcium