title: Arrhythmias in patients with mechanical ventricular dysfunction and myocardial stretch: role of mechano-electric feedback.
abstract: Patients with dilated cardiomyopathy, ventricular volume or pressure overload, or dysynergistic ventricular contraction and relaxation are prone to develop severe ventricular arrhythmias. In these patients it has been suggested that the abnormal mechanics of contraction can disturb 'mechano-electric feedback', also known as 'contraction-excitation feedback', which is defined as the development of electrophysiological changes during or after changes in mechanical loading. This electrical instability, expressed by significant changes in ventricular repolarization and refractoriness and by the development of afterdepolarizations, has been variously reported in isolated tissues and isolated ventricles as well as in hearts in vivo. Furthermore, it is known that many patients with supraventricular tachycardia but otherwise structurally normal hearts can develop atrial fibrillation and that atrial arrhythmias frequently occur in the setting of acute or chronic increases in atrial size and pressure. It is possible that changes in atrial load directly alter the electrophysiological properties of the atrium by an analogue mechanism of contraction-excitation feedback. This paper reviews the literature concerning mechanoelectric feedback involvement in rhythm disorders, with the aim of investigating, through basic and clinical research, the clinical and therapeutic implications.
authors.affiliation: Seconda Università degli Studi di Napoli, Facoltà di Medicina e Chirurgia, Istituto Medico Chirurgico di Cardiologia, Italy. cmone@mbox.vol.it
authors.forename: B
authors.initials: B
authors.lastname: Sarubbi
authors.forename: V
authors.initials: V
authors.lastname: Ducceschi
authors.forename: L
authors.initials: L
authors.lastname: Santangelo
authors.forename: A
authors.initials: A
authors.lastname: Iacono
mesh_terms: D019571:Arrhythmogenic Right Ventricular Dysplasia; D009202:Cardiomyopathies / Q000209:etiology* / Q000503:physiopathology; D005246:Feedback; D006321:Heart / Q000503:physiopathology; D006801:Humans; D018497:Ventricular Dysfunction, Right / Q000150:complications / Q000503:physiopathology*