Mechanical effects on arrhythmogenesis: from pipette to patient

• Published in: Progress in Biophysics and Molecular Biology 2003-05, Vol.82 (1), p.187-195
• Main Authors: Janse, Michiel J, Coronel, Ruben, Wilms-Schopman, Francien J.G, de Groot, Joris R
• Format: Article
• Language: English
• Subjects: 1B arrhythmias; Acute and chronic stretch; Animals; Arrhythmias, Cardiac - etiology; Arrhythmias, Cardiac - pathology; Coronary Disease; Electrophysiology; Humans; Hypertrophy; Ion Channels - physiology; Ischaemia; Myocardial Ischemia; Pressure; Reentry; Tachycardia, Ventricular - pathology; Time Factors
• ISSN: 0079-6107; 1873-1732
• DOI: 10.1016/S0079-6107(03)00015-4

Mechanical stimuli delivered to the precordium can, if strong enough and timed at the beginning of the T-wave, induce ventricular premature beats or runs of ventricular tachycardia and even fibrillation. On the other hand, there are reports that a properly timed “chest thump” can terminate ventricular tachycardia, or can act as pacemaker stimuli during an episode of asystole. It is likely that in these cases mechanical energy is translated to an electrical stimulus. There are more subtle ways in which mechanical stimuli, mediated by stretch, can exert electrophysiological effects, and the most common name to describe these effects is mechanoelectrical feedback. Most studies have concentrated on acute stretch or dilatation, while the effects of chronic stretch, which may clinically be more important, are difficult to evaluate since they are accompanied by other factors, such as hypertrophy, heart failure, fibrosis, neurohumeral disturbances, and electrolyte abnormalities, all of which have arrhythmogenic effects. There are a number of ion channels that are activated following stretch. Stretch during diastole usually leads to a depolarization, resembling a delayed afterdepolarization, which may reach threshold and initiate a ventricular premature beat. Stretch during systole usually shortens the action potential, but action potential prolongation, resulting in early afterdepolarizations has been described as well. The arrhythmias during acute myocardial ischaemia occur in two phases: the 1A phase between 2 and 10 min following coronary artery occlusion, and the 1B phase between 18 and 30 min. Experiments will be described, indicating that the ventricular premature beats of the 1B phase, which may induce ventricular fibrillation, are caused by stretch of the border between ischaemic and normal myocardium. Briefly, 1B arrhythmias are much less frequent in the isolated perfused heart than in the heart in situ, but in working, ejecting isolated hearts, the number of 1B arrhythmias is similar to those in the in situ heart. The ventricular premature beats have a focal origin at the border, and they occur more often after a pause-induced potentiated contraction.