Key result
Mechanoelectric feedback, where mechanical changes in ventricular muscle alter its electrical properties, may drive arrhythmias in myocardial ischemia and failure, offering a new therapeutic avenue.
The concept of mechanoelectric feedback suggests that mechanical changes in the myocardium can initiate electrophysiological changes, providing a potential new avenue for understanding and treating arrhythmias.
The initiating cause of the first ectopic beat and its precipitation of sustained lethal arrhythmia in acute myocardial ischemia is not clear. Comparable uncertainties surround sudden death in myocardial failure. Progress in control of ventricular fibrillation has been slow, perhaps because diagnosis and treatment have been based on the premise that ischemic biochemical changes solely cause the alterations in electrophysiological behavior. Alternative approaches need exploration. Evidence that mechanical changes can initiate electrophysiological changes by a process sometimes referred to as "mechanoelectric feedback" is accumulating. It operates when any primary mechanical change in ventricular muscle, e.g., contraction produces a change in its electrical properties. Mechanical changes are prevalent in ischemia and cardiac failure. If mechanoelectric feedback operates here, it is not surprising that arrhythmias in some of these pathologies parallel the degree of mechanical myocardial dysfunction rather than electrophysiological changes, independent of etiology. This mechanoelectric feedback system may exist as an intrinsic property of normal myocardium, providing a feedback control of activation processes at both the cellular and gross levels. Its disruption during pathological events produces instability in the system and thus ventricular arrhythmia. This concept provides a new potential avenue for arrhythmia therapy.
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Lab et al. (1991) conducted a review in Arrhythmia in acute myocardial ischemia and cardiac failure. Mechanoelectric feedback was evaluated. Mechanoelectric feedback, where mechanical changes in ventricular muscle alter its electrical properties, may drive arrhythmias in myocardial ischemia and failure, offering a new therapeutic avenue.
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