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Myocardial mechanics and arrhythmia
1Department of Physiology, Charing Cross and Westminster Medical School, London, England.
Insights
Mechanoelectric feedback, where mechanical changes influence electrical activity, may explain arrhythmias in heart failure and ischemia. This mechanism offers a new therapeutic target for ventricular arrhythmias.
Area of Science:
- Cardiology
- Electrophysiology
- Cardiac Mechanics
Background:
- The precise cause of ectopic beats and lethal arrhythmias in acute myocardial ischemia and failure remains unclear.
- Current understanding often attributes electrophysiological changes solely to ischemic biochemical alterations, limiting therapeutic progress.
- Ventricular fibrillation control has seen slow progress, suggesting a need for alternative explanations.
Purpose of the Study:
- To explore the role of mechanoelectric feedback in initiating arrhythmias during myocardial ischemia and failure.
- To investigate whether mechanical changes, rather than solely biochemical ones, drive electrophysiological alterations.
- To propose mechanoelectric feedback as a potential therapeutic target for cardiac arrhythmias.
Main Methods:
- Reviewing evidence for mechanoelectric feedback in cardiac muscle.
- Analyzing the prevalence of mechanical changes in ischemia and heart failure.
- Correlating mechanical dysfunction with arrhythmia severity in pathological conditions.
Main Results:
- Accumulating evidence suggests mechanical changes can initiate electrophysiological alterations via mechanoelectric feedback.
- Mechanical changes are common in myocardial ischemia and failure.
- Arrhythmias in some conditions correlate with mechanical dysfunction, independent of etiology.
Conclusions:
- Mechanoelectric feedback may be a key mechanism underlying arrhythmias in myocardial ischemia and failure.
- This feedback system, potentially intrinsic to myocardium, becomes unstable during pathology, leading to arrhythmias.
- Targeting mechanoelectric feedback presents a novel therapeutic strategy for managing ventricular arrhythmias.
Abstract:
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.