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Optical Mapping of the Effects of Mechanoelectric Transduction

Cardiac mechanoelectric transduction (or feedback) refers to the effects that mechanical events can have on the electrical activity of myocardial cells (i.e., the action potential). Mechanical forces could be the result of cell contraction or externally applied mechanical stimulus at the cell (stretching) or tissue level (atrial or ventricular dilation). We often think about electromechanical interactions occurring in a cell as a unidirectional pathway, the excitation-contraction coupling pathway. Electrical activation of cardiac cells leads to activation of the L-type calcium channel and to entry of calcium ions in the cell that in turn triggers further release of calcium from the sarcoplasmic reticulum. Binding of calcium to troponin allows the interaction of actin and myosin that causes contraction. But there is now compelling evidence that the electromechanical pathway is, in fact, bidirectional, and that mechanical forces may influence the electrophysiology of cardiac cells.1-5 The major cellular mechanism of mechanoelectric transduction is the presence of mechanosensitive (or stretch-activated) ionic channels in the cell membrane.6-9 Mechanosensitive channels change their permeability in response to membrane tension and thus could affect the action potential of excitable cells. Mechanosensitive ion channels are present in many biologic systems, including ventricular myocytes,10 where these channels are selective to K+ or nonspecific cations.11 A second cellular mechanism of mechanoelectric transduction results from changes in intracellular calcium during contraction that could affect the action potential by modulating the function of calcium-dependent ionic channels.12 Effects of mechanoelectric transduction have been reported not only at the cellular level but also at the organ level experimentally and in humans.13,14 The occurrence of ventricular arrhythmias in patients with congestive heart failure and other ventricular mechanical dysfunctions indicates that mechanoelectric transduction may play a role in arrhythmogenesis.13,15 Gathering the evidence supporting mechanoelectric transduction in cardiac tissue has been (and still is) traumatic because the required physical contact between recording electrodes (microelectrodes, extracellular electrodes, monophasic action potential electrodes) and myocardium may result in mechanically induced electrical artifact.4 This may have contributed to conflicting experimental results. For example, it is not clear whether conduction velocity increases,16 decreases,17 or does not change at all18 during experimental ventricular loading. In this issue of the Journal,