Abnormal mechanical stretch of the myocardium during cardiac memory results in direct alterations in ion channel properties and activation of angiotensin-dependent signaling cascades.
What are the molecular mechanisms linking mechanical stretch and electrical perturbations to cardiac electrical remodeling and memory?
This review highlights the role of mechanical stretch and angiotensin signaling in cardiac electrical remodeling and memory, linking these processes to heart failure and increased arrhythmia risk.
Ion channels play a central role in the normal electro-mechanical functioning of the heart and are implicated in a variety of disease processes. In response to electrical or mechanical perturbations, cardiac myocytes exhibit remarkable changes in the expression and/or the function of sarcolemmal ion channels, a process that is broadly described as electrical remodeling. This remodeling has beneficial, as well as adverse, effects on myocardial function, including increased risk of fatal arrhythmias. One specific example of cardiac electrical remodeling is cardiac memory, a phenomenon induced in the heart following abnormal myocardial activation patterns produced by artificial pacemakers. Recent studies have shed new light on the molecular mechanisms underlying cardiac memory and suggest intriguing parallels between cardiac memory and heart failure. In both situations, abnormal mechanical stretch of the myocardium results in direct alterations in ion channel properties, as well as in the activation of angiotensin-dependent signaling cascades. With time, altered gene transcription and protein synthesis lead to persistent changes in ion channel levels and activities, changes that can significantly impact normal cardiac function and increase arrhythmia susceptibility.
Marrus et al. (Wed,) conducted a review in Cardiac memory and electrical remodeling. Abnormal myocardial activation (cardiac memory) was evaluated. Abnormal mechanical stretch of the myocardium during cardiac memory results in direct alterations in ion channel properties and activation of angiotensin-dependent signaling cascades.