Abstract
Experimental studies have demonstrated that changes in mechanical loading conditions have important, and potentially arrhythmogenic, electrophysiologic effects. These studies have, for the most part, involved the effects of acute dilatation in the structurally normal heart. The ionic basis of these changes remains incompletely understood. Although there is abundant evidence that mechano-electrical feedback occurs in man, additional studies are required to clarify whether the mechanical and hemodynamic abnormalities present in patients with congestive heart failure are a significant contributor to the clinical arrhythmias in these patients. Ongoing studies should clarify this important issue.

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