Mechanoelectrical feedback (MEF) has become firmly established as a mechanism in which mechanical forces experienced by myocardial tissue or cell membranes convey alterations in electrophysiologic characteristics of such tissue. Observations to date mainly concern mechanically induced changes in action potential duration, resting and active potential amplitude, enhanced pacemaker frequency, or afterdepolarizations. While some of these changes (i.e. after depolarizations) may give rise to premature beats, a role of MEF in explaining sustained ventricular tachyarrhythmias has so far been elusive. Here, we review recent findings showing that acute atrial dilatation facilitates atrial fibrillation (AF) and that two stretch-activated channel (SAC) blockers (gadolinium and GsMTx-4) are able to suppress stretch-facilitated AF. These findings strongly support a role of MEF and SACs in promoting sustained arrhythmias and point to a new class of antiarrhythmic drugs.