Much progress has been made in understanding the mechanisms underlying arrhythmias. It is now clear that electrophysiological properties of the myocardium at a cellular level are very different in different parts of the heart, even over fairly small distances (for example across the thickness of the left ventricular wall). However, most models of arrhythmogenesis do not include the role that mechanical forces on the myocardium play in altering its electrophysiology (a process called mechanoelectric feedback, or MEF). Stretch of the myocardium can alter action potential morphology, propagation velocity and intracellular calcium handling, all of which can contribute to arrhythmogenesis. In particular, it is now becoming clear that MEF is not homogeneous in the heart. It is also clear that MEF is altered in some diseases such as hypertrophy, where it may explain the propensity to arrhythmias in these diseases. Here, we discuss the evidence that MEF is heterogeneous in the heart, in the same way that other electrophysiological properties are heterogeneous. The reasons why this may be are discussed. The possible role that this heterogeneity, and its modulation in some common cardiac diseases, plays in the induction of arrhythmias is also explored.