Effects of stretch on heart rhythm: theory & practice

Effects of stretch on heart rhythm have been known for over a century. They possess considerable clinical importance and range from the increase in heart rate during enhanced venous return to the right atrium (Bainbridge effect) to sudden cardiac death caused by pre-cordial chest thumps (Commotio cordis). The underlying cellular and molecular mechanisms have only recently started to become evident and include stretch-activation of ion channels and mechanical modulation of intracellular calcium handling. We have investigated the effects of stretch-activation of ion channels in working myocardium, pacemaker cells and cardiac fibroblasts, using experimental procedures (single and double cell patch-clamp technique as well as in-situ recordings) and mathematical modelling (single cell `ionic' models, cell pairs, tissue sheets and anatomical models). Our findings illustrate why (i) transient stretch may trigger ectopic excitation via depolarization of resting myocytes or fibroblasts; (ii) sustained stretch may increase the heart's susceptibility to re-entry by generating spatial and temporal dispersion of excitability, refractoriness and electrical load; (iii) combined cyclic and maintained stretch, as occurs during ischaemic bulging of myocardium, is particularly arrhythmogenic; and (iv) areas of increased connective tissue content, like post-ischaemic scars or regions of fibrosis, are prone to act as foci of ectopic excitation