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.