It is known that stretch of the ventricles is arrhythmogenic.1 The role that this plays in healthy heart is unclear, but we hypothesised that an exaggeration of this response in hypertrophic hearts may explain the high risk of SCD in patients with hypertrophy and early failure. The hypertrophied heart indeed shows increased sensitivity to stretch-induced arrhythmias2 and increased stretch-activated currents in myocytes from hypertrophied animal and human hearts has been directly demonstrated.3 We have now extended these observations by examining stretch-induced ectopic beats in isolated hearts from Wistar-Kyoto (control) and SHR.4 Our results show that hypertrophic hearts are more sensitive to mechanically induced arrhythmias and that the putative stretch-activated channel blocker streptomycin reduces this sensitivity. Hearts from SHR had a threshold for stretch-induced ectopic beats of 21.2±3.6 mm Hg (n=5) compared to 49.4±4.7 mm Hg in Wistar Kyoto (n=5), p<0.01). Perfusion of the hearts with 100 μM streptomycin increased the threshold in both (to 39.7±9.0 mm Hg in SHR (n=5); p=0.07 vs 69.4±6.9 mm Hg in control (n=5); p=0.04). These data add to growing evidence that mechanical effects on the myocardium may contribute to arrhythmias in many clinical situations and suggest that efforts at developing anti-arrhythmic agents with this as a target may prove fruitful.5 As yet there is no guidance for the study of such arrhythmias and provision for this is required in the Lambeth Conventions update.
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