Introduction. We have previously shown that rapid stretch of the ventricle or rapid release of tension can induce arrhythmias (Saint, Kelly & Mackenzie, 2010). Hypertrophic hearts show increased sensitivity to stretch induced arrhythmias (Evans, Dalton & Lev, 2000), but how these mechanisms may be altered in hypertrophic hearts is not well understood. Here we investigate mechanically induced arrhythmias in isolated hearts from Wistar-Kyoto (control) and age-matched Spontaneously Hypertensive Rats (SHR).
Methods. Langendorff perfused hearts had a fluid filled balloon placed in the left ventricle, connected to a servo-driven syringe injector. Epicardial monophasic action potentials and intraventricular pressure were monitored to detect ectopic beats. Left Ventricular End Diastolic Pressure (LVEDP) was set at 5 to 10 mm Hg and the minimum step pressure increase which just triggered an ectopic beat was taken as threshold for stretch-induced arrhythmias (St-Ar).
Results. SHR had pronounced cardiac hypertrophy (cardiac index 0.48 ± 0.02%, n=15 in SHR vs 0.41 ± 0.02%, n=11 in Wistar-Kyoto; P <<0.01). Hearts from SHR had a lower threshold for St-Ar (21.2 ± 3.6 mm.Hg (n=5) compared to 49.4 ± 4.7 mm.Hg for control (n=5), p << 0.01). Perfusion of the hearts with 100 μM streptomycin increased the threshold in both groups (39.7 ± 9.0 mm.Hg in SHR (n=5); p = 0.07 and 69.4 ± 6.9 mm.Hg in control (n=5); p = 0.04).
Discussion. Hypertrophic hearts (SHR) are more sensitive to mechanically induced arrhythmias. Streptomycin (a blocker of stretch-activated channels) decreased the sensitivity in both SHR and control.
Evans SJ, Dalton GR & Levi AJ. (2000) Journal of Cardiovascular Risk, 7(3): 163-75.
Saint DA, Kelly D & Mackenzie L. (2010) in Mechanosensitivity of the Heart, pp 275-300 Eds Kamkin and Kiseleva, Springer.