Increased mechanically-induced ectopy in the hypertrophied heart

Abstract

<h4>Introduction</h4>Left ventricular hypertrophy (LVH) predisposes patients to arrhythmias, but the mechanism of these arrhythmias is unclear. Here we show that hearts from spontaneously hypertensive rats (SHR) have a lower threshold for induction mechanically induced arrhythmias compared to age matched Wistar-Kyoto (WKY).<h4>Methods</h4>Recordings were made from isolated hearts from nine month old SHR (n = 18) and WKY (n = 17) rats. A water filled balloon in the left ventricle had its volume controlled by a servo-driven syringe. LVEDP was abruptly increased in increments until an ectopic beat was detected by an epicardial MAP electrode. Alternatively, LVEDP was abruptly reduced back to 5 mm Hg from an elevated pressure.<h4>Results</h4>SHR hearts had a lower threshold for stretch induced ectopics (29.87 ± 2.79 mm Hg vs. 42.23 ± 2.33 mm Hg, p < 0.01) and for release induced ectopics (24.09 ± 1.40 vs. 37.23 ± 3.22, p < 0.01). Perfusion with 100 μM streptomycin increased threshold for stretch induced ectopics in both strains (from 49.4 ± 4.7 to 69.5 ± 6.9 mm Hg in WKY; p < 0.05 and from 21.2 ± 3.5 to 39.7 ± 9.0 mm Hg in SHR; p = 0.07). 100 μM streptomycin also increased threshold for release induced ectopics in SHR (from 23.5 ± 3.6 to 32.6 ± 4.9 mm Hg; p < 0.05) but not in WKY. Perfusion with 0.01 μM isoprenaline decreased the threshold for stretch induced ectopics in both strains (from 40.6 ± 5.0 to 22.6 ± 2.5 mm Hg in WKY; not significant at p < 0.05; p = 0.07 and from 31.0 ± 5.5 to 14.3 ± 2.5 mm Hg in SHR; p < 0.05).<h4>Conclusions</h4>Hearts from SHR are more susceptible to both stretch-induced and release-induced arrhythmia.