Heptanol at 0.05 mM increased the incidence of induced ventricular tachycardia to 50% (6/12 hearts) compared to 0% at baseline by reducing conduction velocity.
Absolute Event Rate: 50% vs 0%
p-value: p=<0.05
In the current study, arrhythmogenic effects of the gap junction inhibitor heptanol (0.05 mM) were examined in Langendorff-perfused mouse hearts. Monophasic action potential recordings were obtained from the left ventricular epicardium during right ventricular pacing. Regular activity was observed both prior and subsequent to application of heptanol in all of the 12 hearts studied during 8 Hz pacing. By contrast, induced ventricular tachycardia (VT) was observed after heptanol treatment in 6/12 hearts using a S1S2 protocol (Fisher's exact test; P0.05). Consequently, excitation wavelengths (λ; CV x ERP) were reduced from 9.1±0.6 to 6.5±0.6 mm (P0.05). Together, these observations demonstrate for the first time, to the best of our knowledge, that inhibition of gap junctions alone using a low heptanol concentration (0.05 mM) was able to reduce CV, which alone was sufficient to permit the induction of VT using premature stimulation by reducing λ, which therefore appears central in the determination of arrhythmic tendency.
Tse et al. (Tue,) conducted a other in Ventricular arrhythmogenicity (n=13). Heptanol vs. Baseline (prior to heptanol application) was evaluated on Induced ventricular tachycardia (VT) using a S1S2 protocol (p=<0.05). Heptanol at 0.05 mM increased the incidence of induced ventricular tachycardia to 50% (6/12 hearts) compared to 0% at baseline by reducing conduction velocity.