Key result
Repolarization variability shifts significantly in the 20 seconds preceding spontaneous ventricular tachyarrhythmias.
Why the study?
Whether measures of repolarization variability can predict ventricular arrhythmogenesis in mice had never been explored.
Do measures of repolarization variability predict ventricular arrhythmogenesis in heptanol-treated Langendorff-perfused mouse hearts?
Do measures of repolarization variability predict ventricular arrhythmogenesis in heptanol-treated Langendorff-perfused mouse hearts?
Non-linear measures of repolarization variability are significantly altered prior to the onset of ventricular arrhythmias in a mouse model, highlighting their potential as predictive markers for impending arrhythmias.
Repolarization variability changes may precede arrhythmias in this model; hypothesis-generating and requires validation before any clinical translation.
Time-domain and non-linear methods can be used to quantify beat-to-beat repolarization variability but whether measures of repolarization variability can predict ventricular arrhythmogenesis in mice have never been explored. Left ventricular monophasic action potentials (MAPs) were recorded during constant right ventricular 8 Hz pacing in Langendorff-perfused mouse hearts, in the presence or absence of the gap junction and sodium channel inhibitor heptanol (0.1, 0.5, 1 or 2 mM). Under control conditions, mean action potential duration (APD) was 39.4 ± 8.1 ms. Standard deviation (SD) of APDs was 0.3 ± 0.2 ms, coefficient of variation was 0.9 ± 0.8% and the root mean square (RMS) of successive differences in APDs was 0.15 ± 0.14 ms. Poincaré plots of APDn+1 against APDn revealed ellipsoid morphologies with a SD along the line-of-identity (SD2) to SD perpendicular to the line-of-identity (SD1) ratio of 4.6 ± 2.1. Approximate and sample entropy were 0.61 ± 0.12 and 0.76 ± 0.26, respectively. Detrended fluctuation analysis revealed short- and long-term fluctuation slopes of 1.49 ± 0.27 and 0.81 ± 0.36, respectively. Heptanol at 2 mM induced ventricular tachycardia in five out of six hearts. None of the above parameters were altered by heptanol during which reproducible electrical activity was observed (KW-ANOVA, P > 0.05). Contrastingly, SD2/SD1 decreased to 2.03 ± 0.41, approximate and sample entropy increased to 0.82 ± 0.12 and 1.45 ± 0.34, and short-term fluctuation slope decreased to 0.82 ± 0.19 during the 20-s period preceding spontaneous ventricular tachy-arrhythmias (n = 6, KW-ANOVA, P < 0.05). Measures of repolarization variability, such as SD2/SD1, entropy, and fluctuation slope are altered preceding the occurrence of ventricular arrhythmogenesis in mouse hearts. Changes in these variables may allow detection of impending arrhythmias for early intervention.
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Tse et al. (2021) studied Ventricular Arrhythmogenesis (n=6). Heptanol vs. Baseline (absence of heptanol) was evaluated on Repolarization variability measures (approximate entropy, sample entropy, SD2/SD1 ratio, and short-term fluctuation slope) preceding spontaneous ventricular tachy-arrhythmias (p=<0.05). During the 20-second period preceding spontaneous ventricular tachy-arrhythmias, repolarization variability was significantly altered, demonstrated by a decrease in SD2/SD1 to 2.03 ± 0.41 and increases in approximate entropy to 0.82 ± 0.12 and sample entropy to 1.45 ± 0.34 (P < 0.05).
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