Why the study?
The relationship between repolarization variability parameters and ventricular arrhythmogenicity in a hypokalaemic model of acquired long QT syndrome remained to be investigated.
Does heptanol prevent ventricular tachycardia and alter repolarization variability in a hypokalaemic mouse model of acquired long QT syndrome?
Does heptanol prevent ventricular tachycardia and alter repolarization variability in a hypokalaemic mouse model of acquired long QT syndrome?
In a mouse model of acquired long QT syndrome, nonlinear analysis of repolarization variability reflects arrhythmic risk, and heptanol prevents VT without altering these parameters.
Answers are grounded in this paper and cite their sources.
May link repolarization variability to arrhythmogenicity in hypokalemic mouse LQTS models; leaves open human translation for risk stratification.
Previous studies have quantified repolarization variability using time-domain, frequency-domain and nonlinear analysis in mouse hearts. Here, we investigated the relationship between these parameters and ventricular arrhythmogenicity in a hypokalaemia model of acquired long QT syndrome. Left ventricular monophasic action potentials (MAPs) were recorded during right ventricular regular 8 Hz pacing during normokalaemia (5.2 mM [K + ]), hypokalaemia modeling LQTS (3 mM [K + ]) or hypokalaemia with 0.1 mM heptanol in Langendorff-perfused mouse hearts. During normokalaemia, mean APD was 33.5 ± 3.7 ms. Standard deviation (SD) of APDs was 0.63 ± 0.33 ms, coefficient of variation was 1.9 ± 1.0% and the root mean square (RMS) of successive differences in APDs was 0.3 ± 0.1 ms. Low- and high-frequency peaks were 0.6 ± 0.5 and 2.3 ± 0.7 Hz, respectively, with percentage powers of 38 ± 22 and 61 ± 23%. Poincaré plots of APD n +1 against APD n revealed ellipsoid morphologies with SD along the line-of-identity (SD2) to SD perpendicular to the line-of-identity (SD1) ratio of 4.6 ± 1.1. Approximate and sample entropy were 0.49 ± 0.12 and 0.64 ± 0.29, respectively. Detrended fluctuation analysis revealed short- and long-term fluctuation slopes of 1.62 ± 0.27 and 0.60 ± 0.18, respectively. Hypokalaemia provoked ventricular tachycardia in six of seven hearts, prolonged APDs (51.2 ± 7.9 ms), decreased SD2/SD1 ratio (3.1 ± 1.0), increased approximate and sample entropy (0.68 ± 0.08 and 1.02 ± 0.33) and decreased short-term fluctuation slope (1.23 ± 0.20) (ANOVA, P < 0.05). Heptanol prevented VT in all hearts studied without further altering the above repolarization parameters observed during hypokalaemia. Reduced SD2/SD1, increased entropy and decreased short-term fluctuation slope may reflect arrhythmic risk in hypokalaemia. Heptanol exerts anti-arrhythmic effects without affecting repolarization variability.
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Tse et al. (2023) studied this question.
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