Key result
Moderate mechanical stretch facilitated the triggering of rapid pulmonary vein firing by 10 µmol/L adrenaline, increasing the arrhythmia index to 4.4 compared to 1.3 in unstretched preparations (P<0.001).
Why the study?
Autonomic tone plays a crucial role in pulmonary vein arrhythmogenesis, but its interplay with myocardial stretch remains uncertain.
Does mechanical stretch combined with adrenaline induce arrhythmogenic activity in isolated rat pulmonary veins?
Does mechanical stretch combined with adrenaline induce arrhythmogenic activity in isolated rat pulmonary veins?
Mechanical stretch facilitates sympathetic-induced arrhythmogenic activity in pulmonary veins, providing a mechanistic link between atrial overload and atrial fibrillation.
Animal data link stretch to enhanced adrenergic PV firing; hypothesis-generating for AF mechanisms, should not change practice.
Rapid firing from pulmonary veins (PVs) frequently initiates atrial fibrillation which is a common comorbidity associated with hypertension, heart failure, and valvular disease, i.e. conditions that pathologically increase cardiomyocyte stretch. Autonomic tone plays a crucial role in PV arrhythmogenesis while its interplay with myocardial stretch remains uncertain. Two-microelectrode technique was used to characterize electrophysiological response of rat PV to adrenaline at baseline and under mild (150 mg of applied weight which corresponds to a pulmonary venous pressure of 1 mmHg) and moderate (10 g, 26 mmHg) stretch. Low adrenaline concentrations (25-100 nmol/L) depolarized the resting membrane potential selectively within distal PV (by 26+/-2 mV at baseline, 18+/-1 mV at 150 mg, P<0.001, and by 5.9+/-1.1 mV at 10 g, P<0.01) resulting in intra-PV conduction dissociation and rare episodes of spontaneous activity (arrhythmia index of 0.4+/-0.2, NS vs. no activity at baseline). In contrast, 1-10 umol/L of adrenaline recovered intra-PV propagation. While mild stretch did not affect PV electrophysiology at baseline, moderate stretch depolarized the resting potential within distal PV (-56+/-2 mV vs. -82+/-1 mV at baseline, P<0.01), facilitated the triggering of rapid PV firing by adrenaline (arrhythmia index: 4.4+/-0.2 vs. 1.3+/-0.4 in unstretched, P<0.001, and 1.7+/-0.8 in mildly stretched preparations, P<0.005, at 10 umol/L adrenaline) and induced frequent episodes of potentially arrhythmogenic atrial ‘echo’ extra beats. Our findings demonstrate complex interactions between the sympathetic tone and mechanical stretch in the development of arrhythmogenic activity within PVs that may impact an increased atrial fibrillation vulnerability in patients with elevated blood pressure.
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Egorov et al. (2020) studied Pulmonary vein arrhythmogenesis (n=7). Adrenaline and mechanical stretch vs. Unstretched baseline was evaluated on Arrhythmia index at 10 µmol/L adrenaline (p=<0.001). Moderate mechanical stretch facilitated the triggering of rapid pulmonary vein firing by 10 µmol/L adrenaline, increasing the arrhythmia index to 4.4 compared to 1.3 in unstretched preparations (P<0.001).
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