Abstract
Ventricular action potential duration (APD) is an important component of many physiological functions including arrhythmogenesis. APD oscillations have recently been reported in humans at the respiratory frequency. This study investigates the contribution of the autonomic nervous system to these oscillations. In 10 patients undergoing treatment for supraventricular arrhythmias, activation recovery intervals (ARI; a conventional surrogate for APD) were measured from multiple left and right ventricular (RV) endocardial sites, together with femoral artery pressure. Respiration was voluntarily regulated and heart rate clamped by RV pacing. Sympathetic and parasympathetic blockade was achieved using intravenous metoprolol and atropine, respectively. Metroprolol reduced the rate of pressure development (maximal change in pressure over time): 1,271 (± 646) vs. 930 (± 433) mmHg/s; P < 0.01. Systolic blood pressure (SBP) showed a trend to decrease after metoprolol, 133 (± 21) vs. 128 (± 25) mmHg; P = 0.06, and atropine infusion, 122 (± 26) mmHg; P < 0.05. ARI and SBP exhibited significant cyclical variations (P < 0.05) with respiration in all subjects with peak-to-peak amplitudes ranging between 0.7 and 17.0 mmHg and 1 and 16 ms, respectively. Infusion of metoprolol reduced the mean peak-to-peak amplitude [ARI, 6.2 (± 1.4) vs. 4.4 (± 1.0) ms, P = 0.008; SBP, 8.4 (± 1.6) vs. 6.2 (± 2.0) mmHg, P = 0.002]. The addition of atropine had no significant effect. ARI, SBP, and respiration showed significant coupling (P < 0.05) at the breathing frequency in all subjects. Directed coherence from respiration to ARI was high and reduced after metoprolol infusion [0.70 (± 0.17) vs. 0.50 (± 0.23); P < 0.05]. These results suggest a role of respiration in modulating the electrophysiology of ventricular myocardium in humans, which is partly, but not totally, mediated by β-adrenergic mechanisms.
Highlights
Ventricular action potential repolarization is critical to electrical stability and arrhythmogenesis
The main findings were as follows: 1) we confirmed the presence of oscillations in ACTION potential duration (APD) and systolic blood pressure (SBP) at each of four controlled respiratory frequencies: 6, 9, 15, and 30 breaths/ min; 2) the -adrenergic blocking agent metoprolol resulted in a decrease in the amplitude of APD oscillation; 3) IV administration of atropine following metoprolol was without effect on LV or RV activation recovery intervals (ARIs) oscillation amplitude; 4) coherence analysis showed a significant linear coupling between respiration, APD, and SBP at the breathing frequency; 5) analysis of the directed coherence showed a high directed coherence from respiration to APD and from respiration to SBP. -Adrenergic blockade reduced the contribution of respiration to APD oscillations
The dynamics of ventricular repolarization play a critical role in maintaining electrical stability
Summary
Ventricular action potential repolarization is critical to electrical stability and arrhythmogenesis. Several considerations suggest the possibility of a role of the autonomic nervous system in respiratory-related ventricular APD oscillations. Ventricular myocardium is known to receive substantial vagal as well as sympathetic innervation [7], raising the possibility of cyclical autonomic influence in the ventricle Both sympathetic and vagal stimulation may modulate ventricular APD [30, 32, 35, 43, 50, 55]. Respiration is known to gate the timing of autonomic motor neurone firing such that inspiration is associated with an increase in sympathetic and decrease in parasympathetic nerve activity [8, 16, 28], again suggesting the possibility of respiratory-related autonomic modulation of ventricular APD. Phase analysis was implemented to investigate the oscillatory behavior of APD in the left and right ventricle
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