Key result
Metoprolol cuts respiratory-related ARI oscillations by ~29%.
Why the study?
Does autonomic blockade with metoprolol and atropine reduce respiratory-related oscillations of ventricular action potential duration in humans?
Does autonomic blockade with metoprolol and atropine reduce respiratory-related oscillations of ventricular action potential duration in humans?
Respiratory-related oscillations in ventricular action potential duration in humans are partially mediated by sympathetic nervous system activity, as demonstrated by their reduction following beta-adrenergic blockade.
Supports beta-adrenergic mediation of respiratory ventricular repolarization effects; extends prior observations but remains hypothesis-generating.
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.
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Duijvenboden et al. (2015) studied Supraventricular arrhythmias (atrial fibrillation) (n=10). Metoprolol and Atropine vs. Baseline (no autonomic blocking agents) was evaluated on Mean peak-to-peak amplitude of respiratory-related activation recovery interval (ARI) oscillations (p=0.008). Infusion of the β-adrenergic blocking agent metoprolol significantly reduced the mean peak-to-peak amplitude of respiratory-related activation recovery interval oscillations from 6.2 ms to 4.4 ms.
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