Enhancement of sympathetic nerve activity by single premature ventricular beats in humans

Abstract

This is the first systematic study of the effects of ventricular premature beats on sympathetic nerve activity in humans. Microneurographic techniques were used to record efferent sympathetic activity from the peroneal nerve, and an intracardiac electrode catheter was used to introduce ventricular premature beats after every 6 to 10 sinus heartbeats. Studies were performed in eight patients, aged 22 to 74 years (mean 57), undergoing cardiac electrophysiologic studies. Three patients did not have apparent heart disease and five had coronary artery disease. During sinus rhythm, 19 to 93% (mean 42%) of heartbeats were followed by a pulse-synchronous burst of sympathetic activity. Provoked ventricular premature beats had obvious effects on this activity. Premature beats with coupling intervals less than 80% of sinus cycle length were consistently followed by a burst of sympathetic activity, and this activity was greater in amplitude, duration and area (all p less than 0.05) than were burst of such activity during sinus rhythm. The magnitude of this burst of activity increased as the coupling interval of the ventricular premature beat decreased (p less than 0.0001). In contrast, postextrasystolic beats were followed by nearly complete neural silence. These effects were seen in all patients regardless of baseline burst incidence and the presence or absence of heart disease. Total nerve activity per 10 heartbeats was 6,520 +/- 770 U during ventricular extrastimulation and 5,720 +/- 440 U during normal sinus rhythm (difference not significant). It is concluded that single ventricular premature beats provoke fluxes of muscle sympathetic nerve activity in humans, comprising surges of sympathetic activity larger than those occurring during sinus rhythm, followed by neural silence.

Sympathetic Response to Ventricular Extrasystolic Beats in Hypertension and Heart Failure

“…Furthermore, in these subjects the above-mentioned changes were followed by a transient diastolic BP increase and a concomitant transient suppression of spontaneous MSNA bursts. These findings are in line with the results of previous studies performed in both experimental animals 17 and humans, 1,18 in which a provoked PVC elicited, along with a diastolic BP reduction, a marked increase in cardiac, renal, and skeletal muscle sympathetic outflow, which was followed by a BP overshoot and a concomitant period of sympathetic silence. We can thus conclude that in healthy subjects, the sympathetic responses to provoked and unprovoked PVCs are qualitatively similar to each other, and thus, artificially induced PVCs represent a valid model for studying the hemodynamic and neural adjustments to spontaneously occurring arrhythmias of this type.…”

“…[12][13][14][15][16] In the present study, we investigated the behavior of the changes in MSNA, as directly quantified by microneurography, that follow spontaneous unprovoked PVCs in healthy subjects and in patients with EH or CHF. Because evidence in animals and man 1,17,18 suggests that the sympathetic changes after provoked PVCs are related to (1) the blood pressure (BP) changes induced by PVCs, (2) their degree of prematurity (expressed by the coupling interval time), and (3) the level of the resting sympathetic tone, we further investigated in the 3 groups the relationships between the MSNA adjustments to spontaneous PVCs and the above-mentioned variables. …”

“…1 These modifications include (1) an enhancement in the amplitude and duration of the sympathetic burst immediately after the PVC and (2) a subsequent period of sympathetic silence, followed by the restoration of the normal pattern of adrenergic discharge. 1 With the exception of 2 studies 2,3 (in which the early sympathoexcitatory responses to spontaneous PVCs were evaluated in 9 patients affected by congestive heart failure [CHF]), no information exists as to whether the MSNA behavior characterizing provoked PVCs is also shared by the spontaneous ones. Furthermore, it is unknown whether the sympathetic responses to PVCs seen in healthy subjects differ from those observed in essential hypertension (EH) and CHF, ie, 2 cardiovascular diseases in which sympathetic neural activity is markedly increased 4 -11 and its role in the arrhythmogenesis has been documented.…”

Reflex Control of Sympathetic Activity During Simulated Ventricular Tachycardia in Humans

“…Burst area was used because ventricular pacing often produces broad arterial pressure oscillations that provoke broad bursts of sympathetic activity. Under these conditions, burst amplitude alone does not correlate well with burst area 4 and does not account for the prolonged activation of sympathetic nerve traffic associated with periods of protracted hypotension.…”

Changes in Autonomic Nervous Activity After Catheter Ablation of Right Ventricular Outflow Tract Tachycardia

“…In an earlier study by Huikuri et al, an increase in sinus rate was demonstrated during induced VT. 41 They suggested that both vagal withdrawal and sympathetic activation may play a role in the increase in sinus rate during VT. Other experimental and clinical studies have shown an increase in sympathetic nerve activity during programmed ventricular stimulation 42 and induced VT, 43 and even in the presence of PVC. 44 In the present study, increased vagal tone and decreased sympathetic tone were demonstrated after the successful ablation.…”