Recruitment pattern of sympathetic muscle neurons during premature ventricular contractions in heart failure patients and controls

Abstract

Premature ventricular contractions (PVC) elicit larger bursts of multiunit muscle sympathetic nerve activity (MSNA), reflecting the ability to increase postganglionic axonal recruitment. We tested the hypothesis that chronic heart failure (CHF) limits the ability to recruit postganglionic sympathetic neurons as a response to PVC due to the excessive sympathetic activation in these patients. Sympathetic neurograms of sufficient signal-to-noise ratio were obtained from six CHF patients and from six similarly aged control individuals. Action potentials (APs) were extracted from the multiunit sympathetic neurograms during sinus rhythm bursts and during the post-PVC bursts. These APs were classified on the basis of the frequency per second, the content per burst, and the peak-to-peak amplitude, which formed the basis of binning the APs into active clusters. Compared with controls, CHF had higher APs per burst and higher number of active clusters per sinus rhythm burst (P < 0.05). Compared with sinus rhythm bursts, both groups increased AP frequency and the number of active clusters in the post-PVC burst (P < 0.05). However, compared with controls, the increase in burst integral, AP frequency, and APs per burst during the post-PVC burst was less in CHF patients. Nonetheless, the PVC-induced increase in active clusters per burst was similar between the groups. Thus, these CHF patients retained the ability to recruit larger APs but had a diminished ability to increase overall AP content.

Premature Ventricular Contraction Coupling Interval Variability Destabilizes Cardiac Neuronal and Electrophysiological Control

“…20 These changes on muscle sympathetic nerve activity were subsequently confirmed in heart failure patients during spontaneous PVCs, providing further support for the validity of our experimental model involving pacing-induced PVCs. 10 …”

“…10 Of these mechanisms, the role of the autonomic nervous system (ANS) is not well understood. The ANS regulates all aspects of cardiac function.…”

Firing patterns of muscle sympathetic neurons during short-term use of continuous positive airway pressure in healthy subjects and in chronic heart failure patients

“…Multiunit-MSNA was quantified as burst frequency by counting the number of bursts during a specified period of time, as burst incidence by expressing the number of burst that occurred per 100 heart beats, and as mean burst area/min (Sundlof and Wallin, 1977). Action potentials (APs) were detected and extracted from the filtered raw MSNA signal using the continuous wavelet transform (CWT) technique for AP detection as reported previously (Steinback et al, 2010; Salmanpour et al, 2010, 2011; Breskovic et al, 2011; Maslov et al, 2012). Briefly, the method uses an original mother wavelet, derived from an average human AP.…”

“…In contrast to the idea that sympathoinhibition should occur if CPAP enhances cardiac index (as above), Heindl et al (2001) found a modest increase in multi-unit MSNA burst frequency in both CHF patients and healthy control subjects. Recently, our studies have explored the potential importance of quantifying actual action potential (AP) patterns in the postganglionic sympathetic nerve activity as an indicator of sympathetic patterns, rather than just the frequency of integrated bursts (Steinback et al, 2010; Salmanpour et al, 2010, 2011; Breskovic et al, 2011; Maslov et al, 2012). Specifically, multi-unit MSNA bursts are composed of several sympathetic neurons firing at the same time with burst-by-burst variations in the numbers of APs recruited (Salmanpour et al, 2010).…”

Influence of spontaneously occurring bursts of muscle sympathetic nerve activity on conduit artery diameter

“…In this regard, in our study of healthy subjects with Յ25 MSNA bursts/min, resting MSNA burst frequency did not influence the diameter or MAP changes following MSNA bursts. However, we speculate that substantially elevated resting MSNA burst frequency, such as observed in aging (12,19) or heart failure (17,21), may supply a neurotransmitter stimulus which overcomes the threshold for smooth muscle contraction in conduit arteries to demonstrate a decrease in compliance relative to healthy subjects, or outright vasoconstriction, depending on the degree of conduit artery smooth muscle contraction. Accordingly, it is possible that spontaneously occurring MSNA bursts may evoke vasoconstriction throughout the arterial tree in pathological overactive sympathetic states, instead of mediating an effect exclusively in resistance arteries as observed in young healthy men.…”