Baseline arterial pressure affects sympathoexcitatory responses to ventricular premature beats

Smith, Michael L.; Ka, Ellenbogen; Eckberg, Dwain L.

doi:10.1152/ajpheart.1995.269.1.h153

Cited by 9 publications

(7 citation statements)

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“…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.…”

Section: Discussionsupporting

confidence: 92%

“…[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. …”

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confidence: 99%

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Sympathetic Response to Ventricular Extrasystolic Beats in Hypertension and Heart Failure

et al. 2002

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Abstract-Provoked premature ventricular contractions (PVCs) evoke, in concomitance with an early and late blood pressure fall and overshoot, an early sympathoexcitation and a later period of sympathoinhibition, respectively. The present study was designed to examine whether in healthy subjects this is the case for spontaneous PVCs. Because of their pathophysiological relevance for arrhythmogenesis, it was also designed to determine whether the sympathetic responses are different from those seen in essential hypertension and congestive heart failure. In 14 untreated mild essential hypertensives (EH; age, 53.8Ϯ2.6 years; meanϮSEM), 20 untreated congestive heart failure patients (CHF; age, 56.7Ϯ2.5 years; New York Heart Association class, II or III), and 16 age-matched healthy subjects (control) in Lown class ϽII, we evaluated the blood pressure (Finapres), heart rate (ECG), and muscle sympathetic nerve traffic (MSNA; by microneurography) responses to isolated monofocal PVCs. MSNA, quantified as bursts/100 heart beats, was significantly increased in EH (57.8Ϯ3.8, PϽ0.05) and CHF patients (77.7Ϯ4.0, PϽ0.01) compared with controls (44.6Ϯ4.4). In controls, the PVC-induced blood pressure fall and overshoot were accompanied by a sympathoexcitation (144.2Ϯ14%), followed by a period of sympathoinhibition (average duration, 12043Ϯ985 ms). The responses were similar in EH but not in CHF, in whom the magnitude of the sympathoexcitation and particularly the duration of the subsequent sympathoinhibition were strikingly reduced (average reduction, Ϫ46.1 and Ϫ72.8%, respectively). The most important factor accounting for this reduction appeared to be an altered baroreflex response to the PVC-induced BP changes. These data demonstrate that the MSNA responses to spontaneous PVCs are similar in controls and EH but markedly impaired in CHF, presumably because of the baroreflex alteration. This may represent an important factor for the genesis of the life-threatening ventricular arrhythmias that characterize CHF. Key Words: arrhythmia Ⅲ heart failure Ⅲ sympathetic nervous system Ⅲ baroreflex M icroneurographic recording of efferent postganglionic sympathetic nerve traffic to the skeletal muscle district (MSNA) has shown that in healthy humans, premature ventricular contractions (PVCs) induced by programmed ventricular stimulation evoke profound modifications in neural adrenergic discharge. 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 d...

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Section: Discussionsupporting

confidence: 92%

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confidence: 99%

Sympathetic Response to Ventricular Extrasystolic Beats in Hypertension and Heart Failure

et al. 2002

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“…The post-VPC drop of diastolic blood pressure initiates a surge of muscle sympathetic nerve activity, which is immediately followed by a period of sympathetic silence (27)(28)(29)(30)(31). The magnitude of this burst, which cannot be observed earlier than at the time of the first post-VPC beat, provokes noradrenaline release in perivascular sympathetic endings, leading to an increase of peripheral vascular resistance.…”

Section: Physiologic Background and Pathophysiology Of Hrtmentioning

confidence: 99%

Heart Rate Turbulence: Standards of Measurement, Physiological Interpretation, and Clinical Use

Bauer¹,

Malík

Schmidt³

et al. 2008

Journal of the American College of Cardiology

397

432

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This consensus statement has been compiled on behalf of the International Society for Holter and Noninvasive Electrophysiology. It reviews the topic of heart rate turbulence (HRT) and concentrates on technologies for measurement, physiologic background and interpretation, and clinical use of HRT. It also lists suggestions for future research. The phenomenon of HRT refers to sinus rhythm cycle-length perturbations after isolated premature ventricular complexes. The physiologic pattern of HRT consists of brief heart rate acceleration (quantified by the so-called turbulence onset) followed by more gradual heart rate deceleration (quantified by the so-called turbulence slope) before the rate returns to a pre-ectopic level. Available physiologic investigations confirm that the initial heart rate acceleration is triggered by transient vagal inhibition in response to the missed baroreflex afferent input caused by hemodynamically inefficient ventricular contraction. A sympathetically mediated overshoot of arterial pressure is responsible for the subsequent heart rate deceleration through vagal recruitment. Hence, the HRT pattern is blunted in patients with reduced baroreflex. The HRT pattern is influenced by a number of factors, provocations, treatments, and pathologies reviewed in this consensus. As HRT measurement provides an indirect assessment of baroreflex, it is useful in those clinical situations that benefit from baroreflex evaluation. The HRT evaluation has thus been found appropriate in risk stratification after acute myocardial infarction, risk prediction, and monitoring of disease progression in heart failure, as well as in several other pathologies.

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“…Several studies indicated that a large multiunit MSNA burst occurred during premature ventricular contraction (PVC; Ando et al, 1997; Grassi et al, 2002) and atrial fibrillation (AF; Grassi et al, 2003; Wasmund et al, 2003) in HF patients. The low diastolic pressure induced by these arrhythmic conditions unloads arterial baroreceptors and evokes a larger and longer multiunit MSNA burst (Welch et al, 1989; Smith et al, 1995). However, only counting multiunit MSNA could cause the actual level of sympathetic nerve activity to be underestimated, because a large sympathetic activity burst could produce prolonged sympathetic inhibition.…”

Section: Assessment Of Muscle Sympathetic Nerve Activity During Irregmentioning

confidence: 99%

Advantage of Recording Single-Unit Muscle Sympathetic Nerve Activity in Heart Failure

Murai¹,

Takamura²,

Kaneko³

2012

Front. Physio.

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Elevated sympathetic activation is a characteristic feature of heart failure (HF). Excessive sympathetic activation under resting conditions has been shown to increase from the early stages of the disease, and is related to prognosis. Direct recording of multiunit efferent muscle sympathetic nerve activity (MSNA) by microneurography is the best method for quantifying sympathetic nerve activity in humans. To date, this technique has been used to evaluate the actual central sympathetic outflow to the periphery in HF patients at rest and during exercise; however, because the firing occurrence of sympathetic activation is mainly synchronized by pulse pressure, multiunit MSNA, expressed as burst frequency (bursts/min) and burst incidence (bursts/100 heartbeats), may have limitations for the quantification of sympathetic nerve activity. In HF, multiunit MSNA is near the maximum level, and cannot increase further than the heartbeat. Single-unit MSNA analysis in humans is technically demanding, but provides more detailed information regarding central sympathetic firing. Although a great deal is known about the response of multiunit MSNA to stress, little information is available regarding the responses of single-unit MSNA to physiological stress and disease. The purposes of this review are to describe the differences between multiunit and single-unit MSNA during stress and to discuss the advantages of single-unit MSNA recording in improving our understanding the pathology of increased sympathetic activity in HF.

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Baseline arterial pressure affects sympathoexcitatory responses to ventricular premature beats

Cited by 9 publications

References 0 publications

Sympathetic Response to Ventricular Extrasystolic Beats in Hypertension and Heart Failure

Sympathetic Response to Ventricular Extrasystolic Beats in Hypertension and Heart Failure

Heart Rate Turbulence: Standards of Measurement, Physiological Interpretation, and Clinical Use

Advantage of Recording Single-Unit Muscle Sympathetic Nerve Activity in Heart Failure

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