Sympathetic Alternans

Ando, Shin-ichi; Dajani, Hilmi R.; Senn, Beverley L.; Newton, Gary E.; Floras, John S.

doi:10.1161/01.cir.95.2.316

Cited by 43 publications

(16 citation statements)

References 23 publications

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“…Similar to what has been recently reported in CHF patients, 2,3 in healthy subjects a spontaneous PVC triggered, along with a diastolic BP reduction, a postextrasystolic MSNA burst characterized by an amplitude markedly and significantly greater than the average amplitude of the MSNA bursts occurring in sinus rhythm. 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.…”

Section: Discussionsupporting

confidence: 86%

“…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.…”

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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: 86%

mentioning

confidence: 99%

Sympathetic Response to Ventricular Extrasystolic Beats in Hypertension and Heart Failure

et al. 2002

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“…It is also quite interesting to point out that Ando et al 34 have reported that patients with heart failure and pulsus alternans present a correlated alternation in the discharge of the muscle sympathetic nerve activity as well, clearly indicating that brisk baroreflex mechanisms are also operative in an advanced phase of the disease. Thus, some of the observed blunting of supraspinal negative-feedback responses, such as the reduced reflex bradycardia, may depend on the activation of sympathetic afferents mediating a reflex increase in cardiac sympathetic drive and a simultaneous decrease in cardiac vagal efferent activity.…”

Section: Pathophysiological Predominance Of Reflex Excitatory Mechanismsmentioning

confidence: 97%

Emerging Excitatory Role of Cardiovascular Sympathetic Afferents in Pathophysiological Conditions

Malliani¹,

Montano²

2002

Hypertension

136

119

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Abstract-There is sound experimental evidence that cardiovascular sympathetic afferent fibers mediate cardiovascular reflexes largely excitatory in nature with positive-feedback characteristics. This afferent neural channel is likely to normally participate in the neural regulation of cardiovascular function. The hypothesis, which is the core of this article, is that in some pathophysiological conditions, sympathetic overactivity may be partly due to an emerging excitatory reflex action of cardiovascular sympathetic afferents. In fact, the early phase of congestive heart failure can be characterized by an increase in arterial pressure and heart rate and/or by a diastolic dysfunction, leaving unchanged the cardiac output; in these conditions, in which no baroreceptor deactivation should occur, it is possible that cardiovascular sympathetic afferents with sensory endings in the thoracic low-pressure areas, highly responsive to volume loading, are responsible for mediating the reflex sympathetic excitation. Similarly, during acute myocardial infarction, ventricular sympathetic afferents are likely to mediate a reflex sympathetic overactivity, which is known to facilitate sudden death. Finally, numerous reports have described in essential arterial hypertension an increased sympathetic activity that may be due, at least in part, to the reinforcing action of sympathosympathetic reflexes. Thus, in pathophysiological conditions, cardiovascular sympathetic afferents would mediate a reflex sympathetic overactivity independently of baroreceptive mechanisms, and such an absence of a homeostatic purpose would provide a better rationale for some beneficial effects of therapeutic correction. Key Words: heart failure Ⅲ ischemia Ⅲ hypertension, arterial Ⅲ heart rate Ⅲ reflex Ⅲ lung T he present article will attempt to support the hypothesis that in the early phase of congestive heart failure and other pathophysiological conditions, such as myocardial ischemia and arterial hypertension, sympathetic excitation seems devoid of an ultimate homeostatic purpose, and its genesis may be, in part, attributable to an enhanced peripheral excitatory function of sympathetic afferent fibers.In physiological conditions, the cardiovascular neural regulation is likely to result from a complex interaction of central integration and peripheral inhibitory and excitatory reflexes. [1][2][3] In this interplay, cardiovascular sympathetic afferent fibers mediate a reflex action that is largely excitatory in nature 1 (Figure). When a sympathetic excitation is part of an integrated physiological pattern with a clear ultimate purpose, such as emotion, the central neural and, in particular, diencephalic mechanisms 4 are likely to play a predominant role. However, the central command is also likely to be reinforced by a synergistic enhancement of peripheral excitatory reflex mechanisms, accompanied by a simultaneous attenuation of mechanisms exerting an inhibitory action. 3,4

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“…Second, MSNA could be modulated through arterial baroreflexes in response to respiratory variations of arterial pressure, because arterial baroreflex control of sympathetic nerve activity is preserved in heart failure. 28,29 Random-interval respiration provided an opportunity to examine the effects of a wide range of blood pressures and lung inflations on MSNA and demonstrated that lung inflation suppressed MSNA more effectively as blood pressure was maintained at an elevated level. These findings suggest that arterial baroreflex and lung stretch reflex modulate MSNA independently but synergistically.…”

Section: Study Limitationsmentioning

confidence: 99%

Respiratory Modulation of Muscle Sympathetic Nerve Activity in Patients With Chronic Heart Failure

et al. 2001

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Background-Sympathoexcitation and respiratory instability are closely related to worsening of chronic heart failure. To elucidate the dynamic nature of respiratory modulation of sympathetic activity in patients with heart failure, we studied within-breath variation of muscle sympathetic nerve activity (MSNA) under various ventilatory volumes. Methods and Results-MSNA, blood pressure, and respiratory flow were recorded in 23 patients with left ventricular ejection fraction Յ45%. Within-breath suppression of MSNA (neural silence) was found in 11 patients (MSNA bursts: 71Ϯ10/100 heartbeats) but not in the remaining 12 patients (MSNA bursts: 88Ϯ8/100 heartbeats). Patients without neural silence had a smaller tidal volume (391Ϯ70 versus 267Ϯ75 mL/m 2 , PϽ0.01) and a higher respiratory rate (15Ϯ2 versus 19Ϯ4 breaths/min, PϽ0.01) during spontaneous respiration than those with neural silence. The relationship between tidal volume and minimal amplitude of MSNA bursts in each breath was obtained during random-interval breathing and fitted by an exponential function. The curve of patients without neural silence was shifted to the right and upward, which suggests that a greater tidal volume was required to suppress MSNA (227Ϯ70 versus 437Ϯ195 mL/m 2 , PϽ0.01). Conclusions-Sympathoexcitation in patients with chronic heart failure is closely related to both a decrease in resting tidal volume and an attenuated sympathoinhibitory effect of lung inflation reflex.

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Sympathetic Alternans

Cited by 43 publications

References 23 publications

Sympathetic Response to Ventricular Extrasystolic Beats in Hypertension and Heart Failure

Sympathetic Response to Ventricular Extrasystolic Beats in Hypertension and Heart Failure

Emerging Excitatory Role of Cardiovascular Sympathetic Afferents in Pathophysiological Conditions

Respiratory Modulation of Muscle Sympathetic Nerve Activity in Patients With Chronic Heart Failure

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