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(Circulation. 2004;109:e171.)
© 2004 American Heart Association, Inc.

Correspondence

Baroreflex Regulation of Sympathetic Nerve Activity in Patients With Vasovagal Syncope

Raffaello Furlan, MD; Francesca Perego, MD; Simona Colombo, MD

Unita Sincopi e Disturbi della Postura, Medicine Interna II, Ospedale "L. Sacco", Universita di Milano, Milan, Italy

To the Editor:

In their study, "Dysfunctional Baroreflex Regulation of Sympathetic Nerve Activity in Patients With Vasovagal Syncope," Béchir et al¹ implied a unilateral causal relationship between reduction of arterial baroreflex control of heart rate and increase of muscle sympathetic nerve activity (MSNA) in patients with syncope. The authors concluded that dysfunctional baroreflex regulation of sympathetic activity provides "new insights into the mechanisms of vasovagal syncope..."

We have two comments.

Baroreflex function can be depressed by suprabulbar central influences and also by vagal, somatic, or sympathetic² afferents. This experimental evidence has provided strong support for the concept that baroreceptive input should be considered as one of the neural mechanisms underlying cardiovascular regulation³ and not the only mechanism, as suggested by the Béchir et al¹ study. The observation of enhanced MSNA values in patients with syncope both at rest and during lower body negative pressure¹ is in contrast to the reduced MSNA already reported⁴ and raises the possibility of an alternative interpretation of the results. Indeed, the depressed baroreflex function observed in patients with syncope¹ may be the consequence of an increase in central sympathetic drive.

In the Béchir et al¹ study, baroreflex inhibitory modulation of MSNA was inferred by using the alpha index that only assesses arterial baroreflex control of heart rate.

A comprehensive approach to arterial baroreflex modulation of heart rate and MSNA in patients with syncope has been previously published in a study⁴ misquoted in the Béchir et al¹ paper. An exhaustive assessment of baroreflex function should consider several aspects besides alpha index, including the definition of the entire sigmoidal baroreflex curve during drug infusion and the evaluation of spontaneous reciprocal changes of heart rate, arterial pressure, central venous pressure, and MSNA during progressive tilt (or lower body negative pressure).⁵

References

1. Béchir M, Binggeli C, Corti R, et al. Dysfunctional baroreflex regulation of sympathetic nerve activity in patients with vasovagal syncope. Circulation. 2003; 107: 1620–1625.[Abstract/Free Full Text]
   
2. Pagani M, Pizzinelli P, Bergamaschi M, et al. A positive feedback sympathetic pressor reflex during stretch of the thoracic aorta in conscious dogs. Circ Res. 1982; 50: 125–132.[Abstract/Free Full Text]
   
3. Malliani A. General concepts and hypothesis in the study of cardiovascular neural regulation. In: Principles of Cardiovascular Neural Regulation in Health and Disease. Boston, Mass: Kluwer Academic Publishers; 2000.
   
4. Mosqueda-Garcia R, Furlan R, Fernandez-Violante R et al. Sympathetic and barorereceptor reflex function in neurally mediated syncope evoked by tilt. J Clin Invest. 1997; 99: 2736–2744.[Medline] [Order article via Infotrieve]
   
5. Mosqueda-Garcia R, Furlan R, Tank J, et al. The elusive pathophysiology of neurally mediated syncope. Circulation. 2000; 102: 2898–2906.[Free Full Text]
   

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Response

Markus Béchir, MD; Christian Binggeli, MD; Roberto Corti, MD; Remy Chenevard, MD; Lukas Spieker, MD; Frank Ruschitzka, MD; Thomas F. Lüscher, MD; Georg Noll, MD

Cardiovascular Center, Department of Cardiology, University Hospital, Zürich, Switzerland

We thank Dr Furlan and colleagues for their comments concerning our study.¹

First, there is no doubt that there are many contributing cofactors in the pathophysiology of vasovagal syncope. Thus, a baroreceptor dysfunction is, indeed, only one underlying factor, but probably an important one. Many other studies (even one of the respondents’) have shown such an impairment.^2,3 Indeed, in our study, we did not suggest impaired baroreceptor sensitivity as the only pathophysiological factor in the genesis of vasovagal syncope

Second, there are stimulus-dependent and -independent baroreceptor testing methods. We used only a stimulus-independent one, because the infusion of vasodilators may lead to syncope, which was not the aim of our study. Furthermore, many substances can interfere pharmacologically with the endings of the baroneurons in the vasculature.⁴ This, in turn, might lead to a change in baroreceptor sensitivity.

References

1. Béchir M, Binggeli C, Corti R, et al. Dysfunctional baroreflex regulation of sympathetic nerve activity in patients with vasovagal syncope. Circulation. 2003; 107: 1620–1625.[Abstract/Free Full Text]
   
2. Mosqueda-Garcia R, Furlan R, Fernandez-Violante R, et al. Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt. J Clin Invest. 1997; 99: 2736–2744.[Medline] [Order article via Infotrieve]
   
3. Thomson HL, Wright K, Frenneaux M. Baroreflex sensitivity in patients with vasovagal syncope. Circulation. 1997; 95: 395–400.[Abstract/Free Full Text]
   
4. Chapleau MW, Cunningham JT, Sullivan MJ, et al. Structural versus functional modulation of the arterial baroreflex. Hypertension. 1995; 26: 341–347.[Abstract/Free Full Text]
   

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