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(Circulation. 2001;104:2694.)
© 2001 American Heart Association, Inc.

Clinical Investigation and Reports

Cerebral Vasoconstriction in Vasovagal Syncope: Any Link With Symptoms?

A Transcranial Doppler Study

Alfonso Lagi, MD; Simone Cencetti, MD; Vanni Corsoni, MD; Dimitrios Georgiadis, MD; Stefano Bacalli, MD

From the Department of Internal Medicine, Autonomic Unit, Santa Maria Nuova Hospital, Firenze, Italy, and the Institute of Neurology, Martin-Luther-University, Halle Wittenberg, Germany (D.G.).

Reprint requests to Dr Alfonso Lagi, Via G. Mameli 44, 50131 Firenze, Italy. E-mail lagi{at}dada.it

Background— Cerebral vasoconstriction has been described previously in vasovagal syncope (VVS). This phenomenon appears paradoxical in view of the well-known decrease of systemic vascular resistances taking places during VVS. We aimed to assess (1) whether cerebral vasoconstriction in VVS is an independent paradoxical phenomenon and (2) whether cerebral vasoconstriction has any link with symptoms and/or VVS onsets.

Methods and Results— Seven young patients with recurrent VVS participated in the study. Each patient underwent monitoring of heart rate, blood pressure, cerebral blood flow velocity (by means of transcranial Doppler), end-tidal PCO₂, peripheral oximetry, respiratory rate, and tidal volumes both at rest and during head-up tilt. All the subjects experienced tilt-induced VVS. A significant increase of respiratory tidal volumes was observed in each subject 160 seconds before VVS. This deep breathing induced a PCO₂ decrease and, consequently, also a decrease in cerebral blood flow velocity and increase in cerebrovascular resistance (expressed by the increase of the pulsatility index). Within 40 seconds, 5 subjects started complaining of discomfort, in the absence of any significant blood pressure drop.

Conclusions— Cerebral vasoconstriction is not a paradoxical phenomenon when it occurs before tilt-induced VVS but rather is only the physiological consequence of the hyperventilation-induced hypocapnia that occurs in habitual fainters. The large lag between the onset of syncope and cerebral vasoconstriction excludes the hypothesis that VVS is dependent on abnormal behavior of cerebral hemodynamics.

Key Words: syncope • cerebrovascular circulation • ultrasonics

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