Cerebral vasoconstriction in vasovagal syncope: Any link with symptoms? A transcranial Doppler study

Citation
A. Lagi et al., Cerebral vasoconstriction in vasovagal syncope: Any link with symptoms? A transcranial Doppler study, CIRCULATION, 104(22), 2001, pp. 2694-2698
Citations number
34
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CIRCULATION
ISSN journal
00097322 → ACNP
Volume
104
Issue
22
Year of publication
2001
Pages
2694 - 2698
Database
ISI
SICI code
0009-7322(20011127)104:22<2694:CVIVSA>2.0.ZU;2-B
Abstract
Background-Cerebral vasoconstriction has been described previously in vasov agal 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 indep endent 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-tida l Pco(2), 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 greater than or equal to 160 seconds before VVS. This deep breathin g induced a Pco(2) decrease and, consequently, also a decrease in cerebral blood flow velocity and increase in cerebrovascular resistance (expressed b y the increase of the pulsatility index). Within 40 seconds, 5 subjects sta rted complaining of discomfort, in the absence of any significant blood pre ssure drop. Conclusions-Cerebral vasoconstriction is not a paradoxical phenomenon when it occurs before tilt-induced VVS but rather is only the physiological cons equence of the hyperventilation-induced hypocapnia that occurs in habitual fainters. The large lag between the onset of syncope and cerebral vasoconst riction excludes the hypothesis that VVS is dependent on abnormal behavior of cerebral hemodynamics.