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  • Title: Cerebral vasoconstriction in neurally mediated syncope: relationship with type of head-up tilt test response.
    Author: Silvani S, Padoan G, Guidi AR, Bianchedi G, Maresta A.
    Journal: Ital Heart J; 2003 Nov; 4(11):768-75. PubMed ID: 14699706.
    Abstract:
    BACKGROUND: The pathophysiology of neurally mediated syncope (NMS) is unclear. Cerebral vasoconstriction has been observed in NMS patients during tilt testing. To shed light on the pathophysiology of NMS, we attempted to establish whether the degree of cerebral vasoconstriction changes with the tilt test positivity type, scored in accordance with Sutton's classification. METHODS: Twenty-one patients (12 males and 9 females, mean age 41 +/- 15 years) consecutively admitted to tilt test evaluation were studied through simultaneous recordings of their electrocardiogram, blood pressure, electroencephalogram and transcranial Doppler sonography (TCD) of the middle cerebral artery. TCD allowed computation of the Gosling's pulsatility index [PI = (systolic velocity--diastolic velocity)/mean velocity], as an index of cerebrovascular resistance. RESULTS: In the 13 tilt-positive patients (62%), TCD revealed a significant PI increase at the onset of prodromic symptoms in comparison with baseline (2.01 +/- 0.94 vs 0.77 +/- 0.20, p < 0.001, paired-sample Student's t-test). No significant TCD alterations were seen in tilt-negative patients. Furthermore, the percentage change in the PI from baseline was significantly higher in cardioinhibitory types (254 +/- 51%, 5 patients) than in mixed and vasodepressor types (101 +/- 22%, 8 patients, p < 0.001, independent-sample Student's t-test). CONCLUSIONS: Our data show that the degree of cerebral vasoconstriction at the onset of prodromic symptoms changes with the tilt test positivity type. We suggest that in NMS patients the degree of cerebral vasoconstriction may depend on the amount of sympathetic activation. The sympathetic modulation of cerebral vasoconstriction may therefore be a turning point in the explanation of the pathophysiology of NMS.
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