These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Modulations of autonomic activity leading to tilt-mediated syncope.
    Author: Folino AF, Russo G, Porta A, Buja G, Cerutti S, Iliceto S.
    Journal: Int J Cardiol; 2007 Aug 09; 120(1):102-7. PubMed ID: 17141893.
    Abstract:
    BACKGROUND: Vasovagal syncope (VVS) results from a complex interaction among afferent vagal and sympathetic signals, cortical modulation and bulbar integration. The aim of our study was to evaluate the modifications of autonomic activity during Upright Tilt Test (UTT) in patients with unexplained syncope, and to correlate these changes with the specific cardiovascular reactions induced. METHODS AND RESULTS: We studied 90 patients with a mean age of 44+/-17 yrs. Frequency domain analysis of heart rate variability (HRV) (normalized units) was performed on 2 periods of 300 beats: at baseline and after 5 min of 60 degrees tilt. UTT was positive in 56 patients (62%). The responses were cardioinhibitory in 8, vasodepressive in 15, mixed in 33. Baseline LF and HF components did not show significant difference between subjects with positive or negative test (HF: 39+/-21 versus 41+/-22; LF: 50+/-22 versus 49+/-23). HRV during UTT showed similar changes in patients with positive or negative test. However, subjects with mixed or cardioinhibitory reactions were characterized by a relevant increase of LF during UTT (from 47+/-23 to 66+/-21), whereas the others by a non-significant decrease of the same component (from 57+/-19 to 51+/-31). CONCLUSIONS: Patients developing a reflex cardioinhibitory reaction during UTT were characterized by an increase of sympathetic activity during the test, that might represent an essential factor to induce a stronger vagal reaction on the sinus node. On the contrary, in subjects with vasodepressive reactions an inadequate enhancement of the sympathetic drive, probably causing a failure of peripheral vasoconstriction, was evidenced.
    [Abstract] [Full Text] [Related] [New Search]