Key result
Epilepsy in vasovagal syncope is linked to lower sympathetic-vagal activation, with ~54% lower tilt LF/HF ratio.
Why the study?
Seizures and syncope can coexist and both may present with autonomic dysfunction, prompting this evaluation of heart rate variability during tilt table testing in patients with vasovagal syncope with and without epilepsy.
Does the presence of epilepsy alter heart rate variability parameters during head-up tilt table testing in patients with vasodepressor syncope?
Cross-Sectional (n=24)
No
Does the presence of epilepsy alter heart rate variability parameters during head-up tilt table testing in patients with vasodepressor syncope?
Patients with coexisting epilepsy and vasodepressor syncope exhibit lower sympathetic-vagal activation (lower supine LF and tilt LF/HF ratio) during tilt table testing compared to patients with vasodepressor syncope without epilepsy, independent of clinical presentation or hemodynamic parameters.
Answers are grounded in this paper and cite their sources.
Epilepsy may modify heart rate variability in vasovagal syncope; hypothesis-generating for autonomic interactions, pending prospective validation.
Background: The main causes of transient loss of consciousness are neurological emergencies involving seizures and syncope. The two clinical conditions can coexist, and both may present with autonomic dysfunction. Aims: to evaluate heart rate variability (HRV) in participants with vasovagal syncope, comparing those with epilepsy (group A) and those without epilepsy (group B), all without structural heart disease or conditions affecting HRV, and matched for sex and age, who undergoing the tilt table testing (HUTT). Methods: 24 patients were included, 8 from group A, undergoing HUTT at 70º, under Holter monitoring. HRV was performed using Fourier transformation [high-frequency (HF) and low-frequency (LF) components and the LF/HF ratio] in the supine position and at the 10th minute of HUTT. Only those with a vasodepressor phenotype who showed a positive response were included. Results: the mean age was 39.3 years (A) and 32.3 years (B), 15 females. There was no difference between the groups regarding the presence of prodromes, physical injury, Calgary score, blood pressure, heart rate and vasovagal response to HUTT. Log-transformed LF was 2.6 ms2 in group A and 3.0 in group B, p=0.02 (supine position); and LF/HF was 2.6 and 5.7, respectively, p=0.01 (HUTT). There was a reduction in the HF component and an increase in the LF/HF ratio with inclination (p < 0.0001 for both). Conclusions: Sympathetic-vagal activation was lower in participants with epilepsy and syncope compared to those without epilepsy and with syncope. There was no influence of premonitory signs, Calgary score, hemodynamic data, or HUTT positivity.
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Silva et al. (2026) conducted a cross-sectional in Vasovagal syncope (vasodepressor phenotype) with and without epilepsy (n=24). Coexisting epilepsy in patients with vasovagal syncope vs. Vasovagal syncope without epilepsy (matched 2:1 for age and sex) was evaluated on Low-frequency to high-frequency (LF/HF) heart rate variability ratio at the 10th minute of head-up tilt table testing (HUTT) (p=0.016). Patients with both epilepsy and vasovagal syncope had lower sympathetic-vagal activation than those with syncope alone, with a lower supine log-LF (2.6 vs 3.0 ms², p=0.02) and HUTT LF/HF ratio (2.6 vs 5.7, p=0.016).
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