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Updated: May 1, 2026

Tilt Testing with Combined Lower Body Negative Pressure: a "Gold Standard" for Measuring Orthostatic Tolerance
Published on: March 21, 2013
P-wave voltage and peaking on electrocardiogram in patients undergoing head-up tilt testing for history of syncope
Cesare de Gregorio1, Concetta Lentini1, Patrizia Grimaldi1
1Department of Clinical and Experimental Medicine, Cardiology Unit, University Hospital of Messina, Messina, Italy.
Background:
Only scanty data are available in the literature on P-wave (PW) morphology at ECG in patients with history of vasovagal syncope undergoing diagnostic functional testing. In this study, we evaluated resting and head-up tilt testing (HUTT) related changes in PW voltage (PWV) and duration (PVD) and their relationship with triggered syncope.
Methods:
55 patients, mean aged 41 ± 19 y (35 F), without patent heart disease or neuropathy, underwent potentiated HUTT according to the Italian protocol. Heart rate (HR), blood pressure (BP), PR-interval, PWV and PWD were measured at rest, 15 min from passive position (15-min) and after nitroglycerine (peak-HR). PW peaking (PWP) was calculated as percent increase in PWV than baseline values. Patients were divided into 2 groups based on tilt-positive (group-A) or negative (group-B) response.
Results:
20 patients (36%) entered the group-A, whereas 35 (64%) the group-B. Higher PWV was observed at baseline in group-A (0.147 ± 0.034 mV vs 0.114 ± 0.036 mV in group-B, p=0.001), with no differences in the remaining ECG measurements. BP was lower in group-A than in B, both at 15-min and peak-HR. HUTT-related PWP in lead II (the most significant among all inferior leads) was 31 ± 30% in group-A vs 95 ± 54% in group-B (p<0.0001) at 15-min, and 52 ± 44% vs 112±72% at peak-HR, respectively (p=0.002). 75% of patients with PWP ≤ 50% experienced HUTT-triggered syncope, vs 5% of those with PWP ≥ 100% (p<0.0001).
Conclusions:
This study shows a potential relationship between HUTT-triggered syncope and low or absent PWP, suggesting a role for atrial chamber functional involvement in the mechanisms underlying the vasovagal syncope.
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