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Updated: Jul 3, 2025
Tilt Testing with Combined Lower Body Negative Pressure: a "Gold Standard" for Measuring Orthostatic Tolerance
Published on: March 21, 2013
Temporal relationship between haemodynamic changes and activation of closed-loop stimulation during a tilt-induced
Vincenzo Russo1, Marco Tomaino2, Erika Parente1
1Cardiology and Syncope Unit, Department of Translational Medical Sciences, University of Campania 'Luigi Vanvitelli'-Monaldi Hospital, 80126 Naples, Italy.
Insights
Closed-loop stimulation (CLS) pacing effectively manages vasovagal syncope (VVS) by increasing heart rate during pre-syncopal phases. This study clarifies the timing and haemodynamic impact of CLS during tilt-induced VVS reflexes.
Area of Science:
- Cardiology
- Electrophysiology
- Medical Devices
Background:
- Vasovagal syncope (VVS) is a common cause of recurrent syncope.
- Dual-chamber pacemakers with closed-loop stimulation (CLS) have shown efficacy in reducing VVS recurrences.
- Understanding the haemodynamic response to CLS during a vasovagal reflex is crucial for optimizing therapy.
Purpose of the Study:
- To investigate the haemodynamic and temporal relationship of CLS during a tilt-induced vasovagal reflex.
- To characterize the onset, rate, and duration of CLS pacing in relation to circulatory instability.
- To assess the effectiveness of CLS in mitigating the haemodynamic effects of VVS.
Main Methods:
- A tilt test was performed on 20 patients with VVS who had previously received a CLS pacemaker.
- Video recording and continuous haemodynamic monitoring (heart rate, blood pressure) were utilized.
- The onset and characteristics of CLS pacing were analyzed in relation to the vasovagal response, including syncope or pre-syncope.
Main Results:
- In 14 out of 17 analyzed patients, CLS pacing initiated during the pre-syncopal phase of circulatory instability.
- CLS pacing rate increased significantly within a median of 0.1 minutes, preceding the lowest systolic blood pressure.
- CLS pacing persisted, though attenuated, at the time of maximum vasovagal effect, with an average rate of 95 bpm.
Conclusions:
- The vasovagal reflex is reproducible, and CLS pacing is activated early during the pre-syncopal phase in most VVS patients.
- CLS pacing demonstrates a haemodynamic impact by increasing heart rate during vasovagal events.
- CLS pacing appears to be an effective therapeutic strategy for managing haemodynamic instability in VVS.
Aims:
A dual-chamber pacemaker with closed-loop stimulation (CLS) mode is effective in reducing syncopal recurrences in patients with asystolic vasovagal syncope (VVS). In this study, we explored the haemodynamic and temporal relationship of CLS during a tilt-induced vasovagal reflex.
Methods And Results:
Twenty patients underwent a tilt test under video recording 3.9 years after CLS pacemaker implantation. Three patients were excluded from the analysis because of no VVS induced by the tilt test (n = 1) and protocol violation (n = 2). In 14 of the remaining 17 patients, CLS pacing emerged during the pre-syncopal phase of circulatory instability when the mean intrinsic heart rate (HR) was 88 ± 12 b.p.m. and systolic blood pressure (SBP) was 108 ± 19 mmHg. The CLS pacing rate thereafter rapidly increased to 105 ± 14 b.p.m. within a median of 0.1 min [inter-quartile range (IQR), 0.1-0.7 min] when the SBP was 99 ± 21 mmHg. At the time of maximum vasovagal effect (syncope or pre-syncope), SBP was 63 ± 17 mmHg and the CLS rate was 95 ± 13 b.p.m. The onset of CLS pacing was 1.7 min (IQR, 1.5-3.4) before syncope or lowest SBP. The total duration of CLS pacing was 5.0 min (IQR, 3.3-8.3). Closed-loop stimulation pacing was not observed in three patients who had a similar SBP decrease from 142 ± 22 mmHg at baseline to 69 ± 4 mmHg at the time of maximum vasovagal effect, but there was no significant increase in HR (59 ± 1 b.p.m.).
Conclusion:
The reproducibility of a vasovagal reflex was high. High-rate CLS pacing was observed early during the pre-syncopal phase in most patients and persisted, although attenuated, at the time of maximum vasovagal effect.
Registration:
ClinicalTrials.gov identifier: NCT06038708.
