Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025
Progressive baroreflex dysfunction and hypotension preceding VVS: a vicious cycle?
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Jardine D L, Stott V, Frampton C
Аннотация
PURPOSE: We aimed to clarify the mechanism for presyncope, defined as the gradual onset of hypotension, starting some minutes before vasovagal syncope. Although there is a fall in cardiac output and usually vasodilatation, the control of sympathetic activity during presyncope is uncertain.
METHODS: We retrospectively compared haemodynamics and muscle sympathetic nerve activity levels from positive tilt tests (without provocation) in patients with known vasovagal syncope (age 41 ± 3 years, 13 female, n = 27) to controls (age 39 ± 3 years, 8 female, n = 13). We used sequence methods to measure vascular sympathetic and cardiovagal baroreflex gain at baseline (lying supine) during tilt, presyncope and recovery.
RESULTS: Patients were tilted for 18.1 ± 1 min, and mean arterial pressure fell to 62 ± 3 mmHg before tilt-back. At baseline and early tilt, all haemodynamic variables were similar to controls, however sympathetic baroreflex gain was increased: -2.7 ± 0.2 bursts/100 beats/mmHg versus -2.0 ± 0.3 (p = 0.03). Cardiovagal baroreflex gain was increased at baseline 11.8 ± 0.6 ms/mmHg versus 9.3 ± 0.8 (p = 0.02). During early presyncope (from 8 to 4 min before tilt-back), sympathetic baroreflex gain fell to -2.4 bursts/100 b/mmHg and thereafter to -0.5 ± 0.3 (p = 0.01) during late presyncope, before losing correlation with mean arterial pressure. In some patients, the regression coefficient reversed before correlation was lost (n = 8) but this did not result in lower levels of nerve activity. At tilt-back, nerve activity fell below baseline levels in at least 63% of patients.
CONCLUSION: Presyncope appeared to be initiated by a fall in sympathetic baroreflex gain despite increased levels at baseline and early tilt.
METHODS: We retrospectively compared haemodynamics and muscle sympathetic nerve activity levels from positive tilt tests (without provocation) in patients with known vasovagal syncope (age 41 ± 3 years, 13 female, n = 27) to controls (age 39 ± 3 years, 8 female, n = 13). We used sequence methods to measure vascular sympathetic and cardiovagal baroreflex gain at baseline (lying supine) during tilt, presyncope and recovery.
RESULTS: Patients were tilted for 18.1 ± 1 min, and mean arterial pressure fell to 62 ± 3 mmHg before tilt-back. At baseline and early tilt, all haemodynamic variables were similar to controls, however sympathetic baroreflex gain was increased: -2.7 ± 0.2 bursts/100 beats/mmHg versus -2.0 ± 0.3 (p = 0.03). Cardiovagal baroreflex gain was increased at baseline 11.8 ± 0.6 ms/mmHg versus 9.3 ± 0.8 (p = 0.02). During early presyncope (from 8 to 4 min before tilt-back), sympathetic baroreflex gain fell to -2.4 bursts/100 b/mmHg and thereafter to -0.5 ± 0.3 (p = 0.01) during late presyncope, before losing correlation with mean arterial pressure. In some patients, the regression coefficient reversed before correlation was lost (n = 8) but this did not result in lower levels of nerve activity. At tilt-back, nerve activity fell below baseline levels in at least 63% of patients.
CONCLUSION: Presyncope appeared to be initiated by a fall in sympathetic baroreflex gain despite increased levels at baseline and early tilt.