Progressive baroreflex dysfunction and hypotension preceding VVS: a vicious cycle?

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.

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.

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.

Presyncope appeared to be initiated by a fall in sympathetic baroreflex gain despite increased levels at baseline and early tilt.