Cerebral Autoregulation Is Impaired In Recurrent Syncope Patients

Abstract

PURPOSE: Cerebral autoregulation is a homeostatic mechanism that serves to maintain cerebral blood flow constant over a wide range of perfusion pressure. Syncope is thought to be caused by cerebral hypoperfusion due to the transient blood pressure drop, and thus impairment of cerebral autoregulation may facilitate syncope. A previous study has reported that a past history of syncope is a strong predictor of future syncope recurrence. However, it is unclear whether impaired cerebral autoregulation would be related with recurrent syncope. The purpose of this study was to test our hypothesis that cerebral autoregulation would be impaired in syncope patients with a past history of syncope as compared with those for the first time. METHODS: We evaluated cerebral autoregulation in 24 syncope patients for the first time (age; 64±19 years old, male/ female; 15/9) and 20 syncope patients with a past history of syncope (age; 52±26 years old, male/female; 11/9). In patients with recurrent syncope, the number of past syncope was 2.9±1.6 times (range 2-7 times). Middle cerebral artery mean blood flow velocity (MCA Vmean) and mean arterial pressure (MAP) were measured by transcranial Doppler ultrasound and tonometry on right radial artery for 3 min in the supine position. In offline analysis after the measurement, the transfer function gain between MAP and MCA Vmean were calculated at very low frequency (0.023-0.07 Hz, VLF) and low frequency (0.07-0.2 Hz, LF) ranges to estimate dynamic cerebral autoregulation. RESULTS: LF gain did not differ between syncope patients with a past history of syncope and those for the first time (P=0.23). In contrast, VLF gain was significantly higher in patients with a past history of syncope than in those for the first time (1.81±1.17 cm/s/mmHg vs. 1.09±0.65 cm/s/mmHg, P=0.02). CONCLUSIONS: These data suggest that impaired cerebral autoregulation at least in part explains physiological mechanisms underlying recurrent syncope.