Impaired arterial baroreceptor sensitivity before tilt-induced syncope

Autonomic dysfunction seems to play a central role in the pathophysiology o f neurocardiogenic syncope (NCS) but conflicting data have recently become available. We evaluated autonomic nervous system (ANS) function (heart rate variability (HRV), systolic blood pressure variability (SBPV) and barorece ptor gain (BRG)) and non-invasive haemodynamics (cardiac output and total p eripheral resistance) in patients with neurocardiogenic syncope. Retrospectively, we evaluated 12 NCS patients (positive head-up tilt withou t pharmacological provocation) in the basal state and at initial tilt, 12 n on-NCS patients with tilt-negative syncope and 12 aged-matched normal contr ols. Prospectively, we evaluated 16 NCS patients to analyse the haemodynami cs and ANS activity throughout the tilt test (beginning of tilt and before syncope occurs). HRV and SBPV were accessed by fast Fourier transforms (FFT ) and spontaneous BRG by temporal sequences. slope and alpha index. Modelfl ow was used to quantify the non-invasive haemodynamics. None of the autonomic and haemodynamic parameters at baseline or in the fir st 10 min of tilt was different among the respective NCS: non-NCS syncope a nd normal control groups, except for SEP, which was higher at baseline in c ontrols. Throughout the tilt test in the prospective NCS group, the heart r ate increased (88-95 beats.min(-1), P<0.05), systolic blood pressure decrea sed (123-109 mmHg, P<0.01), and arterial baroreceptor gain was reduced (7.6 to 5.5 msmmHg(-1), P<0.01) and the absolute high frequency component of HR V (HF HRV) decreased (150-80 ms(-2), P<0.05), before syncope occurred. Ther e was no change in the low frequency component of HRV (LF HRV), SBPV, cardi ac output (CO) or total peripheral resistance (TPR). Tilt-induced syncope could not be predicted by noninvasive haemodynamic or autonomic parameters at rest or in the initial minutes of tilt. The decreas e in arterial baroreceptor gain could be a precocious expression of the tra nsient autonomic dysfunction that characterizes the occurrence of neurocard iogenic syncope. (C) 1999 The European Society of Cardiology.