Spectral and cross-spectral autoregressive analysis of cardiovascular variables in subjects with different degrees of orthostatic tolerance

The mechanisms leading to vasovagal syncope are still unclear. A simple discriminating test for the identification of syncopeprone subjects is not presently available. Fifty-two subjects had a stepwise orthostatic test with 60° tilt and -20 and -40 mm Hg lower-body negative pressure before the appearance of impending syncope symptoms. Spectral and cross-spectral analyses of heart period and systolic pressure time series were performed to estimate the power of the high-frequency (≅ 0.25 Hz) and low-frequency (≅ 0.1 Hz) oscillations, the coherence between heart period and systolic pressure, and the mean low-frequency and high-frequency central frequency, phase shift, and transfer function at maximal coherence. According to time to presyncope, the 52 subjects were divided into two groups: 25 with normal orthostatic tolerance, and 27 with poor orthostatic tolerance. In the supine positions, the mean central low-frequency was significantly lower in poortolerance group than in normal-tolerance group, discriminating poor from normal orthostatic tolerance with 80% specificity and 83% sensitivity, and was significantly correlated to time to presyncope. In the 2 to 3 minutes preceding syncope, subjects with poor orthostatic tolerance had less tachycardia, lower low-frequency power of systolic pressure, higher respiratory frequency, and a less negative phase shift in high-frequency range. In presyncope, sympathetic activation is reduced in subjects with poor orthostatic tolerance. In addition, the higher breathing frequency and the smaller negativity of phase shift in high-frequency range, which may indicate an inadequate engagement of the baroreflex, suggest a causal role of respiration in the development of syncope. Supine central values of low frequency may be proposed as a valuable clinical index of orthostatic intolerance.