Differences in autonomic balance in patients with cardioinhibitory and vasodepressor type of reflex syncope during head-up tilt test and active standing.

OBJECTIVE

To improve the pathophysiological understanding of cardioinhibitory and vasodepressor reflex syncope, by evaluating orthostatic effects on electrical and hemodynamic variables. To unravel the pathogeneses further, we studied these effects during both the passive head-up tilt test and the active standing test.

BACKGROUND

The current knowledge of the compromised autonomic balance in patients with reflex syncope is limited. The orthostatic responses to head-up tilt test in cardioinhibitory and vasodepressor patients differ, suggesting different pathogeneses; however, the more physiological active standing test represents daily life situations better.

METHODS

We included 74 patients; 36 cardioinhibitory and 38 vasodepressor. Patients were compared with respect to vascular hemodynamics and heart rate variability during the change from supine to upright position. Resting electrolytes, brain natriuretic peptide (BNP), pro-atrial natriuretic peptide (pro-ANP), and the C-terminal of pro-vasopressin, copeptin were measured.

RESULTS

Resting systolic blood pressure was higher in cardioinhibitory (117.8 ± 15.7 mmHg) than in vasodepressor patients (109.1 ± 15.3 mmHg, p < 0.001). Changes in heart rate tended to be smaller in cardioinhibitory patients (6.7 ± 9.8 vs. 10.7 ± 8.9 bpm, p = 0.056). Heart rate variability was lower and changed less in cardioinhibitory patients (p < 0.05). Cardioinhibitory patients had higher pro-ANP levels (63.5 ± 18.8 pM) compared to vasodepressor patients (54.2 ± 31.4 pM, p = 0.018). Responses during active standing were attenuated compared to head-up tilt in both groups.

CONCLUSIONS

This study demonstrated that cardioinhibitory patients had higher blood pressure, attenuated hemodynamic responses, and reduced autonomic regulation compared to vasodepressor patients. Furthermore, cardioinhibitory patients showed a sympathetic predominance in their modulation of autonomic responses. Orthostatic responses induced by active standing were modest and did not sufficiently explain potential pathophysiological differences between cardioinhibitory and vasodepressor patients.