Catecholamine response during haemodynamically stable upright posture in individuals with and without tilt-table induced vasovagal syncope.

Abstract

Changes in circulating catecholamine concentrations during vasovagal faints have been the subject of considerable study. However, whether catecholamines are part of the triggering mechanism, or principally reflect attempted compensation for an evolving circulatory crisis is unknown. To address this issue, we determined whether the circulating catecholamine response to upright posture differs among patients with and without inducible vasovagal faints at a time when there is no detectable haemodynamic compromise. Blood samples for measurement of adrenaline and noradrenaline (Norepi) concentrations were obtained in the baseline state, and at both 2-3 min and 4-6 min of upright posture in 22 patients undergoing head-up tilt-table testing for evaluation of syncope of unknown cause. In 11 individuals tilt-testing induced syncope at >5 min head-up posture (Group 1). In 11 other individuals tilt testing did not result in syncope (Group 2). Supine arterial catecholamine levels were comparable in the two groups. However, adrenaline concentrations during upright posture tended to be greater at 2-3 min and were significantly greater at 4-6 min in Group 1 than in Group 2 (P< 0.01). These differences occurred in the absence of significant intergroup differences in mean arterial pressure or cardiac cycle lengths. Norepi concentrations also increased in both groups, but without significant differences. Circulating adrenaline concentrations in posturally induced vasovagal faints rise more rapidly in vasovagal fainters than in comparably posturally stressed non-fainters, and were significantly greater in fainters prior to either detectable haemodynamic compromise or diminution of circulating Norepi levels. These findings suggest that a premonitory rise in adrenaline concentrations occurs in vasovagal fainters unassociated with an evolving circulatory crisis.