Benditt D G, Ermis C, Padanilam B, Samniah N, Sakaguchi S
Cardiac Arrhythmia Center, Department of Medicine (Cardiovascular Division), University of Minnesota Medical School, Minneapolis, Minnesota, USA.
Europace. 2003 Jan;5(1):65-70. doi: 10.1053/eupc.2002.0271.
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.
血管迷走性晕厥期间循环儿茶酚胺浓度的变化一直是大量研究的主题。然而,儿茶酚胺是触发机制的一部分,还是主要反映对不断发展的循环危机的代偿尝试,目前尚不清楚。为了解决这个问题,我们确定了在没有可检测到的血流动力学损害时,有和没有可诱发性血管迷走性晕厥的患者对直立姿势的循环儿茶酚胺反应是否不同。
在22例因不明原因晕厥接受头高位倾斜试验的患者中,于基线状态以及直立姿势2 - 3分钟和4 - 6分钟时采集血样,以测定肾上腺素和去甲肾上腺素(去甲肾上腺素)浓度。在11名个体中,倾斜试验在头高位姿势>5分钟时诱发晕厥(第1组)。在另外11名个体中,倾斜试验未导致晕厥(第2组)。两组仰卧位动脉儿茶酚胺水平相当。然而,第1组在直立姿势时2 - 3分钟的肾上腺素浓度趋于更高,在4 - 6分钟时显著高于第2组(P<0.01)。这些差异出现在两组平均动脉压或心动周期长度无显著差异的情况下。两组去甲肾上腺素浓度也均升高,但无显著差异。
在姿势诱发的血管迷走性晕厥中,血管迷走性晕厥患者循环肾上腺素浓度的升高比姿势应激相当但未晕厥的患者更快,并且在可检测到血流动力学损害或循环去甲肾上腺素水平降低之前,晕厥患者的肾上腺素浓度就显著更高。这些发现表明,血管迷走性晕厥患者会出现与不断发展的循环危机无关的肾上腺素浓度先兆性升高。