Barton David A, Dawood Tye, Lambert Elisabeth A, Esler Murray D, Haikerwal Deepak, Brenchley Celia, Socratous Florentia, Kaye David M, Schlaich Markus P, Hickie Ian, Lambert Gavin W
Human Neurotransmitter Laboratory, Australia.
J Hypertens. 2007 Oct;25(10):2117-24. doi: 10.1097/HJH.0b013e32829baae7.
Evidence exists linking major depressive disorder (MDD) with clinical cardiovascular events. The importance of the sympathetic nervous system in the generation of cardiac risk in other contexts is established.
To examine the importance of the sympathetic nervous system in the generation of cardiac risk in patients with major depressive disorder (MDD).
Studies were performed in 39 patients meeting the Diagnostic and Statistical Manual of Mental Disorders IV (DSM-IV) criteria for MDD and in 76 healthy subjects. Treatment for patients consisted of selective serotonin reuptake inhibition (SSRI) for 12 weeks. Whole body and cardiac sympathetic activity were examined using noradrenaline isotope dilution methodology and sympathetic nerve recording techniques. Measurement of the extraction of infused tritiated noradrenaline by the heart, and estimation of cardiac dihydroxyphenylglycol production provided direct quantification of neuronal noradrenaline reuptake.
Sympathetic activity, particularly in the heart and for the whole body, in patients with MDD followed a bimodal distribution. Elevated values were observed in patients with co-morbid panic disorder (P = 0.006). Consistent with a defect in noradrenaline reuptake, the cardiac extraction of tritiated noradrenaline (0.80 +/- 0.01 versus 0.56 +/- 0.04%, P < 0.001) and cardiac dihydroxyphenylglycol overflow (109 +/- 8 versus 73 +/- 11, P = 0.01) were reduced in patients with MDD. SSRI therapy abolished the excessive sympathetic activation, with whole body noradrenaline spillover falling from 518 +/- 83 to 290 +/- 41 ng/min (P = 0.008).
We have identified a subset of patients with MDD in whom sympathetic nervous activity is extraordinarily high, including in the sympathetic outflow to the heart. Treatment with an SSRI may reduce sympathetic activity in a manner likely to reduce cardiac risk.
有证据表明重度抑郁症(MDD)与临床心血管事件有关。交感神经系统在其他情况下引发心脏风险的重要性已得到证实。
研究交感神经系统在重度抑郁症(MDD)患者心脏风险产生中的重要性。
对39名符合《精神疾病诊断与统计手册》第四版(DSM-IV)重度抑郁症标准的患者和76名健康受试者进行了研究。患者接受了为期12周的选择性5-羟色胺再摄取抑制剂(SSRI)治疗。使用去甲肾上腺素同位素稀释法和交感神经记录技术检测全身和心脏的交感神经活动。通过测量心脏对注入的氚标记去甲肾上腺素的摄取以及估计心脏二羟基苯乙二醇的生成来直接定量神经元去甲肾上腺素的再摄取。
MDD患者的交感神经活动,尤其是心脏和全身的交感神经活动呈双峰分布。合并惊恐障碍的患者中观察到值升高(P = 0.006)。与去甲肾上腺素再摄取缺陷一致,MDD患者心脏对氚标记去甲肾上腺素的摄取(0.80±0.01对0.56±0.04%,P < 0.001)和心脏二羟基苯乙二醇溢出(109±8对73±11,P = 0.01)降低。SSRI治疗消除了过度的交感神经激活,全身去甲肾上腺素溢出从518±83降至290±41 ng/min(P = 0.008)。
我们已经确定了一部分交感神经活动异常高的MDD患者,包括心脏的交感神经输出。SSRI治疗可能以降低心脏风险的方式降低交感神经活动。