Agelink Marcus W, Klimke A, Cordes J, Sanner D, Kavuk I, Malessa R, Klieser E, Baumann B
Department of Psychiatry, Psychotherapy and Psychosomatic Medicine, Ruhr-University of Bochum, Germany.
Eur J Med Res. 2004 Jan 26;9(1):37-50.
Numerous studies provide evidence that major depression (MD) is associated with certain disorders of cardiac autonomic nervous system (ANS) function, in particular, with an autonomic neurocardiac imbalance characterized by a low cardiovagal modulation, a raised sympathetic nerve activity and a high resting heart rate. We assume that such MD-associated cardiac ANS disorders are mainly caused by functional-structural abnormalities within the central autonomic network (CAN), in particular, by well-defined abnormalities of hypothalamic structures in MD. In view of the well-known association between an autonomic neurocardiac imbalance and the risk for cardiac arrhythmias, we assume that MD-associated cardiac ANS disorders are at least partly responsible for the high cardiovascular mortality risk in MD. It is, however, still unclear whether antidepressive treatment will lower the risk for cardiovascular complications in MD. There is convincing evidence that a successful antidepressive treatment with electroconvulsive therapy, cognitive behavioral therapy, or pharmacotherapy with primarily non-antimuscarinergic antidepressants can improve an initially disturbed cardiac ANS function in MD. These studies correspond well to our findings that treatment with both, nefazodone or reboxetine, can induce a reduction of central sympathetic nerve activity and an increase of the initially lowered cardiovagal modulation depending on the improvement of depressive symptoms after treatment. Since both effects occured obviously independent from the primarily serotonergic or noradrenergic action of the antidepressants, our findings suggest the existence of a generally supraordinate and uniform mechanism underlying the ANS effects of antidepressive treatment with drugs inhibiting serotonin- or noradrenaline reuptake.
大量研究表明，重度抑郁症（MD）与心脏自主神经系统（ANS）功能的某些紊乱有关，特别是与一种自主神经心脏失衡有关，其特征是迷走神经调节降低、交感神经活动增强和静息心率升高。我们假设，这种与MD相关的心脏ANS紊乱主要是由中枢自主神经网络（CAN）内的功能结构异常引起的，特别是由MD中下丘脑结构的明确异常引起的。鉴于自主神经心脏失衡与心律失常风险之间的众所周知的关联，我们假设与MD相关的心脏ANS紊乱至少部分是MD中心血管高死亡率风险的原因。然而，抗抑郁治疗是否会降低MD中心血管并发症的风险仍不清楚。有令人信服的证据表明，采用电休克疗法、认知行为疗法或主要使用非抗胆碱能抗抑郁药的药物疗法进行成功的抗抑郁治疗，可以改善MD中最初紊乱的心脏ANS功能。这些研究与我们的发现非常吻合，即使用奈法唑酮或瑞波西汀治疗均可降低中枢交感神经活动，并根据治疗后抑郁症状的改善，增加最初降低的迷走神经调节。由于这两种效应显然独立于抗抑郁药的主要血清素能或去甲肾上腺素能作用，我们的发现表明，存在一种普遍的、更高层次的统一机制，是抑制血清素或去甲肾上腺素再摄取的抗抑郁药物对ANS产生作用的基础。
