Straneva-Meuse Patricia A, Light Kathleen C, Allen Michael T, Golding Michael, Girdler Susan S
University of North Carolina at Chapel Hill, CB #7175, Medical Research Building A, Chapel Hill, NC 27599-7175, USA.
J Affect Disord. 2004 Apr;79(1-3):51-61. doi: 10.1016/S0165-0327(02)00352-X.
There exists a need to identify safe and effective treatments for depression in patients with coronary heart disease (CHD).
Using a cross-sectional design, 17 depressed patients being treated with bupropion (200-450 mg/day) were compared with 17 depressed patients being treated with paroxetine (10-50 mg/day) and with a group of 15 unmedicated, non-depressed controls for cardiovascular, neuroendocrine and heart rate variability (HRV) measures at rest and in response to mental and physical stressors.
Regardless of treatment, both treated groups exhibited blunted plasma cortisol, plasma epinephrine, systolic blood pressure, cardiac output, and pre-ejection period responses to mental stressors relative to controls. Bupropion treated individuals exhibited greater total peripheral resistance (TPR) increases than either the paroxetine or control groups, and greater plasma norepinephrine (NE) increases to mental stressors than the paroxetine group. The bupropion group also displayed reduced HRV at rest relative to the controls and during orthostatic challenge relative to both the control and paroxetine groups.
Despite the fact that the treated groups were well matched for depression and other psychiatric histories, lack of randomization into treatment arms may be associated with a selection bias in the two treated groups.
Although both pharmacological treatments were associated with a blunting of some cardiovascular and neuroendocrine responses to stress relative to controls, which may be reflective of their therapeutic mechanisms of action, the results of our study also suggest that bupropion is associated with a more detrimental autonomic profile than paroxetine, as reflected in increased TPR and NE, and reduced HRV. The results of this study may have implications for the pharmacological treatment of depression in CHD patients.
需要确定冠心病（CHD）患者抑郁症的安全有效治疗方法。
采用横断面设计，将17例接受安非他酮治疗（200 - 450毫克/天）的抑郁症患者与17例接受帕罗西汀治疗（10 - 50毫克/天）的抑郁症患者以及15例未用药的非抑郁症对照组进行比较，测量他们在静息状态以及对精神和身体应激源反应时的心血管、神经内分泌和心率变异性（HRV）指标。
无论接受何种治疗，相对于对照组，两个治疗组在面对精神应激源时，血浆皮质醇、血浆肾上腺素、收缩压、心输出量和射血前期反应均减弱。与帕罗西汀组或对照组相比，接受安非他酮治疗的个体总外周阻力（TPR）增加幅度更大，对精神应激源的血浆去甲肾上腺素（NE）增加幅度比帕罗西汀组更大。与对照组相比，安非他酮组在静息时的HRV降低，与对照组和帕罗西汀组相比，在直立位应激试验期间HRV也降低。
尽管治疗组在抑郁症和其他精神病史方面匹配良好，但未随机分配治疗组可能导致两个治疗组存在选择偏倚。
尽管相对于对照组，两种药物治疗都与对应激的一些心血管和神经内分泌反应减弱有关，这可能反映了它们的治疗作用机制，但我们的研究结果还表明，安非他酮与比帕罗西汀更有害的自主神经特征有关，表现为TPR和NE增加以及HRV降低。本研究结果可能对冠心病患者抑郁症的药物治疗具有启示意义。
