16 research outputs found

    Major depression with ischemic heart disease: Effects of paroxetine and nortriptyline on long-term heart rate variability measures

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    Background: Studies have linked depression to sudden death and serious cardiovascular events in patients with preexisting cardiac illness. Recent studies have shown decreased vagal function in cardiac patients with depression and depressed patients without cardiac illness. Methods: We compared 20-hour, sleeping, and awake heart period variability measures using spectral analysis, fractal dimension, and symbolic dynamics in two patient groups with major depression and ischemic heart disease (mean age 59-60 years) before and after 6 weeks of paroxetine or nortriptyline treatment. Results: Spectral measures showed decreases in awake and sleeping total power (TP: 0.0-0.5 Hz), ultra low frequency power (ULF: 0-0.0033 Hz), very low frequency power (VLF: 0.0033-0.04 Hz), and low-frequency power (LF: 0.04-0.15 Hz) for nortriptyline condition and a decrease in high-frequency power (HF: 0.15-0.5 Hz) for the awake condition in patients who received nortriptyline. A measure of nonlinear complexity, WC-100, significantly increased after paroxetine during the awake condition. Conclusions: These findings suggest that nortriptyline has stronger vagolytic effects on cardiac autonomic function compared with paroxetine, which is in agreement with previous clinical and preclinical reports. Paroxetine may have some cardio-protective effects, especially in cardiac patients

    Major depression with ischemic heart disease: Effects of paroxetine and nortriptyline on measures of nonlinearity and chaos of heart rate

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    Depression is associated with increased cardiovascular mortality in patients with preexisting cardiac illness. A decrease in cardiac vagal function as suggested by a decrease in heart rate variability (HRV) or heart period variability has been linked to sudden death in patients with cardiac disease as well as in normal controls. Recent studies have shown decreased vagal function in cardiac patients with depression as well as in depressed patients without cardiac illness. In this study, we compared 20 h awake and sleep heart period nonlinear measures using quantification of nonlinearity and chaos in two groups of patients with major depression and ischemic heart disease (mean age 59-60 years) before and after 6 weeks of treatment with paroxetine or nortriptyline. Patients received paroxetine, 20-30 mg/day or nortriptyline targeted to 190-570 nmol/l for 6 weeks. For HRV analysis, 24 patients were included in the paroxetine treatment study and 20 patients in the nortriptyline study who had at least 20,000 s of awake data. The ages of these groups were 60.4 +/- 10.5 years for paroxetine and 60.8 +/- 13.4 years for nortriptyline. There was a significant decrease in the largest Lyapunov exponent (LLE) after treatment with nortriptyline but not paroxetine. There were also significant decreases in nonlinearity scores on S-netPR and S-netGS after nortriptyline, which may be due to a decrease in cardiac vagal modulation of HRV. S-netGS and awake LLE were the most significant variables that contributed to the discrimination of postparoxetine and postnortriptyline groups even with the inclusion of time and frequency domain measures. These findings suggest that nortriptyline decreases the measures of chaos probably through its stronger vagolytic effects on cardiac autonomic function compared with paroxetine, which is in agreement with previous clinical and preclinical reports. Nortriptyline was also associated with a significant decrease in nonlinearity scores, which may be due to anticholinergic and/or sympatholytic effects. As depression is associated with a strong risk factor for cardiovascular mortality, one should be careful about using any drug that adversely affects cardiac vagal function. Copyright (C) 2002 S. Karger AG, Basel

    Twenty-four-hour QT interval variability: Increased QT variability during sleep in patients with panic disorder

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    Recent studies on beat-to-beat QT interval variability (QTV) have shown that it can be used as a noninvasive measure of cardiac repolarization lability. It is also a predictor of sudden cardiac death and is higher in patients with anxiety and depression. This study examined the diurnal measures in QTV in 32 normal adults and 22 patients using 24-hour electrocardiogram records. We obtained 8 5-min segments of ECG sampled at 1,000 Hz from the 24-hour records. Our results show that QTV measures at nighttime are significantly higher in patients with panic disorder compared with controls. These findings demonstrate blunted diurnal changes in ventricular repolarization lability in patients resulting in a higher QT variability index during sleep. We speculate that these effects may relate to a relative increase in cardiac sympathetic activity in patients with panic disorder, and may contribute to the increased risk for cardiac mortality in patients with anxiety. Copyright (C) 2002 S. Karger AG, Basel

    Twenty-four hour QT variability: Increased QT variability during sleep in patients with panic disorder

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    Hemodynamic changes in depressive patients

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    Objective: This study is aimed at exploring the relationship between hemodynamic changes and depressive and anxious symptom in depression patients. Methods: The cardiac function indices including the left stroke index (LSI), ejection fraction (EF), heart rate (HR), diastolic pressure mean (DPM), systolic pressure mean (SPM), left ventricle end-diastolic volume (LVDV), effective circulating volume (ECV), resistance total mean (RTM) and blood flow smooth degree (BFSD) were determined in 65 patients with major depressive disorders and 31 healthy normal controls. The clinical symptoms were assessed with Hamilton depression scale (HAMD) and Hamilton anxiety scale (HAMA). Results: In patients with depression without anxiety, LSI, EF, LVDV, DPM, SPM, ECV, BFSD were significantly lower than those in controls, while RTM was higher than that in controls. Patients with comorbidity of depression and anxiety showed decreased LVDV, ECV, BFSD, and increased HR in comparison with the controls. The anxiety/somatization factor score positively correlated with LSI, EF, LVDV, but negatively correlated with RTM. There was negative correlation between retardation factor score and DPM, SPM, LVDV. Conclusion: The study indicated that there are noticeable changes in left ventricle preload and afterload, blood pressure, peripheral resistance, and microcirculation in depressive patients, and that the accompanying anxiety makes the changes more complicated
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