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BACKGROUND: Depression is a common comorbid condition in patients with chronic heart failure (CHF). This pilot study investigated the plasma levels of oxidative stress markers in depressed CHF patients as well as the effects of antidepressant treatment with sertraline on these markers in the same patient population. METHODS AND RESULTS: Patients with positive depression screening [Beck Depression Inventory (BDI) score >10 and/or Zung Self-Rating Depression Scale >40] underwent a psychiatric interview. Patients newly diagnosed as depressed received pharmacologic treatment with sertraline for 3 months (arm A) and were compared with those who did not comply with the antidepressant treatment (arm B). Markers of oxidative stress [malondialdehyde (MDA) and protein carbonyls (PC)], and nitrosative stress [nitrotyrosine (NT)] were assessed at baseline and 3 months later. Fifty-two out of 254 screened hospitalized CHF patients were diagnosed as depressed. Depressed patients had significantly higher levels of MDA compared with age- and gender-matched nondepressed patients (n = 40; 3.2 ± 2.0 vs 2.8 ± 3.8 [mu]mol/L; P = .02). Twenty-eight patients received sertraline (arm A), and 24 refused to receive antidepressant treatment on the top of optimal heart failure treatment (arm B). Although baseline levels of MDA and PC in arm A and arm B did not differ significantly (P > .05), arm A patients demonstrated a significant reduction in MDA (F = 4.657; P = .037) and arm B patients demonstrated no change after 3 months. Regarding the examined scores, arm A patients had a decrease in BDI score (28 ± 11 vs 21 ± 13; P = .008), and arm B patients had no change in BDI score at follow-up (P > .05). Arm A had an increase in 6-minute walking distance (291 ± 110 vs 361 ± 87 m; P = .02), and arm B experienced no change (P > .05). CONCLUSIONS: Increased oxidative stress may play a critical role in the pathophysiology of depression in CHF. Treatment with sertraline improves depressive symptoms and reduces plasma markers of oxidative stress in depressed CHF patients. [ABSTRACT FROM AUTHOR]

Background: The aim of this study was to evaluate the effects of carvedilol therapy on left atrial (LA) function in patients with heart failure from nonischemic dilated cardiomyopathy. Methods and Results: Thirty-five patients (42.4 +/- 13.5 years) in New York Heart Association functional Class II-III have been studied. A low-dose (20 mug.kg.min) echo-dobutamine study has been performed, before and 12 months after carvedilol therapy. Twelve months after carvedilol therapy, a significant improvement in LA and left ventricular (LV) function was observed. To investigate the beneficial effects of carvedilol, patients were separated into 2 groups according to the presence of pretreatment LV contractile reserve (CR) (ejection fraction [EF] increases >20% after dobutamine infusion): Group A consisted of 18 patients with CR and Group B of 17 patients without CR. After carvedilol treatment, both the LV and LA function were improved in group A (P < .01 for all). However, in group B, only the LA function was significantly improved (left atrial ejection volume increased from 10.4 +/- 3 mL to 15.4 +/- 6.7, P < .01 and LA ejection fraction from 19.6 +/- 45.3% to 29.4 +/- 12.5%, P < .01), whereas the LV contractile reserve has partially reappeared (EF from 29.9 +/- 4.5% at baseline, increased after dobutamine infusion to 35.8 +/- 6.8%, P < .0001). Conclusions: In conclusion, carvedilol therapy is associated with improvement in both LV and LA functions in nonischemic dilated cardiomyopathy. In a subgroup of these patients, carvedilol may act differently on LV and LA function. [ABSTRACT FROM AUTHOR]