SummaryCognitive behavioral therapy (CBT), established only a few decades ago, is widely used by clinical psychologists. This study aimed to investigate the effects of CBT on mental status and quality of life (QOL) after percutaneous coronary intervention (PCI) in young and middle-aged patients with coronary heart disease (CHD). Seventy-five anxiety/depression patients (mean age, 52.2 ± 6.2 years, including 8 individuals < 45 years old) with CHD treated with PCI were randomly divided into a CBT group (n = 38) and control group (n = 37). The CBT group received 8 weeks of CBT in addition to the routine postoperative treatment that was also administered to control patients. The 17-item Hamilton Depression Rating Scale (HAM-D17), Hamilton anxiety scale (HAM-A), and Coronary Revascularization Outcome Questionnaire (CROQ-PTCA-POST, Chinese version) were administered before, 3 days, and 8 weeks after intervention. HAM-D17 and HAM-A scores were decreased after treatment, but were more substantially reduced in patients that underwent CBT than those in the control group (11.7 ± 4.5 versus 15.1 ± 3.9, P = 0.001 and 10.6 ± 3.4 versus 16.5 ± 4.6, P = 0.003, respectively). QOL was improved in both groups, but overall satisfaction was higher in the CBT group compared with control patients (89.3 ± 5.2 versus 77.8 ± 9.5, P < 0.05). CBT can relieve depression and anxiety after PCI in young and middle-aged patients with CHD. CBT can improve patient QOL. (Int Heart J 2016; 57: 167-172) Key words: Cognitive behavioral therapy, Percutaneous stent implantation, Anxiety, Depression C oronary heart disease (CHD) is one of the leading causes of death worldwide. The China Cardiovascular Disease report published in 2010 stated that the incidence of CHD in China continues to increase, and that the age at onset is decreasing.1) The relationship between CHD and a change toward a negative mental status has attracted more and more attention, particularly the clinical studies of therapeutic intervention with regards to psychological and social factors of CHD.2-4) Authors agree that many patients with CHD have persistent symptoms of depression and anxiety, 5,6) which significantly influence their quality of life (QOL) and prognosis, often leading to a vicious cycle. 7) However, whether the presence of depressive symptoms is due to depression after CHD or originates from the CHD itself is controversial. 8,9) Nevertheless, there is an association between depressive symptoms and post-CHD mortality. 10,11) Chinese studies performed by Li, et al 12) confirmed that the incidence of anxiety in young and middle-aged CHD patients who underwent percutaneous coronary intervention (PCI) was higher than that of senior patients, which is supported by other studies. [13][14][15] They stated that it might be because young and middle-aged patients are more likely to worry about the effects of stent implantation on their work and social life. These studies also found that the incidence of depression among young and middle-aged people was slightly higher than ...
Oxidative stress causes deregulation of endothelial cell differentiation. Carnosol is a potent antioxidant and antiinflammatory compound. In the present study, we examined whether the antioxidant effect of carnosol might protect bone marrow stem cells against H 2 O 2 -induced oxidative stress and promote endothelial differentiation. We examined cell viability by the MTT assay; oxidative stress and apoptosis were analyzed through changes in ROS levels, apoptotic ratio and caspase-3 activity; changes in protein expression of OCT-4, Flk-1, CD31 and Nrf-2 were assessed by Western blot analysis. H 2 O 2 treatment increased oxidative stress and reduced cell viability, while the stem cell marker OCT-4 and endothelial markers Flk-1, CD31 were significantly downregulated as a result of the treatment with H 2 O 2 . Treatment with carnosol improved the antioxidant status, increased OCT-4 expression and promoted endothelial differentiation. This study provides evidence that carnosol could increase the antioxidant defense mechanism and promote endothelial differentiation.
Objectives To investigate the effects of EGB on advanced glycosylation end products (AGEs)-induced cardiomyocyte injury, and the role of endoplasmic reticulum stress (ERS) in the process. Methods Cultured neonatal rat cardiomyocytes were randomly divided into four groups: control, EGB, AGEs, and AGEs + EGB. MTT assay was used to measure cell viability. Necrosis was determined by LDH release, and apoptosis was detected through TUNEL assay. ERS-related proteins were surveyed by western blot. Results Compared with control group, AGEs (400 μg/ml) resulted in a decrease of cell viability and an increase of LDH release, which was time (48, 72 h) dependent. Moreover, AGEs upregulated ERS-related proteins, including GRP 78, CHOP, leading to cardiomyocyte apoptosis. EGB (50, 100 μg/ml) alone had no effect on cell viability, LDH release, apoptosis, and ERS-related proteins. Cotreatment of EGB and AGEs (400 μg/ml) alleviated AGEs-induced LDH release and apoptosis, improved cell viability, and downregulated ERS-related proteins including GRP 78 and CHOP. Overexpression of CHOP offset the protection of EGB on AGEs-induced injury in H9C2 cells. Conclusions These findings demonstrate that EGB protects cardiomyocytes against AGEs-induced cardiomyocyte apoptosis. It may be associated with attenuation of endoplasmic reticulum stress.
Objectives to evaluate the changes of cardiovascular function and its clinical significance in patients of myocardial infarction (MI) with Wave intensity (WI) and Echo-tracking (ET) technique
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