• 재활간호학회지
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• 제17권2호
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• pp.64-71
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• 2014

Purpose: The purpose of this study was to identify the quality of recovery and influential factors on the quality of recovery after cardiac surgery. Methods: 198 patients undergone cardiac surgery were asked to fill in a self-reported questionnaire about the quality of recovery, anxiety, depression including social support at discharge. The collected data were analyzed with mean, standard deviation, correlation and stepwised multiple regression. Results: The mean scores of quality of recovery at discharge after cardiac surgery was 2.04 on a 3 point scale. Influential factors on the quality of recovery after cardiac surgery were depression(p=.001) and anxiety(p=.027), which disclosed 44.2% of explanation. Depression was the most influential factor. Conclusion: The influential factors on the quality of recovery at discharge after cardiac surgery were depression and anxiety. More studies will be required to reduce depression and anxiety in patients undergone cardiac surgery.

• Archives of Pharmacal Research
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• 제27권3호
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• pp.324-333
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• 2004

To determine whether Insulin-like growth factor (IGF-I) treatment represents a potential means of enhancing the survival of cardiac muscle cells from adriamycin (ADR)-induced cell death, the present study examined the ability of IGF-I to prevent cell death. The study was performed utilising the embryonic, rat, cardiac muscle cell line, H9C2. Incubating cardiac muscle cells in the presence of adriamycin increased cell death, as determined by MTT assay and annexin V-positive cell number. The addition of 100 ng/mL IGF-I, in the presence of adriamycin, decreased apoptosis. The effect of IGF-I on phosphorylation of PI, a substrate of phosphatidylinositol 3-kinase (PI 3-kinase) or protein kinase B (AKT), was also examined in H9C2 cardiac muscle cells. IGF-I increased the phosphorylation of ERK 1 and 2 and $PKC{\;}{\zeta}{\;}kinase$. The use of inhibitors of PI 3-kinase (LY 294002), in the cell death assay, demonstrated partial abrogation of the protective effect of IGF-I. The MEK1 inhibitor-PD098059 and the PKC inhibitor-chelerythrine exhibited no effect on IGF-1-induced cell protection. In the regulatory subunit of PI3K-p85- dominant, negative plasmid-transfected cells, the IGF-1-induced protective effect was reversed. This data demonstrates that IGF-I protects cardiac muscle cells from ADR-induced cell death. Although IGF-I activates several signaling pathways that contribute to its protective effect in other cell types, only activation of PI 3-kinase contributes to this effect in H9C2 cardiac muscle cells.

• Journal of Korean Biological Nursing Science
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• 제9권1호
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• pp.5-31
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• 2007

Purpose: The purpose of this study was to explore the knowledge and learning needs on cardiac rehabilitation of coronary artery bypass graft(CABG) patients. Method: The subjects consisted of 100 CABG patients at A hospital in Seoul. Data were collected by the two different kind of questionnaires which measure knowledge and learning needs on cardiac rehabilitation of CABG patients. The subjects responded the questionnaire on knowledge before CABG and that on learning needs before their discharge. Result: The mean score of knowledge on cardiac rehabilitation was 68.54. Knowledge on risk factor, nature of disease, diet, daily activity, medication, post operative care were great in order. The mean score of learning needs on cardiac rehabilitation was 4.28. Learning needs on diet, medication, nature of disease, post operative care, daily activity, risk factor were great in order. There were significant differences in knowledge according to occupation, economic status and family history(p=.021, p=.017, p=.023). There was a positive correlation between knowledge and learning needs(r=.3009, p=.002). Conclusion: Level of knowledge on cardiac rehabilitation of CABG patients is low and knowledge on postoperative care is the lowest, and learning needs are great in ail categories.

• Journal of Chest Surgery
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• 제33권1호
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• pp.1-6
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• 2000

Background: TNF-$\alpha$ plays a major role in producing left ventricular dysfunction cardio-myopathy pulmonary edema and inhibits the compensatory mechanism of congestive heart failure. IL-6 is an acute reactant of immune reaction and also known to control immune reaction but its function in the myocyte was not clearly investigated. Author's performed this experiment to investigate the contents of TNF-$\alpha$ and IL-6 on the assumption that TNF-$\alpha$ and IL-6 may reside in nonfailing heart that has gone cardiac surgery and play some role in cardiac function. Material and Method : Right auricular tissues were sampled from 12 patients who had undergone total corrective surgery for both congenital and acquired heart diseases from January 1998 to June 1998 in Kosin Universcfy Gospel hospital. The quantitive analysis of TNF-$\alpha$ and IL-6 were assessed by ELISA method in right auricular tissue. Hemodynamic values about the pressure of ventricle atrium aorta pulmonary artery and cardiac index pulmonary and systemic vascular resistance and cardiac output were measured by echocardiography and cardiac catheterization and biochemical analyses of LDH & AST were done before operation. statistical analysis was by Paired Student t-test. Patients were divided into children(under 15 years olds) and adults groups and the data was compared beween two groups. Conclusion: Mild pulmonary hypertension and increased pulmonary vascular resistance were existed in both group. The contents of tissue TNF-$\alpha$ IL-6 in each group were independent of each data.

• 한국응급구조학회지
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• 제24권2호
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• pp.7-26
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• 2020

Purpose: This study aimed to identify the factors affecting the survival outcomes of out-of-hospital cardiac arrest based on the Sudden Cardiac Arrest Survey by the Korean Centers for Disease Control and Prevention from 2012 to 2016. Methods: Out of 84,776 cases, 57,104 cases of cardiac arrest were analyzed. To identify the factors that affect survival outcomes after a sudden cardiac arrest (SCA), we performed a logistic regression using SPSS. We also performed a multilevel analysis using SAS to determine whether the survival outcomes were affected by the socioeconomic level and health index of the communities. Results: When SCA was witnessed by someone, the possibility of discharge with survival outcomes increased by a factor of 4.54. If CPR was administered immediately in emergency situations, this possibility further increased. When defibrillation was performed before hospitalization, the possibility was increased by a factor of 10.31. The multilevel analysis reflected the personal and regional factors that had an impact on the survival outcomes. Conclusion: Because the initial response in SCA is crucial, a community response system is essential before hospitalization. It is necessary to actively publicize and educate the people because the their understanding, sympathy, and cooperation in emergency situations play a role in determining the survival outcomes of the patients.

• 대한핵의학회:학술대회논문집
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• 대한핵의학회 2006년도 제45차 춘계학술대회
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• pp.51-52
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• 2006

• BMB Reports
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• 제54권9호
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• pp.464-469
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• 2021

Cardiomyocyte differentiation occurs through complex and finely regulated processes including cardiac lineage commitment and maturation from pluripotent stem cells (PSCs). To gain some insight into the genome-wide characteristics of cardiac lineage commitment, we performed transcriptome analysis on both mouse embryonic stem cells (mESCs) and human induced PSCs (hiPSCs) at specific stages of cardiomyocyte differentiation. Specifically, the gene expression profiles and the protein-protein interaction networks of the mESC-derived platelet-derived growth factor receptor-alpha (PDGFRα)⁺ cardiac lineage-committed cells (CLCs) and hiPSC-derived kinase insert domain receptor (KDR)⁺ and PDGFRα⁺ cardiac progenitor cells (CPCs) at cardiac lineage commitment were compared with those of mesodermal cells and differentiated cardiomyocytes. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses revealed that the genes significantly upregulated at cardiac lineage commitment were associated with responses to organic substances and external stimuli, extracellular and myocardial contractile components, receptor binding, gated channel activity, PI3K-AKT signaling, and cardiac hypertrophy and dilation pathways. Protein-protein interaction network analysis revealed that the expression levels of genes that regulate cardiac maturation, heart contraction, and calcium handling showed a consistent increase during cardiac differentiation; however, the expression levels of genes that regulate cell differentiation and multicellular organism development decreased at the cardiac maturation stage following lineage commitment. Additionally, we identified for the first time the protein-protein interaction network connecting cardiac development, the immune system, and metabolism during cardiac lineage commitment in both mESC-derived PDGFRα⁺ CLCs and hiPSC-derived KDR⁺PDGFRα⁺ CPCs. These findings shed light on the regulation of cardiac lineage commitment and the pathogenesis of cardiometabolic diseases.

• 대한간호학회지
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• 제41권5호
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• pp.704-714
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• 2011

Purpose: The purpose of this study was to determine whether psychological distress is an independent risk factor for recurrent cardiac events in patients with coronary artery disease (CAD). Methods: A prospective cohort of studies that measured psychological distress and the incidence of recurrent cardiac events in the adult population were included. Three computerized databases were assessed (PubMed, CINAHL, and PSYCINFO). Meta-analysis was conducted using a random-effects model to determine summary estimates of risks of major recurrent cardiac events associated with each psychological distress. Of 506 publications identified, 33 met inclusion criteria, and 24 studies were used to estimate effect size of psychological distress on recurrent cardiac events. Results: Mean number in the research sample was 736 and mean time of follow-up was 4.0 years. Depression, anxiety, anger, and hostility as psychological factors were studied. According to estimation of effect size using random model effect, depression (OR=1.39, 95% CI: 1.22-1.57), anxiety (OR=1.22, 95% CI: 0.96-1.56), and anger/hostility (OR=1.29, 95% CI: 1.07-1.57) CAD patients in significantly increased risk for recurrent cardiac events. Conclusion: Finding suggests that psychological distress in forms of depression, anxiety, anger, and hostility impact unfavorably on recurrent cardiac events in CAD patients.

• The Korean Journal of Physiology and Pharmacology
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• 제26권6호
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• pp.469-478
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• 2022

WNT signaling plays an important role in cardiac development, but abnormal activity is often associated with cardiac hypertrophy, myocardial infarction, remodeling, and heart failure. The effect of WNT signaling on regulation of atrial natriuretic peptide (ANP) secretion is unclear. Therefore, the purpose of this study was to investigate the effect of Wnt agonist 1 (Wnta1) on ANP secretion and mechanical dynamics in beating rat atria. Wnta1 treatment significantly increased atrial ANP secretion and pulse pressure; these effects were blocked by U73122, an antagonist of phospholipase C. U73122 also abolished the effects of Wnta1-mediated upregulation of protein kinase C (PKC) β and γ expression, and the PKC antagonist Go 6983 eliminated Wnta1-induced secretion of ANP. In addition, Wnta1 upregulated levels of phospho-transforming growth factor-β activated kinase 1 (p-TAK1), TAK1 banding 1 (TAB1) and phospho-activating transcription factor 2 (p-ATF2); these effects were blocked by both U73122 and Go 6983. Wnta1-induced ATF2 was abrogated by inhibition of TAK1. Furthermore, Wnta1 upregulated the expression of T cell factor (TCF) 3, TCF4, and lymphoid enhancer factor 1 (LEF1), and these effects were blocked by U73122 and Go 6983. Tak1 inhibition abolished the Wnta1-induced expression of TCF3, TCF4, and LEF1 and Wnta1-mediated ANP secretion and changes in mechanical dynamics. These results suggest that Wnta1 increased the secretion of ANP and mechanical dynamics in beating rat atria by activation of PKC-TAK1-ATF2-TCF3/LEF1 and TCF4/LEF1 signaling mainly via the WNT/Ca²⁺ pathway. It is also suggested that WNT-ANP signaling is implicated in cardiac physiology and pathophysiology.

• The Korean Journal of Physiology and Pharmacology
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• 제14권6호
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• pp.377-384
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• 2010

The present study examined whether metformin treatment prevents isoporterenol-induced cardiac hypertrophy in mice. Chronic subcutaneous infusion of isoproterenol (15 mg/kg/24 h) for 1 week using an osmotic minipump induced cardiac hypertrophy measured by the heart-to-body weight ratio and left ventricular posterior wall thickness. Cardiac hypertrophy was accompanied with increased interleukin-6 (IL-6), transforming growth factor (TGF)-${\beta}$, atrial natriuretic peptide (ANP), collagen I and III, and matrix metallopeptidase 2 (MMP-2). Coinfusion of metformin (150 mg/kg/24 h) with isoproterenol partially inhibited cardiac hypertrophy that was followed by reduced IL-6, TGF-${\beta}$, ANP, collagen I and III, and MMP-2. Chronic subcutaneous infusion of metformin did not increase AMP-activated protein kinase (AMPK) activity in heart, although acute intraperitoneal injection of metformin (10 mg/kg) increased AMPK activity. Isoproterenol increased nitrotyrosine levels and mRNA expression of antioxidant enzyme glutathione peroxidase and metformin treatment normalized these changes. These results suggest that metformin inhibits cardiac hypertrophy through attenuating oxidative stress.