Observation on the curative effect of basic treatment combined with ultrafiltration in patients with stubborn heart failure and high edema

Purpose: We aimed to comprehensively evaluate the curative effect of torasemide, tolvaptan, furosemide and azosemide on patients with heart failure. Methods: Relevant studies were retrieved by searching the electronic databases until May 2018. Quality assessment and data extraction of selected studies were evaluated by two reviewers. Heterogeneity across studies was assessed utilizing the I2 statistic and Q-test, and appropriate effect model was selected to calculate the pooled effect size. Network meta-analysis was conducted and the convergence degree of model was evaluated. Results: A total of 12 studies were enrolled in this study. Significant heterogeneity was not identified across the studies. Significantly greater differences were found in left ventricular ejection fraction (LVEF) for furosemide VS. azosemide, in brain natriuretic peptide (BNP) for furosemide VS. azosemide and furosemide VS. torasemide, and in adverse effects for furosemide VS. torasemide through Meta-analysis of direct comparison. In addition, network meta-analysis results suggested there were no significant differences in adverse effects, mortality, BNP and LVEF among these groups. However, the relatively low mortality and small improvement of BNP and LVEF were found in HF patients treated with torasemide. Conclusion: Torasemide might be an optimal treatment for HF patients considering its comprehensive curative effect.

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Mitochondria in Cardiomyopathy: Alterations in Size, Number and Internal Structures

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100100378 ◽

1968 ◽

Vol 26 ◽

pp. 126-127

Author(s):

George Hug ◽

William K. Schubert

Keyword(s):

Heart Failure ◽

Biochemical Analysis ◽

Left Ventricular ◽

Size Number ◽

Internal Structures ◽

Left Ventricular Outflow ◽

Chest X Ray ◽

Myocardial Fibers ◽

Muscle Biopsies ◽

Needle Liver Biopsy

A white boy six months of age was hospitalized with respiratory distress and congestive heart failure. Control of the heart failure was achieved but marked cardiomegaly, moderate hepatomegaly, and minimal muscular weakness persisted.At birth a chest x-ray had been taken because of rapid breathing and jaundice and showed the heart to be of normal size. Clinical studies included: EKG which showed biventricular hypertrophy, needle liver biopsy which showed toxic hepatitis, and cardiac catheterization which showed no obstruction to left ventricular outflow. Liver and muscle biopsies revealed no biochemical or histological evidence of type II glycogexiosis (Pompe's disease). At thoracotomy, 14 milligrams of left ventricular muscle were removed. Total phosphorylase activity in the biopsy specimen was normal by biochemical analysis as was the degree of phosphorylase activation. By light microscopy, vacuoles and fine granules were seen in practically all myocardial fibers. The fibers were not hypertrophic. The endocardium was not thickened excluding endocardial fibroelastosis. Based on these findings, the diagnosis of idiopathic non-obstructive cardiomyopathy was made.

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Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100166397 ◽

1996 ◽

Vol 54 ◽

pp. 786-787

Author(s):

Chi-Ming Wei ◽

Margarita Bracamonte ◽

Shi-Wen Jiang ◽

Richard C. Daly ◽

Christopher G.A. McGregor ◽

...

Keyword(s):

Nitric Oxide ◽

Heart Failure ◽

Nitric Oxide Synthase ◽

Endothelial Nitric Oxide Synthase ◽

Cardiac Tissues ◽

Mammalian Tissues ◽

End Stage Heart Failure ◽

End Stage ◽

Oxide Synthase ◽

Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

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Expression of Concern: Normal-sodium diet compared with low-sodium diet in compensated congestive heart failure: is sodium an old enemy or a new friend?

Clinical Science ◽

10.1042/cs-20070193_eoc ◽

2020 ◽

Vol 134 (13) ◽

pp. 1841-1841

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Sodium Diet ◽

Low Sodium Diet ◽

Low Sodium

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Protective role of peroxiredoxin-4 in heart failure

Clinical Science ◽

10.1042/cs20191072 ◽

2020 ◽

Vol 134 (1) ◽

pp. 71-72

Author(s):

Naseer Ahmed ◽

Masooma Naseem ◽

Javeria Farooq

Keyword(s):

Heart Failure ◽

Cardiac Fibroblasts ◽

Protective Role ◽

Oxidative Stress Markers ◽

Stress Markers ◽

Total Antioxidant ◽

Galectin 3 ◽

Consequent Increase ◽

And Oxidative Stress

Abstract Recently, we have read with great interest the article published by Ibarrola et al. (Clin. Sci. (Lond.) (2018) 132, 1471–1485), which used proteomics and immunodetection methods to show that Galectin-3 (Gal-3) down-regulated the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts. Authors concluded that ‘antioxidant activity of Prx-4 had been identified as a protein down-regulated by Gal-3. Moreover, Gal-3 induced a decrease in total antioxidant capacity which resulted in a consequent increase in peroxide levels and oxidative stress markers in cardiac fibroblasts.’ We would like to point out some results stated in the article that need further investigation and more detailed discussion to clarify certain factors involved in the protective role of Prx-4 in heart failure.

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