scholarly journals Ablation of telomerase and telomere loss leads to cardiac dilatation and heart failure associated with p53 upregulation

2003 ◽  
Vol 22 (1) ◽  
pp. 131-139 ◽  
Author(s):  
A. Leri
Keyword(s):  
Heart Failure ◽  
Telomere Loss ◽  
Cardiac Dilatation

scholarly journals The pathogenic basis for the development of cardiovascular disease in obesity: difficulties of diagnosis and treatment

2016 ◽  
Vol 12 (4) ◽  
pp. 47-51
Author(s):  
Irina Ziatovna Bondarenko ◽  
Ol'ga Viktorovna Shpagina
Keyword(s):  
Heart Failure ◽  
Cardiovascular Disease ◽  
Morbid Obesity ◽  
Coronary Heart Disease ◽  
Morphological Changes ◽  
Cardiac Complications ◽  
Body Fat Mass ◽  
Obese Patients ◽  
Unexplained Death ◽  
Cardiac Dilatation

Cardiovascular abnormalities associated with morbid obesity include cardiac hypertrophy, cardiac dilatation, diastolic dysfunction. Also obesity predispose to numerous cardiac complications such as coronary heart disease, heart failure, and sudden death. The cardiovascular clinical evaluation of obese patients may be limited by morphological changes, which are specific for increased amount of body fat mass. The incidence of sudden and unexplained death in morbid obesity may be a manifestation of occult cardiovascular disease in this population.

Changes in the sensitivity of left atrial receptors following reversal of heart failure

1979 ◽  
Vol 237 (5) ◽  
pp. H555-H559 ◽  
Author(s):  
I. H. Zucker ◽  
A. M. Earle ◽  
J. P. Gilmore
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Left Atrial ◽  
Vena Cava ◽  
Clinical Signs ◽  
Av Fistula ◽  
Stimulus Response ◽  
Atrial Receptors ◽  
Shunt Closure ◽  
Cardiac Dilatation

Recordings were made from left atrial type B receptors in six mongrel dogs after recovery from the cardiac effects of a chronic AV fistula. All animals showed hemodynamic and clinical signs of congestive heart failure after 44.5 +/- 3.6 days with a patent Dacron shunt between the aorta and inferior vena cava below the level of the renal arteries. The stimulus-response curves of the left atrial stretch receptors (change in spikes/cardiac cycle or in spikes/minute vs. change in left atrial pressure) after 45.2 +/- 7.2 days of shunt closure were similar to those seen in sham-operated dogs from a previous study. However, the slope of the stimulus-response curve of the dogs in which the AV fistula was closed was significantly greater than the slope of the curve from the AV fistula dogs with heart failure. Radiographs indicated that after shunt closure, cardiac dilatation had regressed. This study incidates that a decrease in the sensitivity of left atrial receptors in dogs with congestive heart failure is a reversible phenomenon and that the initial depression is most likely related to the concomitant cardiac dilatation that accompanies the failure state.

Postsystolic myocardial augmentation: physiological considerations and technique

1962 ◽  
Vol 17 (1) ◽  
pp. 61-66 ◽  
Author(s):  
David H. Watkins ◽  
E. Ronald Duchesne
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Blood Flow ◽  
Systolic Blood Pressure ◽  
Electronic Circuit ◽  
Venous Blood ◽  
Ascending Aorta ◽  
Qrs Complex ◽  
Short Period ◽  
Cardiac Dilatation

Technique and appropriate equipment are reported which remove blood from the circulation during cardiac systole, thereby reducing intraventricular systolic blood pressure and the work of systolic ejection. Blood is reinjected during ventricular diastole, so that the diastolic blood pressure and coronary blood flow are increased. An electronic circuit enables the phasing of the augmenting systole to be placed accurately in relationship to the QRS complex of the EKG. Application of the technique to experimental heart failure induced by norepinephrine and hemorrhage is illustrated. Cardiac dilatation, elevated end-diastolic pressures, and arterial hypotension are reversed by the use of this technique. In addition, it is possible to supply an unlimited quantity of oxygenated, banked, standard venous blood to the ascending aorta via intra-arterial cannulas. The technique which we have developed overcomes difficulties previously experienced by those who wished to withdraw blood during systole and reinject it during diastole. The size of the pump is adequate to change the blood pressure effectively; the timing of reinjection is such as to accomplish reinjection during the short period of ventricular diastole. Submitted on May 8, 1961

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

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.

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

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).

Protective role of peroxiredoxin-4 in heart failure

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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