Activation of lymphocyte autophagy/apoptosis reflects haemodynamic inefficiency and functional aerobic impairment in patients with heart failure

2014 ◽  
Vol 127 (10) ◽  
pp. 589-602 ◽  
Author(s):  
Tzu-Pin Weng ◽  
Tieh-Cheng Fu ◽  
Chao-Hung Wang ◽  
Chih-Chin Hsu ◽  
Jong-Shyan Wang

Increased sympathetic activation and oxidative stress/pro-inflammatory status cause lymphocytopenia by activating programmed lymphocyte death in patients with HF. Moreover, a low lymphocyte count correlates with reduced haemodynamics and aerobic capacity, which reflects poor generic/disease-specific QoL in the HF patients.

Global Heart ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e20
Author(s):  
Vitor G. Angarten ◽  
Almir Schmitt Netto ◽  
Anderson Z. Ulbrich ◽  
Sabrina W. Sties ◽  
Lourenço S. de Mara ◽  
...  

Author(s):  
Giane Ribeiro-Samora ◽  
Mariana Hoffman Barbosa ◽  
Luiza Antas Rabelo ◽  
Glaucevane Silva Guedes ◽  
Michelle Favero ◽  
...  

2011 ◽  
Vol 4 (8) ◽  
pp. 1088-1100 ◽  
Author(s):  
Kazufumi Nakamura ◽  
Masato Murakami ◽  
Daiji Miura ◽  
Kei Yunoki ◽  
Kenki Enko ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Damien Vitiello ◽  
François Harel ◽  
Rhian M. Touyz ◽  
Martin G. Sirois ◽  
Joel Lavoie ◽  
...  

Background. Changes in cardiopulmonary reserve and biomarkers related to wall stress, inflammation, and oxidative stress concomitantly with the evaluation of peripheral arterial blood flow have not been investigated in patients with heart failure with preserved ejection fraction (HFpEF) compared with healthy subjects (CTL).Methods and Results. Eighteen HFpEF patients and 14 CTL were recruited. Plasma levels of inflammatory and oxidative stress biomarkers were measured at rest. Brain natriuretic peptide (BNP) was measured at rest and peak exercise. Cardiopulmonary reserve was assessed using an exercise protocol with gas exchange analyses. Peripheral arterial blood flow was determined by strain gauge plethysmography. Peak VO2(12.0±0.4versus19.1±1.1 mL/min/kg,P<0.001) and oxygen uptake efficiency slope (1.55±0.12versus2.06±0.14,P<0.05) were significantly decreased in HFpEF patients compared with CTL. BNP at rest and following stress, C-reactive-protein, interleukin-6, and TBARS were significantly elevated in HFpEF. Both basal and posthyperemic arterial blood flow were not significantly different between the HFpEF patients and CTL.Conclusions. HFpEF exhibits a severe reduction in cardiopulmonary reserve and oxygen uptake efficiency concomitantly with an elevation in a broad spectrum of biomarkers confirming an inflammatory and prooxidative status in patients with HFpEF.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takashi Yokota ◽  
Shintaro Kinugawa ◽  
Kagami Hirabayashi ◽  
Mayumi Yamato ◽  
Shingo Takada ◽  
...  

AbstractOxidative stress plays a role in the progression of chronic heart failure (CHF). We investigated whether systemic oxidative stress is linked to exercise intolerance and skeletal muscle abnormalities in patients with CHF. We recruited 30 males: 17 CHF patients, 13 healthy controls. All participants underwent blood testing, cardiopulmonary exercise testing, and magnetic resonance spectroscopy (MRS). The serum thiobarbituric acid reactive substances (TBARS; lipid peroxides) were significantly higher (5.1 ± 1.1 vs. 3.4 ± 0.7 μmol/L, p < 0.01) and the serum activities of superoxide dismutase (SOD), an antioxidant, were significantly lower (9.2 ± 7.1 vs. 29.4 ± 9.7 units/L, p < 0.01) in the CHF cohort versus the controls. The oxygen uptake (VO2) at both peak exercise and anaerobic threshold was significantly depressed in the CHF patients; the parameters of aerobic capacity were inversely correlated with serum TBARS and positively correlated with serum SOD activity. The phosphocreatine loss during plantar-flexion exercise and intramyocellular lipid content in the participants' leg muscle measured by 31phosphorus- and 1proton-MRS, respectively, were significantly elevated in the CHF patients, indicating abnormal intramuscular energy metabolism. Notably, the skeletal muscle abnormalities were related to the enhanced systemic oxidative stress. Our analyses revealed that systemic oxidative stress is related to lowered whole-body aerobic capacity and skeletal muscle dysfunction in CHF patients.


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