Oxidative stress and inflammation in the evolution of heart failure: From pathophysiology to therapeutic strategies

2019 ◽  
Vol 27 (5) ◽  
pp. 494-510 ◽  
Author(s):  
Alberto Aimo ◽  
Vincenzo Castiglione ◽  
Chiara Borrelli ◽  
Luigi F Saccaro ◽  
Maria Franzini ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Current Knowledge ◽  
Interleukin 1 ◽  
Prognostic Significance ◽  
Deep Understanding ◽  
Future Research ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Both oxidative stress and inflammation are enhanced in chronic heart failure. Dysfunction of cardiac mitochondria is a hallmark of heart failure and a leading cause of oxidative stress, which in turn exerts detrimental effects on cellular components, including mitochondria themselves, thus generating a vicious circle. Oxidative stress also causes myocardial tissue damage and inflammation, contributing to heart failure progression. Furthermore, a subclinical inflammatory state may be caused by heart failure comorbidities such as obesity, diabetes mellitus or sleep apnoeas. Some markers of both oxidative stress and inflammation are enhanced in chronic heart failure and hold prognostic significance. For all these reasons, antioxidants or anti-inflammatory drugs may represent interesting additional therapies for subjects either at high risk or with established heart failure. Nonetheless, only a few clinical trials on antioxidants have been carried out so far, with several disappointing results except for vitamin C, elamipretide and coenzyme Q10. With regard to anti-inflammatory drugs, only preliminary data on the interleukin-1 antagonist anakinra are currently available. Therefore, a comprehensive, deep understanding of our current knowledge on oxidative stress and inflammation in chronic heart failure is key to providing some suggestions for future research on this topic.

scholarly journals Increased Mortality and Cardiovascular Morbidity Associated With Use of Nonsteroidal Anti-inflammatory Drugs in Chronic Heart Failure

2009 ◽  
Vol 169 (2) ◽  
pp. 141 ◽  
Author(s):  
Gunnar H. Gislason ◽  
Jeppe N. Rasmussen ◽  
Steen Z. Abildstrom ◽  
Tina K. Schramm ◽  
Morten L. Hansen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Cardiovascular Morbidity ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

514 Prognostic significance of bioelectrical evaluation of body composition in chronic heart failure

2003 ◽  
Vol 2 (1) ◽  
pp. 105
Author(s):  
F MASSARI ◽  
P GUIDA ◽  
F MASTROPASQUA ◽  
M IACOVIELLO ◽  
B RIZZON ◽  
...  
Keyword(s):  
Heart Failure ◽  
Body Composition ◽  
Chronic Heart Failure ◽  
Prognostic Significance

scholarly journals Association of Nonsteroidal Anti-inflammatory Drugs With First Occurrence of Heart Failure and With Relapsing Heart Failure

2002 ◽  
Vol 162 (3) ◽  
pp. 265 ◽  
Author(s):  
Johan Feenstra ◽  
Eibert R. Heerdink ◽  
Diederick E. Grobbee ◽  
Bruno H. Ch. Stricker
Keyword(s):  
Heart Failure ◽  
First Occurrence ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

scholarly journals Uric Acid, Oxidative Stress and Inflammation in Chronic Heart Failure with Reduced Ejection Fraction

2015 ◽  
Vol 23 (4) ◽  
pp. 397-406 ◽  
Author(s):  
Adriana Iliesiu ◽  
Alexandru Campeanu ◽  
Daciana Marta ◽  
Irina Parvu ◽  
Gabriela Gheorghe
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Uric Acid ◽  
Chronic Heart Failure ◽  
Ejection Fraction ◽  
Xanthine Oxidase ◽  
Left Ventricular ◽  
Paraoxonase 1 ◽  
Lv Function ◽  
The Relationship

Abstract Background. Oxidative stress (OS) and inflammation are major mechanisms involved in the progression of chronic heart failure (CHF). Serum uric acid (sUA) is related to CHF severity and could represent a marker of xanthine-oxidase activation. The relationship between sUA, oxidative stress (OS) and inflammation markers was assessed in patients with moderate-severe CHF and reduced left ventricular (LV) ejection fraction (EF). Methods. In 57 patients with stable CHF, functional NYHA class III, with EF<40%, the LV function was assessed by N-terminal of the prohormone brain natriuretic peptide (NT-proBNP) levels and echocardiographically through the EF and E/e’ ratio, a marker of LV filling pressures. The relationship between LV function, sUA, malondialdehyde (MDA), myeloperoxidase (MPO), paraoxonase 1 (PON-1) as OS markers and high sensitivity C-reactive protein (hsCRP) and interleukin 6 (IL-6) as markers of systemic inflammation was evaluated. Results. The mean sUA level was 7.9 ± 2.2 mg/dl, and 61% of the CHF patients had hyperuricemia. CHF patients with elevated LV filling pressures (E/e’ ≥ 13) had higher sUA (8.6 ± 2.3 vs. 7.3 ± 1.4, p=0.08) and NT-proBNP levels (643±430 vs. 2531±709, p=0.003) and lower EF (29.8 ± 3.9 % vs. 36.3 ± 4.4 %, p=0.001). There was a significant correlation between sUA and IL-6 (r = 0.56, p<0.001), MDA (r= 0.49, p= 0.001), MPO (r=0.34, p=0.001) and PON-1 levels (r= −0.39, p= 0.003). Conclusion. In CHF, hyperuricemia is associated with disease severity. High sUA levels in CHF with normal renal function may reflect increased xanthine-oxidase activity linked with chronic inflammatory response.

scholarly journals Developmental Origins of Kidney Disease: Why Oxidative Stress Matters?

Antioxidants ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 33
Author(s):  
Chien-Ning Hsu ◽  
You-Lin Tain
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Current Knowledge ◽  
Future Research ◽  
Antioxidant Systems ◽  
Developmental Origins ◽  
Adult Onset ◽  
Functional Changes ◽  
Health And Disease ◽  
Developing Kidney

The “developmental origins of health and disease” theory indicates that many adult-onset diseases can originate in the earliest stages of life. The developing kidney has emerged as being particularly vulnerable to adverse in utero conditions leading to morphological and functional changes, namely renal programming. Emerging evidence indicates oxidative stress, an imbalance between reactive oxygen/nitrogen species (ROS/RNS) and antioxidant systems, plays a pathogenetic role in the developmental programming of kidney disease. Conversely, perinatal use of antioxidants has been implemented to reverse programming processes and prevent adult-onset diseases. We have termed this reprogramming. The focus of this review is twofold: (1) To summarize the current knowledge on oxidative stress implicated in renal programming and kidney disease of developmental origins; and (2) to provide an overview of reprogramming effects of perinatal antioxidant therapy on renal programming and how this may prevent adult-onset kidney disease. Although early-life oxidative stress is implicated in mediating renal programming and adverse offspring renal outcomes, and animal models provide promising results to allow perinatal antioxidants applied as potential reprogramming interventions, it is still awaiting clinical translation. This presents exciting new challenges and areas for future research.

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