The relationship between tumor necrosis factor-α, brain natriuretic peptide and atrial natriuretic peptide in patients with chronic heart failure

Competence Network Heart Failure, Department of Cardiology, Campus Virchow-Klinikum, Charité - Universitätsmedizin Berlin, Berlin, Germany.
International journal of cardiology (Impact Factor: 4.04). 01/2009; 141(1):39-43. DOI: 10.1016/j.ijcard.2008.11.146
Source: PubMed


Cytokines such as tumor necrosis factor-alpha (TNF) contribute to cardiac dysfunction in chronic heart failure (CHF). Brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) are thought to reflect cardiac functional and structural damage.
To study the relationship between BNP, ANP, and TNF, these parameters were measured in fasting venous blood samples of 25 CHF patients (age 66+/-2 years, pVO(2) 17.4+/-2.1 mL/kg/min, NYHA class 2.8+/-0.2, all mean+/-SEM) and 8 healthy controls (age 71+/-2 years). Patients with CHF had higher plasma levels of BNP (p<0.05), ANP (p<0.05), norepinephrine (p<0.01), and echocardiographic left ventricular end-diastolic diameter (LVEDD, p<0.05) compared to controls, whereas TNF and epinephrine were not significantly different. There were significant correlations between natriuretic peptides and markers of inflammation and myocardial dysfunction in CHF patients: BNP vs. TNF (r=0.64, p=0.0006), vs. LVEDD (r=0.59, p=0.0025); ANP vs. TNF (r=0.60, p=0.0016), vs. LVEDD (r=0.65, p=0.0006); TNF vs. LVEDD (r=0.57, p=0.004). After adjustment for NYHA, creatinine clearance, and age TNF correlated with BNP (all p=0.01) and ANP (all p<0.002). The cachectic CHF patients (n=7,>6% weight loss) had the highest BNP (p<0.001 vs. controls, p<0.05 vs. non-cachectic CHF) and ANP levels (p=0.01 vs. controls). Concentrations of uric acid, epinephrine, and norepinephrine also correlated with ANP and BNP.
In CHF, TNF is closely related to BNP and ANP (independently of CHF severity and ventricular dysfunction), particularly in patients with cardiac cachexia. TNF may causally contribute to intrinsic cardiac dysfunction thereby stimulating BNP and ANP secretion.

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    • "As the most extensively studied cytokine, TNF-α is a noteworthy pro-inflammatory cytokine with various pathogenic effects. On one side, TNF-α is a valuable biomarker, for its correlation with enhanced brain natriuretic peptide and adverse clinical outcome in patients with heart failure [26,27]. On the other side, TNF-α is a strong mediator in the progression of heart failure. "
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    ABSTRACT: Aims Given the importance of inflammation in the onset and progression of diabetic cardiomyopathy, we investigated the potential protective effects of triptolide, an anti-inflammatory agent, in streptozotocin-induced diabetic rat model and in H9c2 rat cardiac cells exposed to high glucose. Methods and results Diabetic rats were treated with triptolide (100, 200, or 400 μg/kg/day respectively) for 6 weeks. At the end of this study, after cardiac function measurements were performed, rats were sacrificed and their hearts were harvested for further histologic and molecular biologic analysis. Enhanced activity and expression of nuclear factor-kappaB (NF-κB) p65 in diabetic hearts were associated with increased inflammatory response, as demonstrated by increased pro-inflammatory cytokines, cell adhesion molecules and invading inflammatory cells, as well as increased fibrosis, in line with impaired left ventricular function. Triptolide attenuated these morpho-functional alterations. Furthermore, triptolide (20 ng/ml) also attenuated high glucose-induced inflammation in H9c2 rat cardiac cells. Conclusion Our data demonstrate that anti-inflammatory effects of triptolide involving the NF-κB signaling pathway can improve left ventricular function under diabetic conditions, suggesting triptolide treatment might be beneficial in diabetic cardiomyopathy.
    Cardiovascular Diabetology 03/2013; 12(1):50. DOI:10.1186/1475-2840-12-50 · 4.02 Impact Factor
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    • "The neurohormonal basis of weight loss in cardiac cachexia has been well evaluated [30, 31]. This as in severe heart failure, and indeed even in cancer cachexia [32], is associated with cardiopulmonary reflex abnormalities including Cheyne-Stokes respiration [33]. "
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    ABSTRACT: Background The awareness of cardiac cachexia, i.e. involuntary weight loss in patients with underlying cardiovascular disease, has increased over the last two decades. Methods and results This mini-review looks at recent research in the cardiovascular literature that is relevant to the areas of interest of the Journal of Cachexia, Sarcopenia and Muscle. It identifies significant research in the last 3 years on the obesity paradox, the causes and effects of skeletal muscle wasting, animal models of cachexia and emerging treatment ideas in cardiac cachexia. Conclusions Assuming a similar literature in the fields of cancer, chronic obstructive pulmonary disease, chronic renal failure and chronic liver failure, the emergence of cachexia as a vibrant area of clinical and experimental research seems assured.
    11/2012; 3(4). DOI:10.1007/s13539-012-0090-6
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    • "Neurohormonal activation initially has protective effects but prolonged (over-)activity translates into clinically apparent damage mediated through neurohormonal and other mechanisms. This seems to be particularly important in the setting of cachexia, when highest concentrations of natriuretic peptides and markers of inflammation are detected [40]. Our knowledge about the activation and the interplay of existing systems [27, 41] and the level of induction remains insufficient, particularly so among patients with preserved left ventricular ejection fraction. "
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    ABSTRACT: Background Chronic heart failure (CHF) is increasing in prevalence. Patients with CHF usually have co-morbid conditions, but these have been subjected to little research and consequently there is a paucity of guidance on how to manage them. Obesity and diabetes mellitus are common antecedents of CHF and often complicate management and influence outcome. Cachexia is an ominous and often missed sign in patients with CHF. Methods This manuscript describes the rationale and the design of Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF), a prospective, multicentre, multinational, longitudinal, pathophysiological evaluation study, which is being conducted in 11 centres across six countries in the European Union and in Russia. We aim to recruit >1,600 patients with CHF due to various common aetiologies, irrespective of left ventricular ejection fraction, and with or without co-morbidities at study entry. In addition, >300 patients with type 2 diabetes mellitus without CHF and >150 healthy subjects will serve as control groups. Participants will be systematically investigated at annual intervals for up to 48 months. Additional investigations focusing on cellular and subcellular mechanisms, adipose and skeletal muscle tissue, and in endothelial progenitor cells will be performed in selected subgroups. Conclusions SICA-HF will provide insights into common co-morbidities in CHF with a specific emphasis on diabetes mellitus and body mass. This will provide a more thorough pathophysiological understanding of the complexity of CHF that will help develop therapies tailored to manage specific co-morbidities.
    12/2010; 1(2):187-194. DOI:10.1007/s13539-010-0013-3
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