Proinflammatory cytokine levels in patients with depressed left ventricular ejection fraction: A report from the studies of left ventricular dysfunction (SOLVD)

Torre‐Amione, Guillermo; Kapadia, Samir; Benedict, Claude R.; Oral, Hakan; Young, James B.; Mann, Douglas L.

doi:10.1016/0735-1097(95)00589-7

Cited by 1,097 publications

(685 citation statements)

References 21 publications

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“…Elevated levels of peripherally circulating TNF-α are associated with increased severity of heart failure. 85 Three sources of TNF-α after myocardial injury in heart failure are proposed: (1) TNF-α produced locally in the myocardium triggers the HPA axis and leads to secondary activation of the immune system in the periphery 86 ; (2) decreased cardiac output causes underperfusion of systemic tissues and leads to elaboration of the factor 87 ; and/or (3) activation of the immune system occurs in response to injury from some index event. 88 Complex and not fully understood, depression is accompanied by moderate activation of proinflammatory cytokines, in particular TNF-α, IL-1, and IL-6.…”

Section: Activation Of Cytokine Cascadesmentioning

confidence: 99%

Pathophysiological Relationships Between Heart Failure and Depression and Anxiety

Chapa

Akintade

Son

et al. 2014

Critical Care Nurse

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H eart failure is an epidemic with national and global implications. Compared with the situation in other cardiac diseases, the incidence and prevalence of heart failure continue to increase despite recent advancements in understanding and treatment. Increased survival after myocardial infarction, aging of the population, and increased incidence of diabetes are contributing factors. This article has been designated for CNE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives:1. Describe the biopsychosocial holistic model for cardiovascular health 2. Identify 2 neurohormonal pathways and their impact in heart failure 3. Identify nursing implications for heart failure, depression, and anxiety CNE Continuing Nursing EducationCover Depression and anxiety are common comorbid conditions in patients with heart failure. Patients with heart failure and depression have increased mortality. The association of anxiety with increased mortality in patients with heart failure is not established. The purpose of this article is to illustrate the similarities of the underlying pathophysiology of heart failure, depression, and anxiety by using the Biopsychosocial Holistic Model of Cardiovascular Health. Depression and anxiety affect biological processes of cardiovascular function in patients with heart failure by altering neurohormonal function via activation of the hypothalamic-pituitary-adrenal axis, autonomic dysregulation, and activation of cytokine cascades and platelets. Patients with heart failure and depression or anxiety may exhibit a continued cycle of heart failure progression, increased depression, and increased anxiety. Understanding the underlying pathophysiological relationships in patients with heart failure who experience comorbid depression and/or anxiety is critical in order to implement appropriate treatments, educate patients and caregivers, and educate other health professionals. (Critical Care Nurse. 2014;34[2]:14-25)

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Section: Activation Of Cytokine Cascadesmentioning

confidence: 99%

Pathophysiological Relationships Between Heart Failure and Depression and Anxiety

Chapa

Akintade

Son

et al. 2014

Critical Care Nurse

View full text Add to dashboard Cite

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“…It has been proposed that a heightened pro‐inflammatory state may play a role in the progression of HF, including acute decompensations 1, 2, 3, 4, 5, 6, 7, 8, 9. Impairment of nitric oxide bioavailability due to oxidative stress, leading to impaired cyclic guanosine monophosphate‐protein kinase G signaling29 is one potential mechanism underlying the link between inflammation and HF progression.…”

Section: Introductionmentioning

confidence: 99%

Pro‐Inflammatory Biomarkers in Stable Versus Acutely Decompensated Heart Failure With Preserved Ejection Fraction

Abernethy

Raza

Sun

et al. 2018

JAHA

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BackgroundUnderlying inflammation has been increasingly recognized in heart failure with a preserved ejection fraction (HFpEF). In this study we tested the hypothesis that pro‐inflammatory biomarkers are elevated in patients with acutely decompensated HFpEF (AD‐HFpEF) compared with patients with stable HFpEF (S‐HFpEF).Methods and ResultsUsing a post hoc analysis the serum biomarkers tumor necrosis factor‐alpha, high‐sensitivity C‐reactive protein interleukin 6 and pentraxin 3 (PTX3) and clinical, demographic, echocardiographic‐Doppler and clinical outcomes data were analyzed in HFpEF patients enrolled in NHLBI Heart Failure Research Network clinical trials which enrolled patients with either AD‐HFpEF or S‐HFpEF. Compared to S‐HFpEF, AD‐HFpEF patients had higher levels of PTX3 (3.08 ng/mL versus 1.27 ng/mL, P<0.0001), interleukin‐6 (4.14 pg/mL versus 1.71 pg/mL, P<0.0001), tumor necrosis factor‐alpha (11.54 pg/mL versus 8.62 pg/mL, P=0.0015), and high‐sensitivity C‐reactive protein (11.90 mg/dL versus 3.42 mg/dL, P<0.0001). Moreover, high‐sensitivity C‐reactive protein, interleukin‐6 and PTX3 levels were significantly higher in AD‐HFpEF compared with S‐HFpEF patients admitted for decompensated HF within the previous year. PTX3 was positively correlated with left atrial volume index (r=0.41, P=0.0017) and left ventricular mass (r=0.26, P=0.0415), while tumor necrosis factor‐alpha was inversely correlated with E/A ratio (r=−0.31, P=0.0395).ConclusionsLevels of pro‐inflammatory biomarkers are strikingly higher in AD‐HFpEF compared with S‐HFpEF patients. PTX3 and tumor necrosis factor‐alpha are correlated with echocardiographic‐Doppler evidence of diastolic dysfunction. Taken together these data support the concept that a heightened pro‐inflammatory state has a pathophysiologic role in the development of AD‐HFpEF.

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“…3 Cardiac cytokines that are stimulated by Ang II, such as interleukin (IL)1b and transforming growth factor (TGF)b1, are involved in the development of cardiac fibrosis and in cardiac failure. 4,5 The LVH and myocardial fibrosis may also occur because of non-hemodynamic factors such as parathyroid hormone, endothelin, aldosterone and an increased sympathetic nerve discharge. 6 Increasing evidences have proved that Ang II is an independent risk factor for cardiovascular disease.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin (1−7) prevent heart dysfunction and left ventricular remodeling caused by renal dysfunction in 5/6 nephrectomy mice

et al. 2009

Hypertens Res

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The renin-angiotensin system (RAS) plays a critical role in chronic renal failure associated with heart failure. In the past few years, angiotensin (Ang) (1-7) have been reported to counteract the effects of angiotensin II (Ang II) and were even considered as a new therapeutical target in RAS. The purposes of this study were to examine whether the Ang (1-7) improves the heart function and remodeling of the left ventricle (LV) in mice with 5/6 nephrectomy (NC). We used a 5/6 nephrectomy to induce significant renal dysfunction in wildtype mice (WT). Twelve weeks after NC, WT showed high blood pressure, significant leftventricular dilation and dysfunction, which were accompanied by cardiomyocyte hypertrophy, diffuse interstitial fibrosis and oxidative damage of cardiomyocytes. Exogenous Ang (1-7) injection improved the heart function and remodeling of LV in mice with 5/6 NC accompanied by a reduction in cardiac interstitial fibrosis, inflammatory cytokine expression and oxidative damage levels of cardiomyocytes, decrease in the profibrotic signaling molecule transforming growth factor (TGF)-b and increase in the collagen degradation signaling molecule matrix metalloproteinase (MMP)-2, -9. However, these beneficial effects did not occur in hydralazine-treated mice. These findings suggest that (1) Exogenous Ang (1-7) injection improve the heart function and remodeling of LV in mice with 5/6 NC. (2) These beneficial effects are independent of its anti-blood pressure effect.

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Proinflammatory cytokine levels in patients with depressed left ventricular ejection fraction: A report from the studies of left ventricular dysfunction (SOLVD)

Abstract: Circulating levels of proinflammatory cytokines increase in patients as their functional heart failure classification deteriorates. Moreover, activation of the neurohumoral axis is unlikely to completely explain the elaboration of proinflammatory cytokines in heart failure.

Cited by 1,097 publications

References 21 publications

Pathophysiological Relationships Between Heart Failure and Depression and Anxiety

Pathophysiological Relationships Between Heart Failure and Depression and Anxiety

Pro‐Inflammatory Biomarkers in Stable Versus Acutely Decompensated Heart Failure With Preserved Ejection Fraction

Angiotensin (1−7) prevent heart dysfunction and left ventricular remodeling caused by renal dysfunction in 5/6 nephrectomy mice

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