Inflammatory Biomarkers in Heart Failure

Petersen, John W.; Felker, G. Michael

doi:10.1111/j.1527-5299.2006.05595.x

Cited by 69 publications

(53 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Many studies have shown that factors such as the inflammatory status, poor nutritional state and, obviously, the extent of cardiac dysfunction herald a poor prognosis in CHF [7][8][9][10][11][12][13]. However, none of these conventional indicators and, interestingly, also not LVF or RVF, carried any prognostic potential in our patient group.…”

Section: Discussionmentioning

confidence: 58%

Prognosis in patients with congestive heart failure and subacute renal failure treated with hemodialysis

Lindner

Doberer

Vychytil

et al. 2009

Wien Klin Wochenschr

View full text Add to dashboard Cite

Non-critically ill CHF patients with (sub-)acute renal dysfunction progressing to dialysis dependency have a grave prognosis. Renal failure itself had such a strong prognostic impact that conventional factors such as poor myocardial function or inflammation were concealed. Recovery of renal function and, surprisingly, anemia were beneficial factors. Alternative treatment strategies must be designed to improve the devastating prognosis for this special subset of patients with CHF.

show abstract

Section: Discussionmentioning

confidence: 58%

Prognosis in patients with congestive heart failure and subacute renal failure treated with hemodialysis

Lindner

Doberer

Vychytil

et al. 2009

Wien Klin Wochenschr

View full text Add to dashboard Cite

show abstract

“…These mediators are involved in, but not limited to, recruiting cells to inflammatory sites and stimulating cell division, proliferation, and differentiation [1]. Increased circulating and intracardiac levels of proinflammatory cytokines have been associated with chronic heart failure [2][3][4][5]. In addition, coronary artery disease (CAD) and dilated cardiomyopathy (DCM), the most common causes of chronic heart failure, are believed to be of an inflammatory origin.…”

Section: Introductionmentioning

confidence: 99%

Proinflammatory cytokines in heart failure: double-edged swords

et al. 2010

View full text Add to dashboard Cite

Increased circulating and intracardiac levels of proinflammatory cytokines have been associated with chronic heart failure. Following an initial insult, the increased production of proinflammatory cytokines, including TNF-α, IL-6, IL-1, and IL-18, jeopardizes the surrounding tissue through propagation of the inflammatory response and direct effects on the cardiac myocyte structure and function. Cardiac myocyte hypertrophy, contractile dysfunction, cardiac myocyte apoptosis, and extracellular matrix remodeling contribute enormously to the development and progression of chronic heart failure. Despite the identification of efficacious pharmacological regimens and introduction of mechanical interventions, chronic heart failure remains among the leading causes of mortality worldwide. To introduce novel therapeutic strategies that modulate the inflammatory response in the context of the failing heart, it is of prime importance to determine the contributions of TNF-α, IL-6, IL-1, and IL-18 in mediating cardiac adaptive and maladaptive responses, as well as delineating their downstream intracellular signaling pathways and their potential therapeutic implications.

show abstract

“…Elevated plasma levels of C-reactive protein (CRP) have been observed and are predictive of poor outcomes in patients with cardiovascular diseases, including CHF; 5 however, CRP has other specific functions, such as amplifying the production of monocyte proinflammatory cytokines such as TNF-α and IL-6, [6][7][8][9][10][11][12] thus suggesting that CRP may not be simply a biomarker, but may play a significant role in the pathogenesis and development of CHF.…”

Section: Editorial P 622mentioning

confidence: 99%

Short-Term Amiodarone Treatment Attenuates the Production of Monocyte Cytokines and Chemokines by C-Reactive Protein and Improves Cardiac Function in Patients With Idiopathic Dilated Cardiomyopathy and Ventricular Tachycardia

Hirasawa

Nakagomi

Kobayashi

et al. 2009

Circ J

View full text Add to dashboard Cite

Background: Increased expression of cytokines and chemokines has been observed in chronic heart failure (CHF). Amiodarone reduces circulating cytokine levels, so it may attenuate the production of monocyte cytokines and chemokines by C-reactive protein (CRP) and thus improve the left ventricular ejection fraction (LVEF) in dilated cardiomyopathy (DCM) patients with ventricular tachycardia (VT). Methods and Results: Peripheral blood mononuclear cells (PBMCs) were stimulated by 25 μg/ml CRP in 23 patients with DCM, who were divided into 2 groups based on whether or not amiodarone was included in their treatment (Amiodarone group n=8; No amiodarone group n=15). Tumor necrosis factor (TNF)-α and monocyte chemoattractant protein (MCP)-1 on monocytes at baseline and after 4 weeks of treatment was measured by ELISA and expressed as mean ± SD (pg · ml -1 · 10 -6 PBMCs). The LVEF and the CRP-induced monocyte cytokine and chemokine production were unchanged in the No amiodarone group after 4 weeks; however, LVEF in the Amiodarone group was increased (32.7±6.9 to 39.2±6.9%; P=0.005), and TNF-α and MCP-1 production in the Amiodarone group were decreased (P=0.012, respectively). Conclusions: Amiodarone attenuates the production of monocyte cytokines and chemokines by CRP, and improves LVEF in CHF patients with VT. (Circ J 2009; 73: 639 -646)

show abstract

Inflammatory Biomarkers in Heart Failure

Cited by 69 publications

References 43 publications

Prognosis in patients with congestive heart failure and subacute renal failure treated with hemodialysis

Prognosis in patients with congestive heart failure and subacute renal failure treated with hemodialysis

Proinflammatory cytokines in heart failure: double-edged swords

Short-Term Amiodarone Treatment Attenuates the Production of Monocyte Cytokines and Chemokines by C-Reactive Protein and Improves Cardiac Function in Patients With Idiopathic Dilated Cardiomyopathy and Ventricular Tachycardia

Contact Info

Product

Resources

About