Positioning of Inflammatory Biomarkers in the Heart Failure Landscape

Hartupee, Justin; Mann, Douglas L.

doi:10.1007/s12265-013-9467-y

Cited by 76 publications

(71 citation statements)

References 43 publications

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“…More recently, the contribution of a pro‐inflammatory state to the pathophysiology of HFpEF has been emphasized 6, 8, 17, 23, 31, 34, 35, 36, 45. In patients with ADHF, biomarkers reflecting activation of the renin‐angiotensin aldosterone system (RAAS) (plasma renin activity, aldosterone levels), oxidative stress (uric acid) and collagen synthesis (N‐terminal procollagen III) appear to be elevated to a similar extent in HFrEF and HFpEF 33.…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

“…Recently, there has been an effort to better characterize biomarkers in HF with preserved EF (HFpEF)2, 9, 31, 32). While inflammation plays a role in both HFpEF and HFrEF,33 there appear to be distinct differences in their pathogenesis 2, 34, 35, 36.…”

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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“…24,25 Recently, several studies suggested that circulating concentration of PTH was correlated with the severity of CHF and it could serve as a useful biomarker of the disease. 26 -28 In the present meta-analysis, our pooled results revealed that vitamin D supplementation was associated with a significant decrease in serum levels of TNF-α, CRP, and PTH.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D Supplementation in the Treatment of Chronic Heart Failure: A Meta‐analysis of Randomized Controlled Trials

Jiang

Zhang

et al. 2015

Clinical Cardiology

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Background: In recent years, there has been growing evidence that vitamin D deficiency is associated with the development and progression of chronic heart failure (CHF). Hypothesis: Additional supplementation of vitamin D may have protective effects in patients with CHF. Methods: We searched PubMed, Embase, and Cochrane databases through June 2015 and included 7 randomized controlled trials that investigated the effects of vitamin D on cardiovascular outcomes in patients with CHF. Then, we performed a meta-analysis of clinical trials to confirm whether vitamin D supplementation is beneficial in CHF patients. The weighted mean difference (WMD) and 95% confidence interval (CI) were calculated using fixed-or random-effects models. Results: Our pooled results indicated that additional supplementation of vitamin D was not superior to conventional treatment in terms of left ventricular ejection fraction, N-terminal pro-B-type natriuretic peptide, and 6-minute walk distance. Moreover, vitamin D supplementation was associated with significant decreases in the levels of tumor necrosis factor-α (WMD: −2.42 pg/mL, 95% CI: −4.26 to −0.57, P < 0.05), C-reactive protein (WMD: −0.72 mg/L, 95% CI: −1.42 to −0.02, P < 0.05), and parathyroid hormone (WMD: −13.44 pg/mL, 95% CI: −21.22 to −5.67, P < 0.05). Conclusions: Vitamin D supplementation may decrease serum levels of parathyroid hormone and inflammatory mediators in CHF patients, whereas it has no beneficial effects on improvement of left ventricular function and exercise tolerance.

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“…Less is known about the role of galectins in HIV infection. Galectin-3 (Gal-3) is secreted by macrophages; promotes eosinophil, neutrophil, and monocyte adhesion and recruitment, thereby enhancing inflammation [24]; and is a known marker of heart failure prognosis [25]. Gal-3 binding protein (Gal-3BP) is a soluble marker of M1-polarized macrophages [26], which are thought to be associated with inflamed, vulnerable plaques [27]; serum Gal-3BP levels have been found to be elevated in individuals with cancer or HIV infection [28,29].…”

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confidence: 99%

Association of Macrophage Inflammation Biomarkers With Progression of Subclinical Carotid Artery Atherosclerosis in HIV-Infected Women and Men

Hanna

Lin

Post

et al. 2017

The Journal of Infectious Diseases

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(See the editorial commentary by Feinstein and Lloyd-Jones on pages 1343-5.)Background. Monocytes and monocyte-derived macrophages promote atherosclerosis through increased inflammation and vascular remodeling. This may be especially true in chronic human immunodeficiency virus (HIV) infection.Methods. We examined 778 women (74% HIV + ) in the Women's Interagency HIV Study and 503 men (65% HIV + ) in the Multicenter AIDS Cohort Study who underwent repeated B-mode carotid artery ultrasound imaging in 2004-2013. We assessed baseline associations of the serum macrophage inflammation markers soluble (s)CD163, sCD14, galectin-3 (Gal-3), and Gal-3 binding protein (Gal-3BP) with carotid plaque formation (focal intima-media thickness >1.5 mm) over 7 years.Results. Marker levels were higher in HIV + persons versus HIV -persons. Presence of focal plaque increased over time: from 8% to 15% in women, and 24% to 34% in men. After adjustment for demographic, behavioral, and cardiometabolic factors, and CRP and interleukin-6, each standard deviation increase in sCD14 was associated with increased plaque formation (risk ratio [RR] 1.24, 95% confidence interval [CI] 1.07-1.43). This pattern was consistentby sex. sCD163 was associated with plaque formation in virally suppressed HIV + men (RR 1.52, 95% CI 1.04-2.22); Gal-3BP and Gal-3 were not associated with increased plaque.Conclusions. sCD14 and sCD163 may play important roles in atherogenesis among HIV + persons.

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Positioning of Inflammatory Biomarkers in the Heart Failure Landscape

Cited by 76 publications

References 43 publications

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

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

Vitamin D Supplementation in the Treatment of Chronic Heart Failure: A Meta‐analysis of Randomized Controlled Trials

Association of Macrophage Inflammation Biomarkers With Progression of Subclinical Carotid Artery Atherosclerosis in HIV-Infected Women and Men

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