Inflammation and anaemia in a broad spectrum of patients with heart failure

Kleijn, Lennaert; Belonje, Anne M.; Voors, Adriaan A.; Boer, Rudolf A. de; Jaarsma, Tiny; Ghosh, Sudip; Kim, Joseph; Hillege, Hans L.; Gilst, Wiek H. van; Veldhuisen, Dirk J. van; Meer, Peter van der

doi:10.1136/heartjnl-2012-301954

Cited by 21 publications

(14 citation statements)

References 39 publications

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“…The IL-6 levels reported here were lower than those obtained in the Coordinating Study Evaluating Outcomes of Advising and Counseling in HF (median, 12.0 [7.1-25.5] pg/mL) 18 ; which included patients hospitalized for HF. This difference can be explained by the fact that patients in our study had chronic stable HF rather than acute HF.…”

Section: Discussioncontrasting

confidence: 72%

“…This difference can be explained by the fact that patients in our study had chronic stable HF rather than acute HF. In Coordinating Study Evaluating Outcomes of Advising and Counseling in HF, 18 high-sensitivity-C-reactive protein also differed between patients with anemia and without anemia with a median of 3.4 (1.3-6.6) mg/L in patients with acute HF and anemia. We observed lower levels of high-sensitivity-C-reactive protein in patients with chronic HFrEF and anemia (median value of 2.6 (1.1-5.2) mg/L), which did not differ from patients in either groups 2 or 3.…”

Section: Discussionmentioning

confidence: 99%

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Heart Failure With Anemia

O’Meara

Rouleau

White

et al. 2014

Circ: Heart Failure

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Background— Anemia is a highly prevalent and strong independent prognostic marker in heart failure (HF), yet this association is not completely understood. Whether anemia is simply a marker of disease severity and concomitant chronic kidney disease or represents the activation of other detrimental pathways remains uncertain. We sought to determine which pathophysiological pathways are exacerbated in patients with HF, reduced ejection fraction (HFrEF) and anemia in comparison with those without anemia. Methods and Results— In a prospective study involving 151 patients, selected biomarkers were analyzed, each representing proposed contributive mechanisms in the pathophysiology of anemia in HF. We compared clinical, echocardiographic, and circulating biomarkers profiles among patients with HFrEF and anemia (group 1), HFrEF without anemia (group 2), and chronic kidney disease with preserved EF, without established HF (chronic kidney disease control group 3). We demonstrate here that many processes other than those related to chronic kidney disease are involved in the anemia–HF relationship. These are linked to the pathophysiological mechanisms pertaining to left ventricular systolic dysfunction and remodeling, systemic inflammation and volume overload. We found that levels of interleukin-6 and interleukin-10, specific markers of cardiac remodeling (procollagen type III N-terminal peptide, matrix metalloproteinase-2, tissue inhibitor of matrix metalloproteinase 1, left atrial volume), myocardial stretch (NT-proBNP [N-terminal probrain natriuretic peptide]), and myocyte death (troponin T) are related to anemia in HFrEF. Conclusions— Anemia is strongly associated not only with markers of more advanced and active heart disease but also with the level of renal dysfunction in HFrEF. Increased myocardial remodeling, inflammation, and volume overload are the hallmarks of patients with anemia and HF. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00834691.

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Section: Discussioncontrasting

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Heart Failure With Anemia

O’Meara

Rouleau

White

et al. 2014

Circ: Heart Failure

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“…Interleukin-6, C-reactive protein, and transforming growth factor-β1 were measured in a 96-well polystyrene microtiter plate using searchlight proteome arrays, as previously described. 10,11 Measurement of N-terminal probrain-type natriuretic peptide (NT-proBNP) was done using the Elecsys proBNP ELISA (Roche diagnostics, Mannheim, Germany). Estimated glomerular filtration rate was calculated using the modification of diet in renal disease formula.…”

Section: Biochemical Analysismentioning

confidence: 99%

Fibrosis Marker Syndecan-1 and Outcome in Patients With Heart Failure With Reduced and Preserved Ejection Fraction

Tromp

Pol

Klip

et al. 2014

Circ: Heart Failure

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Background-Syndecan-1 is a member of the proteoglycan family involved in cell-matrix interactions. Experimental studies showed that syndecan-1 is associated with inflammation in acute myocardial infarction and remodeling. The goal of this study was to explore the role of syndecan-1 in human heart failure (HF). Methods and Results-We analyzed plasma syndecan-1 levels in 567 patients with chronic HF. Primary end point was a composite of all-cause mortality and rehospitalization for HF at 18 months. Mean age was 71.0±11.0 years, 38% was women, and mean left ventricular ejection fraction was 32.5±14.0%. Median syndecan-1 levels were 20.1 ng/mL (interquartile range, 13.9-27.7 ng/mL). Patients with higher syndecan-1 levels were more often men, had higher N-terminal probrain-type natriuretic peptide levels, and worse renal function. Multivariable regression analyses showed a positive correlation between syndecan-1 levels and markers of fibrosis and remodeling but no correlation with inflammation markers. Interaction analysis revealed an interaction between left ventricular ejection fraction and syndecan-1 (P=0.047). A doubling of syndecan-1 was associated with an increased risk of the primary outcome in patients with HF with preserved ejection fraction (hazard ratio, 2.10; 95% confidence interval, 1.14-3.86; P=0.017) but not in patients with HF with reduced ejection fraction (hazard ratio, 0.95; 95% confidence interval, 0.71-1.27; P=0.729). Finally, syndecan-1 enhanced risk classification in patients with HF with preserved ejection fraction when added to a prediction model with established risk factors. Conclusions-In patients with HF, syndecan-1 levels correlate with fibrosis biomarkers pointing toward a role in cardiac remodeling. Syndecan-1 was associated with clinical outcome in patients with HF with preserved ejection fraction but not in patients with HF with reduced ejection fraction. (Circ Heart Fail. 2014;7:457-462.)

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“…Anemia is more prevalent in HFpEF than in HFrEF patients [77] and associated with increased risk of HF hospitalization [78] and overall mortality [79]. Inflammation importantly contributes to anemia in HF [80], through impaired production of erythropoietin and causing bone marrow dysfunction [81]. The presence of anemia is frequently accompanied by iron deficiency [82].…”

Section: Copd Anemia and Renal Failurementioning

confidence: 99%