Pathogenesis of Anemia in Heart Failure

Anand, Inder S.; Rector, Thomas S.

doi:10.1161/circheartfailure.114.001645

Cited by 13 publications

(14 citation statements)

References 6 publications

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“…Erythropoiesis is affected by circulating pro‐inflammatory cytokines as tumor necrosis factor‐alpha interleukin‐1 and interferon‐gamma, which hinder erythroid proliferation and differentiation (Means, ; Selleri et al ). Considering the lack of effective treatment for HFpEF (Ponikowski et al ), further research is warranted to determine the role of potential phenotypic modifications of the hematopoietic bone marrow in this population (Anand and Rector ). This could disclose novel biological targets, notably for those anemic patients in whom EPO treatment is ineffective or detrimental (Borovka et al ; Swedberg et al ).…”

Section: Discussionmentioning

confidence: 99%

Hypovolemia and reduced hemoglobin mass in patients with heart failure and preserved ejection fraction

et al. 2019

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A fundamental tenet of heart failure (HF) pathophysiology hinges on a propensity for fluid retention leading to blood volume (BV) expansion and hemodilution. Whether this can be applied to heart failure patients with preserved ejection fraction (HFpEF) remains uncertain. The present study sought to determine BV status and key hormones regulating fluid homeostasis and erythropoiesis in HFpEF patients. BV and hemoglobin mass (Hb mass ) were determined with high-precision, automated carbon monoxide (CO) rebreathing in 20 stable HFpEF patients (71.5 AE 7.3 years, left ventricular ejection fraction = 55.7 AE 4.0%) and 15 healthy age-and sex-matched control individuals. Additional measurements comprised key circulating BV-regulating hormones such as pro-atrial natriuretic peptide (proANP), copeptin, aldosterone and erythropoietin (EPO), as well as central hemodynamics and arterial stiffness via carotid-femoral pulse wave velocity (PWV). Carotid-femoral PWV was increased (+20%) in HFpEF patients versus control individuals. With respect to hematological variables, plasma volume (PV) did not differ between groups, whereas BV was decreased (À14%) in HFpEF patients. In consonance with the hypovolemic status, Hb mass was reduced (À27%) in HFpEF patients, despite they presented more than a twofold elevation of circulating EPO (+119%). Plasma concentrations of BV-regulating hormones, including proANP (+106%), copeptin (+99%), and aldosterone (+62%), were substantially augmented in HFpEF patients. HFpEF patients may present with hypovolemia and markedly reduced Hb mass , underpinned by a generalized overactivation of endocrine systems regulating fluid homeostasis and erythropoiesis. These findings provide a novel perspective on the pathophysiological basis of the HFpEF condition.

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Section: Discussionmentioning

confidence: 99%

Hypovolemia and reduced hemoglobin mass in patients with heart failure and preserved ejection fraction

et al. 2019

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“…In addition to other medical complications, anemia dominates for the accumulation damage course of cerebral autoregulation. With the progress of the disease, patients with anemia will suffer from many complications, such as heart failure 31 , chronic kidney disease 32 and vascular endothelial cells 33 34 , which play a more important role than anemia in the development of stroke. This effect may partly explain why Sico and colleagues found a positive relationship in patients with less severe stroke but not in severe stroke 17 .…”

Section: Discussionmentioning

confidence: 99%

Anemia increases the mortality risk in patients with stroke: A meta-analysis of cohort studies

Zhou

et al. 2016

Sci Rep

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The impact of anemia on the outcome of patients with stroke remains inconsistent. We performed a meta-analysis of cohort studies to assess the mortality risk in stroke patients with and without anemia. Systematic searches were conducted in the PubMed, China National Knowledge Infrastructure, Web of Science and Wanfang databases to identify relevant studies from inception to November 2015. The estimated odds ratio with a 95% confidence interval was pooled. subgroup analyses and sensitivity analyses were also conducted. We used Begg’s funnel plot and Egger’s test to detect the potential publication bias. Thirteen cohort studies with a total of 19239 patients with stroke were included in this meta-analysis. The heterogeneity among studies was slight (I2 = 59.0%, P = 0.031). The results from a random-effect model suggest that anemia is associated with an increased mortality risk in patients with stroke (adjusted odds ratio = 1.39, 95% confidence interval: 1.22–1.58, P < 0.001). The subgroup analyses are consistent with the total results. This meta-analysis of 13 cohort studies finds that anemia increases the mortality risk in patients with stroke. Future studies should perform longer follow-up to confirm this finding and explore its possible mechanism.

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“…Anemia in HF has the same profile as in chronic disease with defective utilization of iron, impaired erythropoietin responsiveness, and depressed bone marrow function 232, 233, 234. Neurohormonal activation, renal dysfunction, hemodilution, and systemic inflammation contribute to the development of anemia in HFpEF 232, 233, 234. Functional iron deficiency with upregulation of myocardial transferrin receptor has been reported in the absence of anemia in HFpEF patients 235.…”

Section: Comorbid Conditionsmentioning

confidence: 98%

“…Anemia is mostly prevalent in elderly women with advanced HFpEF, CKD, and diabetes 232, 233, 234. Anemia in HF has the same profile as in chronic disease with defective utilization of iron, impaired erythropoietin responsiveness, and depressed bone marrow function 232, 233, 234. Neurohormonal activation, renal dysfunction, hemodilution, and systemic inflammation contribute to the development of anemia in HFpEF 232, 233, 234.…”

Section: Comorbid Conditionsmentioning

confidence: 99%