Heart Failure With Anemia

Abstract

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.

Clinical Phenotypes in Heart Failure With Preserved Ejection Fraction

“…Its prevalence is similar to that of CKD, diabetes, and COPD 229, 230, 231. 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.…”

“…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.…”

“…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.…”

2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure

“…Jest częstsza u kobiet, pacjentów w starszym wieku i u chorych z niewydolnością nerek. Niedokrwistość wiąże się z zaawansowanym remodelingiem mięśnia sercowego, zapaleniem i przewodnieniem [474], a ponadto z bardziej nasilonymi objawami, gorszym stanem czynnościowym, większym ryzykiem hospitalizacji z powodu HF oraz zmniejszoną przeżywalnością. Wskazana jest diagnostyka w kierunku poszukiwania przyczyn niedokrwistości (utrata krwi, niedobór żelaza, niedobór kwasu foliowego/witaminy B12, zaburzenia składu krwi), przy czym u wielu pacjentów nie udaje się znaleźć konkretnej przyczyny.…”

Rationale of the FIBROTARGETS study designed to identify novel biomarkers of myocardial fibrosis

“…One of the many challenges is that fibrosis is a mechanism involved in a number of overlapping and/or coexisting risk and disease states and co‐morbidities48, 49 such as hypertension, chronic kidney disease, diabetes mellitus, obesity, atrial fibrillation, ischaemic heart disease, and prevalent HF, such that a number of circulating biomarkers can be present in these various conditions 26, 46, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61. Our hypothesis is that novel ‘mechanistic’ markers of cardiac fibrosis are differentially expressed in various risk and disease states and co‐morbidities.…”