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[1] KDOQI; National Kidney Foundation. KDOQI Clinical Practice Guidelines and Clinical Practice Recommendations for Anaemia in Chronic Kidney Disease. Am J Kidney Dis. 2006;47(5 Suppl 3):S11–145 [2] Felker GM, Adams KF Jr, Gattis WA, O’Connor CM. Anaemia as a risk factor and therapeutic target in heart failure. J Am Coll Cardiol. 2004;44:959–966 [3] Yi-Da Tang, Katz SD. Anaemia in chronic heart failure. Circulation 2006;113:2454–2461 [4] Go AS, Yang J, Ackerson LM

References 1. Metra M, Ponikowski P, Beckenstein K et al. Advanced chronic heart failure: a position statement from the study Group on Advanced Heart Failure of the Heart Failure Association of the European Society of Cardiology, Eur J Heart Fail. 2007, 9: 684-94 2. Allen LA, Stevenson LW, Grady KL et al – Decesion making in advanced heart failure: a scientific statement from the American Heart Association, Circulation 2012, 125 (15): 1928-52 3. Fang JC – Advanced (stage D) heart failure: a statement from the Heart Failure Society of America guidelines committee

Bibliography 1. Chugh SS, Roth Ga, Gillum Rf, Mensah Ga, Global burden of atrial fibrillation in developed and developing nations, Glob Heart, 2014; 1: 113119 2. Maisel Wh, Stevenson Lw, Atrial fibrillation in heart failure: epidemiology, pathophysiology, and rationale for therapy. AmJ Cardiol 2003; 6A: 2D-8D 3. Agency for Healthcare Research and Quality. Weighted national estimates. HCUP National Inpatient Sample, 2012 4. A.J Camm, G.YH Lip, R. De Caterina, et al., Actualizarea ghidului de management al fibrilaţiei atriale al Societãţii Europene de Cardiologie

guidelines for the diagnosis and treatment of acute and chronic heart failure 2008. Eur Heart J. 2008; 29:2388-2442. 5. World Health Organization. Obesity: preventing and managing the global epidemic. Report of a WHO consultation. World Health Organ Technical Report Series 2000; 894: i-xii,1-253. 6. RUPERT JL, KIDD KK, NORMAN LE, MONSALVE MV, HOCHACHKA PW, DEVINE DV. Genetic polymorphisms in the renin-angiotensin system in high altitude and low altitude native American populations. Ann Hum Genet 2003; 67: 17-25. 7. PROCOPCIUC LM, CARACOSTEA G, ZAHARIE G, PUSCAS M, IORDACHE

–9. 11 Gibbons GH, Liew CC, Goodarzi MO, Rotter JI, Hsueh WA, Siragy HM, et al. Genetic markers: progress and potential for cardiovascular disease. Circulation 2004; 109(Suppl 1): IV47–58. 12 Liew CC, Dzau V. Molecular genetics and genomics of heart failure. Nat Rev Genet 2004; 5: 1–16. 13 Friddle CJ, Koga T, Rubin EM, Bristow J. Expression profiling reveals distinct sets of genes altered during induction and regression of cardiac hypertrophy. Proc Natl Acad Sci USA 2000; 97: 6745–50. 14 Yang J, Moravec CS, Sussman MA, DiPaola NR, Fu D, Hawthorn L, et al. Decreased

Introduction Chronic heart failure (CHF) is a disease with the highest mortality rate for elderly people, with a prevalence of 5–10% for persons aged 65 and older. As a primary single causal and curative therapy is rarely possible, the treatment often simply aims for the prevention of complications (palliation). Therefore, the diagnosis and treatment of concomitant diseases (comorbidities) are of an outstanding importance. Besides that, an early detection of an exacerbation of the clinical pattern is central. The care and the backing of affected patients

REFERENCES 1. Beedkar A, Parikh R, Deshmukh P. Heart Failure and the Iron Deficiency. J Assoc Physicians India . 2017;65:79-80. 2. Weiss G, Goodnough LT. Anemia of chronic disease. N Engl J Med . 2005;352:1011-1023. 3. Cairo G, Bernuzzi F, Recalcati S. A precious metal: Iron, an essential nutrient for all cells. Genes Nutr . 2006;1:25-39. 4. Moos T. Brain iron homeostasis. Dan Med Bull . 2002;49;279-301. 5. Klip IT, Comin-Colet J, Voors AA, et al. Iron deficiency in chronic heart failure: an international pooled analysis. Am Heart J . 2013;165:575-582.e3 6

References 1. Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland JGF, Coats AJS, et al. - 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur Heart J. 2016;37(27):2129-2200 2. Morrow DA, de Lemos JA. Benchmarks for the assessment of cardiovascular biomarkers. Circulation. 2007;115(8):949–952 3. Correale M

patients with heart failure referred for cardiac transplantation: preliminary observations. Clin Cardiol 2003; 26:407–10. 8. Bokhari SW, Bokhari ZW, Zell JA, Lee DW, Faxon DP. Plasma homocysteine levels and left ventricular systolic function in coronary artery disease patients. Coron Artery Dis 2005; 16:153–61. 9. Gibelin P, Serre S, Candito M, Houcher B, Berthier F, Baudouy M. Prognostic value of homocysteinemia in patients with congestive heart failure. Clin Chem Lab Med 2006; 44:813–6. 10. Vasan RS, Beiser A, D'Agostino R, Levy D, Selhub J, Jacques PF, et al. Plasma

and paracrine effector. ADM is a hemodynamically active vasodilatory peptide with potent hypotensive effects [1]. It also demonstrates acute inotropic, vasodilatory, diuretic, and natriuretic effects, and it inhibits aldosterone production. Chronically, ADM also has antihypertrophic, anti-apoptotic, antifibrotic, antioxidant, and angiogenesis effects. ADM also may have utility as a disease maker. Elevated measurements have been described in hypertension, chronic renal disease, and heart failure [1]. Its concentrations are elevated in chronic heart failure [2], and