title: Effects of optimized heart failure therapy and anemia correction with epoetin beta on left ventricular mass in hemodialysis patients.
abstract: BACKGROUND
  In chronic hemodialysis (HD) patients, the presence and degree of left ventricular hypertrophy (LVH) correlates with mortality. Previous studies have shown that interventions, such as anemia correction or treatment of hypertension and/or chronic heart failure (CHF), can result in moderate regression of LVH. The primary objective of our study was to investigate the effects of a multi-interventional treatment strategy on LVH in HD patients.
  
  
  RESULTS
  In a series of 202 consecutive HD patients, we combined optimized CHF therapy, including beta-blockers (BB), ACE inhibitors and angiotensin receptor blockers (ARBs), to target doses with full anemia correction by epoetin beta (hemoglobin (Hb) target males 14.5 g/dl, females 13.5 g/dl). Serial echocardiograms were recorded every 3-6 months. Mean follow-up was 3.4 +/- 1.2 years. Mean Hb at baseline was 11.4 +/- 1.4 vs. 14.6 +/- 1.6 g/dl (p < 0.001) at study end. There was a significant reduction in left ventricular mass index (LVMI, 159 +/- 65 vs. 132 +/- 46 g/m2 (p < 0.001)), an improvement in left ventricular ejection fraction (LVEF, 60 +/- 15 vs. 66 +/- 12% (p < 0.01)) and in NYHA class (2.8 +/- 0.76 vs. 1.96 +/- 0.76 (p < 0.01)) from baseline to follow-up in the overall study population. In a subgroup of 70 patients, LVMI returned to normal (169 +/- 33 vs. 114 +/- 14 g/m2 (p < 0.001)) after 1.4 +/- 1 years.
  
  
  CONCLUSIONS
  Our study shows that optimized CHF therapy, in combination with anemia correction to normal Hb targets, results in a significant reduction of LVH, an increase in LVEF and an improvement in NYHA class. Moreover, in contrast to previous studies, our data also demonstrate that complete regression and prevention of LVH in HD patients is possible.
authors.affiliation: Department of Nephrology and Medical Intensive Care, Charité University Clinic, Berlin, Germany. h.hampl@je-web.de
authors.forename: Hannelore
authors.initials: H
authors.lastname: Hampl
authors.forename: Lars
authors.initials: L
authors.lastname: Hennig
authors.forename: Christian
authors.initials: C
authors.lastname: Rosenberger
authors.forename: Masoud
authors.initials: M
authors.lastname: Amirkhalily
authors.forename: Lutz
authors.initials: L
authors.lastname: Gogoll
authors.forename: Eberhard
authors.initials: E
authors.lastname: Riedel
authors.forename: Armin
authors.initials: A
authors.lastname: Scherhag
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000740:Anemia / Q000097:blood / Q000188:drug therapy*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D002303:Cardiac Output, Low / Q000188:drug therapy* / Q000503:physiopathology; D002317:Cardiovascular Agents / Q000627:therapeutic use*; D004452:Echocardiography; D004921:Erythropoietin / Q000627:therapeutic use*; D005260:Female; D006439:Hemodynamics; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging*; D007501:Iron / Q000097:blood; D007676:Kidney Failure, Chronic / Q000628:therapy; D008297:Male; D008875:Middle Aged; D011994:Recombinant Proteins; D006435:Renal Dialysis; D013318:Stroke Volume; D016896:Treatment Outcome
chemical_list: D000319:Adrenergic beta-Antagonists; D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D002317:Cardiovascular Agents; D011994:Recombinant Proteins; C103998:epoetin beta; D004921:Erythropoietin; D007501:Iron