title: Cardiovascular adaptation to chronic anemia in the elderly: an echocardiographic study.
abstract: OBJECTIVE
  To study the effects of chronic severe anemia on the aging heart.
  
  
  METHODS
  We studied 41 elderly patients (mean age 69.8 yr, standard deviation [SD] 3.9 yr) suffering from chronic severe anemia (mean hemoglobin 6.3, SD 0.5 g/dL) with no history of cardiac disease, along with 63 healthy age- and sex-matched controls. Assessment included physical examination, electrocardiogram and Doppler echocardiography.
  
  
  RESULTS
  Although heart rates were similar between patients and controls, arterial blood pressures were significantly lower in patients (mean pressure 92.7 mm Hg, SD 7.9, v. mean 102.1 mm Hg, SD 3.5; p < 0.001). No patient was found to have congestive heart failure. Patients with chronic anemia had larger diameters of the left (end-systolic 35.28, SD 4.20, v. 33.73, SD 2.08 mm, p < 0.05; end-diastolic 53.33, SD 4.55, v. 50.37, SD 2.10 mm, p < 0.001) and right ventricles (30.76, SD 3.98, v. 29.04, SD 2.04 mm; p < 0.05), and greater left-ventricular mass (277.64, SD 62.85, v. 212.91, SD 24.87 g; p < 0.001). Fractional shortening did not differ significantly (0.33, SD 0.04, v. 0.33, SD 0.03). The load-independent end-systolic index was lower in patients (2.67, SD 0.56, v. 3.87, SD 0.49 kdyn x m2/cm5; p < 0.001) along with end-systolic stress and total systemic resistance (p < 0.001) than controls, whereas the cardiac index was higher (4.31, SD 1.29, v. 2.73, SD 0.51 L/min/m2; p < 0.001). Differences between the 2 groups in diastolic function indices and pulmonary arterial pressures were not statistically significant.
  
  
  CONCLUSIONS
  Chronic severe anemia is well tolerated by the aging heart. Neither congestive heart failure nor clearly evident left-ventricular dysfunction were encountered. The heart exhibited an adaptive potential through remodelling by means of the Frank-Starling mechanism and afterload reduction. However, the lower end-systolic index in patients suggests that ventricular performance was marginally compromised. This state of high output was achieved mainly by increased stroke volume, with little contribution from heart rate.
authors.affiliation: First Department of Internal Medicine, University of Athens Medical School, Athens, Greece. aaisopos@cc.uoa.gr
authors.forename: Athanasios
authors.initials: A
authors.lastname: Aessopos
authors.forename: Spyros
authors.initials: S
authors.lastname: Deftereos
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Farmakis
authors.forename: Costas
authors.initials: C
authors.lastname: Corovesis
authors.forename: Stergios
authors.initials: S
authors.lastname: Tassiopoulos
authors.forename: Maria
authors.initials: M
authors.lastname: Tsironi
authors.forename: Dimitra
authors.initials: D
authors.lastname: Georgonikou
authors.forename: John
authors.initials: J
authors.lastname: Moyssakis
mesh_terms: D000222:Adaptation, Physiological; D000368:Aged; D000740:Anemia / Q000503:physiopathology*; D002320:Cardiovascular Physiological Phenomena; D016022:Case-Control Studies; D002908:Chronic Disease; D005260:Female; D006801:Humans; D008297:Male