28 anemic [hematocrit (Hct) < 25%] and normotensive patients on maintenance hemodialysis with uremia-associated left-ventricular (LV) hypertrophy were treated with recombinant human erythropoietin. Before correction of anemia, after 4 months at a target Hct of 35% and 16 months (Hct still 35%) patients were assessed by echocardiography and physical stress testing. Partial correction of anemia resulted in a decrease in the LV end-diastolic diameter from 52.6 ± 3.4 SD mm to 49.6 ± 3.4 mm at 4 months (p < 0.01) and 47.9 ± 2.9 mm at 16 months (p < 0.001). Concomittently there was a slight decrease of LV end-systolic diameter (30.4 ± 3.1 vs. 32.6 ± 3.5 mm, p < 0.05) and LV posterior wall thickness (12.1 ± 0.9 vs. 12.8 ± 0.8 mm, p < 0.05) at 16 months. The calculated LV muscle mass index was reduced from 199 ± 35 g/m2 to 173 ± 34 g/m2 at 4 months (p < 0.01) and 160 ± 28 g/m2 at 16 months (p < 0.001). Heart rate at rest was reduced significantly from 80 ± 12 to 73 ± 11 min (p < 0.01) at 4 and 16 months. LV ejection fraction, thickness of LV septum and blood pressure did not change. Partial correction of anemia led to an increase of maximal physical stress tolerance from 1.4 ± 0.4 to 1.85 ± 0.5 W/kg b.w. at 4 months (p < 0.01), which was maintained at 16 months. It is concluded that correction of anemia leads only to a partial morphologic regression of LV hypertrophy, which underlines the multifactorial pathogenesis of LV hypertrophy in uremic patients.

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