The cardiovascular and hemodynamic effects of erythropoietin in chronic renal failure

Left ventricular hypertrophy (LVH) has been identified as an independent risk factor for mortality in patients with chronic renal failure (CRF) and anemia has been proposed to contribute to LVH. The cardiovascular and hemodynamic effects of correction of anemia with recombinant human erythropoietin (rHU EPO) was assessed in a 12 week prospective study in patients with CRF.

Biochemical parameters and echocardiography were studied at the start and after three months therapy with EPO in 24 patients with CRF--11 predialysis (Group I) and 13 dialysis (Group II).

The mean haemoglobin (Hb)--g/dl increased significantly from 7.5 +/- 1.0 to 10.1 +/- 1.1 in group I and from 6.7 +/- 0.6 to 9.4 +/- 0.8 in group II (p < 0.05) on EPO therapy. The left ventricular mass index (LVMi)--g/m2 reduced significantly from 185.6 +/- 44.6 to 158.3 +/- 4.1 in group I and from 158.0 +/- 26.9 to 131.6 +/- 22.1 in group II (p < 0.05 in both). The interventricular septal thickness (IVST) also showed a significant decline in both groups, 1.17 +/- 0.06 to 1.14 +/- 0.05 (group I) and 1.09 +/- 0.25 to 1.01 +/- 0.21 (group II), p < 0.05 in both. The thickness of the left ventricular posterior wall remained unchanged. The left ventricular end diastolic and systolic diameters (LVEDD and LVESD) significantly reduced from their baseline values in both the groups (p < 0.05). The diastolic filling parameters across the mitral valve remained unchanged in both the groups. The cardiac index (CI)--L/min/m2 decreased from 3.53 +/- 0.3 to 3.03 +/- 0.27 in group I and from 3.31 +/- 0.64 to 2.80 +/- 0.60 in group II (p < 0.05) and the total peripheral resistance (TPR)--dynes/cm5/sec increased from 1567 +/- 164.8 to 1883 +/- 190.7 in group I and from 1618 +/- 375.7 to 2004 +/- 437.3 in group II. The differences in all the parameters at the start and after 3 months of EPO were comparable in groups I and II. The mean arterial pressure (MAP) changed insignificantly in both the groups.

To conclude, this study has shown that the decrease in LVMi with EPO reflects the role of anemia in the genesis of LVH and that the correction of anemia with EPO in CRF results in regression of LVMi and has a favourable effect on cardiovascular hemodynamics.