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heart failure and this condition increases with the degree of severity of illness. Anemia in congestive heart failure is often not tertangi with treatment, and of course, never existed studiyang show that the anemia will contribute to the severity or degree of severity of illness. Study of the Studies Of Left ventricular dysfunction (SOLVD), indicates that anemia is an independent risk factor in patients with left ventricular dysfunction. Compounding the mechanism of the CHF anemia, including anemia due to hypoxia would lead to exacerbation of the heart muscle or peripheral, thus increasing venous return will increase the workload on the heart of LVH. Hypoxia can also be a trigger of the activation of neurohormonal and cytokine that what is called memjadikan syndrome abnemia cardio-renal. Normalization of hemoglobin levels may improve this cycle.

Erythropoietin (EPO) is a glycoprotein that functions as a growth factor produced by the kidneys to regulate red blood cell production. In patients with chronic diseases such as: failure ginjak terminal, malignancy, HIV infection can increase the provision of EPO and hemoglobin levels increase the quality of life. Stdu-subject study in the number of participants who have done little, gives the EPO and the provision of intravenous iron improved ejection fraction, functional repair other organs, and lower hospitalisasi CHF patients.



How EPO granting benefits to CHF patients in improving patient activity?. With the assumption of EPO can improve the provision of oxygen transport and reduce oxidative stress is predicted that the provision EPO can improve the quality of patients with CHF events.


Study the use of EPO in CHF patients whereas severe degree, performed by including as many as 26 CHF patients with anemia. Study design was randomized, single undercover, and a comparative study between the EPO with placebo. Measured parameters in addition to hematology parameters, plasma volume, vasodilatation function was also measured clinically during promorfa patients with active parameters (peak oxygen consumption [VO2], exercise duration, 6-minute walk), muscle aerobic metabolism (half-time of V ˙ O2 and near infrared recovery), and forearm vasodilatation function.

A total of 12 patients who showed improvement emndapatkan EPO compared with only one patient in the placebo group (P <0.05). Repair Hb levels also occurred in the group receiving EPO compared to placebo jka respectively: (11.0 ± 0.5 to 14.3 ± 1.0 g / dL, P <0.05). In the EPO group, peak VO2 (11.0 ± 1.8 to 12.7 ± 2.8 mL / min / kg, P <0.05) and duration of activity of 590 ± 107 to 657 ± 11, P0.004) but not in the control group significant improvements.

Conclusion:
EPO significantly increased capacity at the time of activity in patients with chronic heart failure. One mechanism of improvement in VO2 is increased transport of oxygen due to increased concentration of hemoglobin.