Chronic heart failure secondary to ventricular dysfunction is characterized by neurohormonal activation, reflected mainly as increased sympathetic and renin-angiotensin system activation. Increased plasma levels of several neurohormones have been associated with increased morbidity and mortality. Neurohormone activation is part of the mechanism of compensation that is activated to maintain hemodynamic stability when heart output is reduced. Despite the initial benefits of this mechanism, neurohormone activation has been shown to contribute to progressive impairment of ventricular function and symptoms of heart failure, such that the greater the degree of activation, the worse the prognosis.Despite their important implications for prognosis, plasma neurohormone levels are not measured in clinical practice as part of the clinical evaluation of patients with heart failure. Medical treatment with ACE inhibitors and beta blockers, by lowering the plasma levels of some neurohormones, reduces their prognostic usefulness in establishing risk. Thus, no ideal biomarker is yet available that is stable and easy to measure, and that accurately established risk in patients with heart failure. Such a marker should also have an acceptable cost/benefit ratio.