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Time for primary review 28 days. Chronic heart failure (CHF) is a complex syndrome characterised by objective evidence of ventricular dysfunction and associated clinical symptoms 1. Activated neurohormonal mechanisms play an important role in the maintenance of circulatory homeostasis. They can be divided into the vasoconstrictive, sodium retaining and the opposing vasodilatory, natriuretic systems. Vasoconstrictive and sodium retentive actions are provided by the renin–angiotensin–aldosterone system, the sympathetic nervous system, vasopressin, thromboxane and endothelin 2–5. Initially, in patients with heart failure, these act as important compensatory mechanisms maintaining blood pressure and adequate tissue perfusion. However, prolonged activation of these systems has deleterious effects on haemodynamics and directly on the heart itself. Enhanced vasoconstriction and fluid retention result in adverse loading conditions in the failing ventricle, whilst high levels of angiotensin II directly induce cardiac myocyte necrosis and adversely alter the myocardial matrix structure 6–9. Angiotensin II also potentiates sympathetic drive by direct stimulation and by impairing its control by the baroreceptors 10. In view of these adverse effects, it might be anticipated that measurement of plasma levels of neurohormones would be a helpful adjunct during prognostic assessment and even in the tailoring of therapy in CHF. Several studies have demonstrated an impaired prognosis in patients with CHF who have elevated plasma levels of norepinephrine and endothelin-1 11, 12. Cardiac cachexia is a wasting condition that occurs in a significant percentage of patients with CHF, and is associated with a particularly poor prognosis 13. This group appears to have marked neurohormonal abnormalities, with patients demonstrating elevated levels of norepinephrine and a reduction in plasma sodium concentration 14. However, drugs that reduce plasma catecholamine levels are not necessarily associated with an improved prognosis, suggesting that the mechanisms involved in blunting the effects of the sympathetic nervous system … *Corresponding author. Tel.: +44-207-351-8127; fax: +44-207-351-8733 p. kalraatic. ac. uk
Paul R. Kalra (Wed,) studied this question.