Chronic heart failure (CHF) is frequently associated with poor exercise tolerance and debilitating symptoms despite optimal modern treatment. In the past we expected that this was due to the direct consequences of poor cardiac output and congested lungs. Other important pathophysiological disturbances in CHF occur as both short and long term consequences of the initial cardiac dysfunction. These include neurohormonal activation, cytokine release and trophic changes in skeletal muscle and the peripheral vasculature, and disturbances in reflex control systems.

The severity of symptomatic exercise limitation varies between patients, and bears little relation to the extent of the left ventricular systolic dysfunction measured at rest, or to markers of central haemodynamic disturbance.¹ Although there are several reasons for this, much recent research has suggested that changes which occur in the periphery as a consequence of the systemic effects of heart failure, may have become the principal factors limiting exercise.² Many changes have been described in skeletal muscle, peripheral arterial and endothelial function, and in reflex cardiopulmonary control systems. These have all been implicated in being limiting features to exercise tolerance in CHF patients. In its most severe form this can lead to cardiac cachexia.³ Major abnormalities in anabolic and catabolic hormones⁴ and in immune activation⁵ have been proposed to explain these developments in CHF. Therapeutic advances in managing heart failure have followed these pathophysiological studies, as neurohormonal blockade rather than positive inotropic treatment is now the mainstay of CHF therapy.

“HEART FAILURE SYNDROME”

One manifestation of the “heart …