The clinical syndrome of heart failure has been investigated so extensively that it may now almost be regarded as a metabolic disorder. Although an initial insult reduces cardiac pump efficacy, the resultant physiological response culminates in complex neurohormonal dysfunction. This has created confusion and prevented the acceptance of a universal definition of cardiac failure. With much current research concentrating on the pharmacological modification of neuro-endocrine imbalance, it is easy to lose sight of the fundamental principles behind heart failure management, namely, to improve cardiac function. In attempting to achieve this, the issues of morbidity and mortality must be addressed jointly; they are not mutually exclusive entities. Discrepant results between mortality studies and changes in exercise capacity have undermined the value of exercise testing. Because a treatment enhances longevity we should not ignore its effect on symptomatic status, and likewise we should not discard a therapy, which improves function because adverse events result in occasional premature deaths. Informed patient choice must exist.
Historically, exercise testing has been quintessential in our understanding and evaluation of heart failure. Peak oxygen consumption remains the best overall indicator of symptomatic status, exercise capacity, prognosis and hospitalisation. Unfortunately, muddling of surrogate and true end-points has confused many of these issues. Improved comprehension may be gained by applying the concept of cardiac reserve which has been described in a variety of heart conditions and used in cardiac failure patients to provide an indication of prognosis and functional capacity.


Keywords: exercise testing; heart failure