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Design
Review
Offers historical context on HF therapies without new data; leaves open prospective trials of exercise retraining.
If the failing left ventricle could be given an effective push , other approaches to the treatment of heart failure would not be needed. We have inotropes only for short‐term parenteral use. We have no safe inotrope for chronic oral use. The effect of digitalis is only feeble and the phosphodiesterase inhibitors seem to increase mortality from sudden death. Diuretics are dramatic for acute pulmonary oedema and the mainstay for chronic fluid retention but do not improve the pump and by reducing blood volume stimulate the renin angiotensin system leading to vasoconstriction, further fluid retention and hypokalaemia. Nitrates drop pre‐load without reducing blood volume but tolerance is a problem and stroke volume does not increase. Reduction of afterload helps the failing ventricle to empty, the pull and output increases. The angiotensin converting enzyme inhibitors (ACEI) are now the cornerstone of heart failure treatment, reducing mortality in severe heart failure (CONSENSUS) and superior to standard vasodilator therapy (V‐HeFT‐2) at improving the survival of patients with mild to moderate heart failure. ACEI can reduce the incidence of ventricular ectopy and probably do this through improving left ventricular function, from decreasing sympathetic tone, reducing myocardial oxygen demand or increasing serum potassium but ACEI did not dimmish the incidence of sudden death in the SOLVD trial despite reducing mortality. Disappointingly little improvement in exercise tolerance and persistence of chronic fatigue in heart failure concentrated attention on the periphery . That the changes found in skeletal muscles are consequent upon the combination of inability to increase perfusion on exercise together with the effects of chronic inactivity are beyond question (though it has been suggested otherwise). Retraining by suitable daily exercise has been shown to improve exercise tolerance in chronic stable heart failure with restoration of lost oxidative fast muscle fibres and capillary network. Rest is no longer the order of the day.
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Celia M. Oakley (1992) studied this question.
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