New insights into the mechanisms of action of beta-blockers, and the potential consequences for clinical practice, are continually evolving. Originally, this class of drugs was targeted towards treatment or prevention of hypertension, arrhythmias and myocardial ischaemia. Their therapeutic potential then expanded towards the reduction of mortality after myocardial infarction and heart failure.1 Although these indications are now widely accepted, they were not immediately apparent. So why may the use of beta-blockers be beneficial in patients already suffering from impaired myocardial contractility? Clinical observations suggested that the beneficial effect of beta-blockers was greater in patients with the worst cardiac performance.2 Concurrent findings that chronic use of an oral beta-agonist was associated with increased mortality led to re-evaluation of the paradigm,34 fuelled new research that unravelled the concept of maladaptive sympathetic overstimulation in heart failure,5 and changed clinical practice towards the use of beta-blockade.
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