Sympathetic activation produces short term beneficial
effects by maintaining cardiac output and systemic
blood pressure in acute heart failure.[11,13-15]
On the other hand, chronic sympathetic activation
and excessive adrenergic stimulation in CHF ultimately
produces deleterious effects resulting in
worsening of the heart failure and increasing morbidity
and mortality.[11,13-15] These effects include
desensitisation of the -adrenergic signal transduction
mechanisms, resulting in a decreased cardiac
reserve and impairment of exercise tolerance, and
toxic effects on the cardiac myocyte, resulting in
progressive left ventricular dysfunction and chamber
remodelling.[14,15]The systemic effects of sympathetic
activation also cause increased peripheral
vascular resistance and increased afterload, thus,
worsening the function of the weakened heart.[14-15]
That -blockade may prevent or reverse these effects
forms the pathophysiological rationale for the use
of -blockers in CHF.[14,15] Whether or not such
benefits can be attained clinically can only be tested
by clinical trials