Sympathetic activation produces short term beneficial
effects by maintaining cardiac output and systemic
blood pressure in acute heart failure.
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. 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. Whether or not such
benefits can be attained clinically can only be tested
by clinical trials