Abstract
The past several decades have shown the functional status of sympathetic activity in congestive heart failure. The results, particularly through clinical and basic studies in heart failure, indicate an increased sympathetic neural activity. The definitive and compelling evidence of the involvement of catecholamines is the demonstration that many drugs that are therapeutically useful in the treatment of heart failure also affect the sympathetic nervous system at various sites, including its synthesis, release and uptake of catecholamines and a decreased plasma norepinephrine level. Although it is not surprising that the sympathetic system is altered as cardiac function is compromised in heart failure, it now appears that this system may overreact in chronic situations. The detrimental cardiovascular problems result in the production of aminochrome and free radicals. Antioxidant therapy to target the production of aminochrome from autooxidation of catecholamines should provide an insight into the future therapeutic goal in situations like congestive heart failure.