|do you want to run that by me again...?
||[Apr. 2nd, 2005|06:21 am]
8 or so bees in my bonnet
|||||aim-cold water music||]|
Sympathetic activation in heart failure is intimately linked to disease progression and to adverse outcome.1–3 Contemporary management of heart failure relies on three antiadrenergic strategies, predicated on the hypothesis that interventions that counter sympathetic overactivity will improve both symptoms and prognosis. First, excessive central sympathetic outflow to the heart and periphery can be reduced by normalizing elevated cardiac filling pressures,4 by abolishing coexisting obstructive sleep apnea with nocturnal continuous positive airway pressure,5 or by attenuating sympathoexcitatory reflexes activated by exercising muscle through conditioning. Although rational, thus far these interventions have not been proven to improve survival.