Abstract
The prognosis in patients with heart failure, independent of etiology, is determined mainly by the extent of sympatho-adrenergic stimulation. In the development of heart failure sympathetic cardiac stimulation precedes systemic sympatho-adrenergic activation. Increased concentrations of the neurotransmitter norepinephrine can be found in the myocardium. This is a result of both increased release from sympathetic nerves as well as reduced neuronal reuptake. We were able to show that in advanced heart failure these effects are distributed heterogeneously in the heart. It has been shown experimentally that the effects on sympathetic neurotransmission are similar for both ischemia and heart failure. Therefore, these findings could indicate an important role of sympatholytic measures in patients with ischemia induced heart failure.
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