[Role of the sympathetic nervous system in heart failure]

An increased activity of the sympathetic nervous system has been regarded as a sensible compensatory mechanism in heart failure. Further stimulation of this system by therapeutic interventions has proven useful in the situation of acute heart failure; however, the contractile reserve elicited by beta-stimulation is markedly reduced. By long-term stimulation of the sympathetic nervous system in the treatment of chronic heart failure mostly unfavorable effects are evoked, i.e.: 1) An increase in impedance for the failing heart by stimulation of peripheral alpha 1-adrenoreceptors. 2) An increase in myocardial oxygen consumption which causes further deterioration of the energy balance in the failing heart. 3) A fall in serum potassium concentration by stimulation of beta 2-receptors combined with a reduction of the fibrillation threshold favor the genesis of malignant arrhythmias. 4) Stimulation of myocardial alpha 1-adrenoreceptors may lead to a de-differentiation with a preferential synthesis of fetal myosins. Because of a reduced rate of calcium removal during diastole, increases in heart rate lead to an elevated myocardial stiffness. An increased sympathetic activity in patients with heart failure represents an independent marker of a reduced life expectancy. Interventions that either cause a reduction in sympathetic activity or which protect the heart from high catecholamine concentrations in heart failure are associated with an improvement of survival and quality of life.