[Neurohumoral mechanisms in cardiocirculatory decompensation]

Congestive heart failure is characterized by profound alterations in systemic haemodynamics as well as in neurohumoral profile with activation of the sympathetic nervous system, reninangiotensin axis, plasma vasopressin and atrial natriuretic peptides, i.e. factors involved in homeostatic control of the cardiovascular system. The sympathetic stimulation, which has been documented by a variety of methodological approaches (plasma norepinephrine measurement, norepinephrine spillover technique, microneurographic recording of efferent post-ganglionic muscle sympathetic nerve traffic) is already evident in the initial stages of the disease (NYHA classes I-II) and more manifest in severe heart failure (NYHA classes III-IV). Although representing in mild heart failure a compensatory mechanism aimed at preserving cardiac output, the sympathetic and neurohumoral activation, which can be likely ascribed to arterial baroreceptor dysfunction, may represent, in the clinical course of the disease, a maladaptative phenomenon. Thus pharmacological treatment of heart failure should be aimed not only at improving systemic haemodynamics but also at reversing neurohumoral activation and baroreflex impairment. Recent experimental clinical evidence suggests that these therapeutical goals can be satisfactorily achieved by digitalis glycosides and ACE-inhibitors.