[Beta-blockers in CHF: kidney's consequences]

In the 1980s congestive heart failure (CHF) was exclusively interpreted in hemodynamic terms. In accordance with this pathophysiologic hypothesis, cardiovascular drugs, mainly positive inotropics and/or vasodilators were used but not with significant results. From the mid 1980s, attention started focusing on the neurohumoral asset, strongly activated in patients suffering from CHF, and that it was itself the cause of CHF and responsible for the poor prognosis in these patients; therefore, to become the therapeutic target and to represent the rationale for using angiotensin-converting enzyme inhibitors (ACE-I), beta-blockers and angiotensin II receptor blockers (ARBs). Evidence has been provided that these drugs can reduce morbidity and mortality. However, this evidence derives only from studies on the general population. In uremic patients, there are no dedicated controlled trials, assuming that the effect can be extended to these patients, but this is not necessarily true. The evidence based on retrospective analysis is a better survival in patients using ACE-I, but there are no prospective trials on mortality and morbidity available. Even less evidence is available on ARBs, in spite of their favorable pharmacokinetic characteristics. Uremia has been suggested as state of excess sympathetic activation; therefore, the benefit derived from beta-blockers should be even greater in uremic than in non-renal patients. Therapy with beta-blockers significantly reduces morbidity and mortality in the general population. These results are also specifically demonstrated in dialysis patients. Finally, only specifically designed trials will be able to answer the questions that cardiologists and nephrologists ask themselves in their daily practice.