HF remains the most common cause of hospitalisation in patients over the age of 65 and the main symptoms are vascular congestion. Fluid overload is a major pathophysiological mechanism underlying both acute decompensation in HF and the progression of the syndrome. Although there has been a lot of controversy on the possible negative effects of diuretic therapy, due to the reduced intra-arterial volume with neuro-endocrine hyperactivation, no definite causal relationship has been established between diuretic therapy, its dosage and cardiovascular mortality.
Although there are three main classes of diuretics (loop diuretics, thiazide diuretics with metolazone and potassium-sparing diuretics), loop diuretics are most commonly used, because they have the most potent natriuretic action. Conversely, despite having a weak diuretic effect, potassium sparing diuretics have been shown to be significantly efficacious in improving the long-term prognosis in symptomatic HF patients.
Nowadays, the primary role of thiazide-like diuretics in CHF is to attempt to overcome diuretic resistance, thus performing a sequential nephron blockade when administered in association with loop diuretics.
Despite various attempts, due to the many confounding factors and the extreme heterogeneity of studied population, randomised trials failed to find any significant differences on optimal dosages and modality of administration of loop diuretics in acute HF.
More data will be needed before using arginine vasopressin antagonist clinically, since the results of randomised trials failed to show the expected benefits. The same is true for UF – until stronger clinical data are available, its use will be limited to selected cases in accordance with current guidelines.
Research of new physiology-based approaches designed to offset the primary determinants of water retention could improve the management of patients affected by CHF. Until then, diuretic therapy will remain the cornerstone in CHF.