Vasopressin antagonists in acute heart failure syndromes

Abstract

The contribution of neurohormonal abnormalities in the pathophysiology of chronic heart failure (CHF) is well established. Attenuation of the excessive and continuous activation of angiotensin II and β-adrenergic receptors in patients with CHF with angiotensin-converting enzyme (ACE) inhibitors and beta-blockers, respectively, has resulted in substantial reductions in morbidity and mortality. However, it is not clear whether intervention with other neuroendocrine modulators (e.g., tumor necrosis factor [TNF] or endothelin) could result in similar benefits. © 2008 Springer-Verlag London.