Abstract

Acute heart failure (AHF) represents a major burden in developed countries. However, pharmacological approaches have remained almost same for 30 years and are still based on consensus rather than evidence, given that no medical therapy has been shown to positively affect clinical outcomes. Current pharmacological approaches are still based on decongestion by using diuretics in almost all patients, plus either vasodilators or inotropic agents to hemodynamics according to perfusion status. The role of loop diuretics (furosemide) and nitrates (nitroglycerin and nitroprusside) is well established, but new agents such as vasopressin and adenosine antagonists, as well as nesiritide, have failed to show any additional value. In presence of hypoperfusion, use of inotropics must be considered despite lack of benefit in terms of survival, and use of phosphodiesterase inhibitors and levosimendan has not shown any significant advantages over catecholamines (dobutamine). AHF involves a wide spectrum of patients and syndromes, and this probably accounts for failure of trials set up to evaluate new therapeutic approaches for improving outcomes: therapies need to be tailored to specific patients. At this time, serelaxin represents a promising new agent which has a multifaceted effect, including organ protection, and has shown encouraging results when tailored for a well defined population. In addition, role of ularitide, a synthetic form of natriuretic peptide urodilatin, and new cardiac myosin activators, as a new class of inotropic agents, will be established in near future by ongoing trials. Therefore, AHF continues to be an unsolved problem and, in light of lessons learned, new pharmacological approaches should be tai- lored to well defined AHF populations, incorporating concepts such as the sooner better, improve and stabilize, and prevent organ damage, in order to be able to clinical outcomes, including both mortality and readmission rates.

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