New pharmacologic therapies for acute heart failure.
Given the limitations of high-dose diuretics and vasodilators and the increasing literature showing that inotropes, regardless of the dose used, have a detrimental effect on mortality, a variety of new agents are under investigation for the treatment of pulmonary and systemic congestion and restoration of cardiac output in the setting of acute heart failure syndromes. The new therapeutic approach is based on two goals: short-term improvement in symptoms together with long-term improvement of cardiac function. This review describes new agents that are in preclinical and in clinical phases with realistic prospects: anti-endothelin, natriuretic peptides, istaroxime, levosimendan, myosin activators, and vasopressin antagonists. Those new therapeutic strategies aim to act at the cellular level to improve vessel and heart functions, with minimal side effects, together with improved sodium and water balance.
D000208:Acute Disease; D000241:Adenosine / Q000037:antagonists & inhibitors; D000251:Adenosine Triphosphatases / Q000187:drug effects; D065092:Antidiuretic Hormone Receptor Antagonists; D024722:Cardiac Myosins / Q000187:drug effects / Q000378:metabolism; D002316:Cardiotonic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D065128:Endothelin Receptor Antagonists; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D006835:Hydrazones / Q000627:therapeutic use; D045265:Natriuretic Peptides / Q000627:therapeutic use; D011724:Pyridazines / Q000627:therapeutic use; D000077464:Simendan
D065092:Antidiuretic Hormone Receptor Antagonists; D002316:Cardiotonic Agents; D065128:Endothelin Receptor Antagonists; D006835:Hydrazones; D045265:Natriuretic Peptides; D011724:Pyridazines; D000077464:Simendan; D000251:Adenosine Triphosphatases; D024722:Cardiac Myosins; D000241:Adenosine