title: Inotropic therapy for the failing myocardium.
abstract: Congestive heart failure (CHF) is a common clinical entity with diverse causes. Patients may present with acute decompensation or have a more indolent course, with diminishing exercise tolerance and increasing dyspnea. The management of this clinical entity traditionally has focused on restricting fluid intake, decreasing dietary sodium, decreasing afterload with vasodilatory agents, and supporting the failing myocardium with agents which produce a positive inotropic response. In the acutely decompensated patient, short-term therapy with positive inotropics is clearly beneficial. The role of long-term inotropic therapy for chronic CHF remains less clear. A number of clinical trials have recently evaluated the effects of long-term therapy on morbidity and mortality, with disappointing results. For a number of the newer, nonglycocide oral positive inotropics, at doses of drug which produce measurable hemodynamic improvement, increased mortality in treatment groups has been unacceptably high. Ironically, patients with worse left ventricular dysfunction show the most clinical improvement, but have the highest increased mortality. However, as with digoxin, there is some evidence that employing lower doses of drug that do not produce measurable improvement in hemodynamic parameters may result in both improved clinical state and decreased mortality. This review discusses the role of both oral and intravenous inotropic agents, discusses the difficulty in translating short-term hemodynamic improvement into long-term clinical benefit, and presents a rationale for the use of lower-dose inotropic therapy to improve long-term clinical outcome.
authors.affiliation: Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298, USA.
authors.forename: J B
authors.initials: JB
authors.lastname: Shipley
authors.forename: M L
authors.initials: ML
authors.lastname: Hess
mesh_terms: D000318:Adrenergic beta-Agonists / Q000627:therapeutic use; D002302:Cardiac Output; D002316:Cardiotonic Agents / Q000627:therapeutic use*; D004071:Digitalis Glycosides / Q000627:therapeutic use; D004280:Dobutamine / Q000627:therapeutic use; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D009200:Myocardial Contraction; D010726:Phosphodiesterase Inhibitors / Q000627:therapeutic use; D014665:Vasodilator Agents / Q000627:therapeutic use; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology
chemical_list: D000318:Adrenergic beta-Agonists; D002316:Cardiotonic Agents; D004071:Digitalis Glycosides; D010726:Phosphodiesterase Inhibitors; D014665:Vasodilator Agents; D004280:Dobutamine