title: Etiology and response to drug treatment in heart failure.
abstract: Clinical trials in heart failure (HF) tend to randomize patients according to demographic characteristics and severity of left ventricular dysfunction, without taking account of the precise diagnosis. This article reviews results from recent trials suggesting that the etiology of HF, and particularly whether it is ischemic or nonischemic, may influence the long-term prognosis and the response to treatment. Some studies, but not all, suggest that nonischemic HF has a better prognosis than ischemic HF. The data on the benefits of angiotensin-converting enzyme inhibitors in ischemic versus nonischemic HF are conflicting. Carvedilol, and recently, bisoprolol have been shown to reduce mortality in ischemic and nonischemic HF, whereas metoprolol has, to date, improved prognosis only in dilated cardiomyopathy. Better responses to digoxin, amlodipine and amiodarone have been reported in non-ischemic HF. There is at present no clear explanation for the apparent therapeutic differences between ischemic and nonischemic HF. Absence of a rigorous definition of "nonischemic HF" in many studies makes interpretation of the results difficult. Further studies to clarify the effects of etiology of HF on the response to treatment could be particularly important for preventing progression to more advanced stages, in which any type of drug therapy may have limited value in prolonging survival. An individualized therapeutic approach, based on etiology of HF and possibly other factors such as plasma drug levels or the levels of neurohormones, could result in major progress in treating HF patients.
authors.affiliation: Department of Internal Medicine, University Hospital, Zürich, Switzerland.
authors.forename: F
authors.initials: F
authors.lastname: Follath
authors.forename: J G
authors.initials: JG
authors.lastname: Cleland
authors.forename: W
authors.initials: W
authors.lastname: Klein
authors.forename: R
authors.initials: R
authors.lastname: Murphy
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D002301:Cardiac Glycosides / Q000627:therapeutic use; D002311:Cardiomyopathy, Dilated / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy; D002317:Cardiovascular Agents / Q000627:therapeutic use*; D003937:Diagnosis, Differential; D004232:Diuretics / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D006333:Heart Failure / Q000175:diagnosis / Q000188:drug therapy* / Q000209:etiology*; D006801:Humans; D017202:Myocardial Ischemia / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy; D011379:Prognosis; D016032:Randomized Controlled Trials as Topic
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D002121:Calcium Channel Blockers; D002301:Cardiac Glycosides; D002317:Cardiovascular Agents; D004232:Diuretics