title: [Diuretics in the treatment of heart failure: current pathophysiological aspects].
abstract: From a pathophysiologic point of view heart failure can be divided into systolic and diastolic dysfunction. Systolic dysfunction is characterized by a decreased ejection fraction and increased chamber volume which can be typically found in young people with congestive cardiomyopathy. Diastolic dysfunction is associated with an enhanced filling pressure but with a normal systolic pump function. This disorder can be typically found in elderly patients with myocardial hypertrophy. Treatment of congestive heart failure includes. 1.) reduction of central blood volume (preload reduction) 2.) decrease of peripheral resistance afterload reduction) 3.) regression of myocardial hypertrophy (improving myocardial stiffness) 4.) maintenance of atrial contraction (atrial kick) 5.) decrease of heart rate (prolongation of diastolic filling time and increase in contractility) 6.) improvement of LV relaxation (positive lusitropic effect) and 7.) prevention of myocardial ischemia (improvement in contractility and relaxation). The primary goal of medical therapy is symptomatic improvement. Reduction in morbidity and mortality is only a secondary consideration. To achieve this goal ACE-inhibitors and in certain cases betablockers (cave: neg. inotropic action) are suited best. Additionally, digitalis-especially in the presence of atrial fibrillation- and vasodilators can be used to further improve quality of life. In the case of severe heart failure with or without atrial fibrillation oral anticoagulation is indicated to prevent systemic embolication. Diuretics are often used for symptomatic improvement but have no effect on long-term survival. Aldosterone antagonists (e.g, spironolactone) have a beneficial effect on LV remodeling and probably also on mortality. The role of endothelin antagonists and atriopeptidase inhibitors in the treatment of heart failure are not yet clear.
authors.affiliation: Kardiologie, Inselspital Bern.
authors.forename: L
authors.initials: L
authors.lastname: Mandinov
authors.forename: C
authors.initials: C
authors.lastname: Matter
authors.forename: P
authors.initials: P
authors.lastname: Kaufmann
authors.forename: O M
authors.initials: OM
authors.lastname: Hess
mesh_terms: D000328:Adult; D000368:Aged; D002311:Cardiomyopathy, Dilated / Q000503:physiopathology; D002316:Cardiotonic Agents / Q000627:therapeutic use; D004071:Digitalis Glycosides / Q000627:therapeutic use; D004232:Diuretics / Q000627:therapeutic use*; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology*; D006801:Humans; D008875:Middle Aged; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use; D009200:Myocardial Contraction; D015260:Neprilysin / Q000037:antagonists & inhibitors; D009569:Nitric Oxide / Q000378:metabolism; D017466:Receptors, Endothelin / Q000187:drug effects
chemical_list: D002316:Cardiotonic Agents; D004071:Digitalis Glycosides; D004232:Diuretics; D004791:Enzyme Inhibitors; D000451:Mineralocorticoid Receptor Antagonists; D017466:Receptors, Endothelin; D009569:Nitric Oxide; D015260:Neprilysin