title: The therapeutic role of RAS blockade in chronic heart failure.
abstract: Cardiovascular disease represents a continuum that starts with risk factors such as hypertension and progresses to atherosclerosis, end-organ damage, and ultimately to chronic heart failure (CHF) and premature death. Renin-angiotensin system (RAS) blockade with angiotensin converting enzyme (ACE) inhibitors and/or angiotensin II type 1 receptor blockers (ARBs) has turned out to be beneficial at all stages of this continuum. Several mechanisms govern the progression of structural myocardial damage to end-stage CHF. Chronic neuroendocrine activation fosters left ventricular remodeling and dilatation and leads to clinical symptoms of CHF via forward/backward failure. RAS inhibition is a cornerstone of neuroendocrine blockade in CHF patients, and combined RAS blockade is especially effective in patients presenting with repetitive cardiac decompensations. This review focuses on the therapeutic role of inhibitors of different RAS components in chronic heart failure caused by systolic left ventricular dysfunction.
authors.affiliation: Kardiologische Forschung Kardiologie, Angiologie und Internistische Intensivmedizin Innere Medizin - Universitätsklinikum des Saarlandes Kirrberger Str. D-66421 Homburg, Germany. cwerner@med-in.uni-saarland.de
authors.forename: Christian M
authors.initials: CM
authors.lastname: Werner
authors.forename: Michael
authors.initials: M
authors.lastname: Böhm
mesh_terms: D000804:Angiotensin II / Q000502:physiology; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D002986:Clinical Trials as Topic; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy; D012084:Renin-Angiotensin System / Q000187:drug effects*
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000804:Angiotensin II