title: Antiarrhythmic therapy in heart failure.
abstract: Heart failure is the term used for a cardiovascular syndrome whose definition lacks uniform criteria. It is associated with a very high mortality rate. Approximately 50% of deaths in patients with heart failure are sudden, mostly due to ventricular tachycardia (VT). In severe heart failure, death may also occur due to bradyarrhythmias. Other arrhythmias complicating heart failure include atrial and ventricular extrasystoles, atrial fibrillation, and sustained or non-sustained VT. Depending on the etiology of heart failure, different preconditions, including ischemia or structural alterations (such as fibrosis) may be prominent. Re-entrant mechanisms around scar tissue, afterdepolarizations, and triggered activity due to changes in calcium metabolism significantly contribute to arrhythmogenesis. The treatment of the underlying disease process and optimal management of heart failure is of major importance. Revascularization, beta-blocker therapy, and angiotensin converting enzyme inhibitors are all essential to appropriate therapy. Treatment of arrhythmias is performed either because patients are symptomatic or to reduce the risk of sudden cardiac death. The implantable cardioverter-defibrillator (ICD) is the best available therapy to prevent sudden cardiac death from VT. Devices with back-up pacing also offer protection against bradyarrhythmias. There is evidence that patients with sustained VT or a history of resuscitation have the best outcome with ICD therapy regardless of the degree of heart failure. Many of these patients require additional antiarrhythmic therapy (e.g. amiodarone) because of atrial fibrillation or non-sustained VT that may activate the device.
authors.affiliation: Hospital of the Westfälische Wilhelms-University, Department of Cardiology and Institute for Arteriosclerosis Research, Münster, Germany.
authors.forename: Lars
authors.initials: L
authors.lastname: Eckardt
authors.forename: Wilhelm
authors.initials: W
authors.lastname: Haverkamp
authors.forename: Günter
authors.initials: G
authors.lastname: Breithardt
mesh_terms: D000465:Algorithms; D000638:Amiodarone / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D001145:Arrhythmias, Cardiac / Q000175:diagnosis / Q000188:drug therapy / Q000401:mortality / Q000503:physiopathology / Q000628:therapy*; D001281:Atrial Fibrillation / Q000188:drug therapy; D002986:Clinical Trials as Topic; D016757:Death, Sudden, Cardiac / Q000209:etiology / Q000517:prevention & control; D017147:Defibrillators, Implantable; D004562:Electrocardiography; D004594:Electrophysiology; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000188:drug therapy / Q000401:mortality / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D008297:Male; D010919:Placebos; D011322:Primary Prevention; D011379:Prognosis; D016032:Randomized Controlled Trials as Topic; D012307:Risk Factors; D017180:Tachycardia, Ventricular / Q000150:complications / Q000628:therapy; D013997:Time Factors; D016277:Ventricular Function, Left
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000889:Anti-Arrhythmia Agents; D010919:Placebos; D000638:Amiodarone