title: Arrhythmias in heart failure: current concepts of mechanisms and therapy.
abstract: About one half of deaths in patients with heart failure are sudden, mostly due to ventricular tachycardia (VT) degenerating to ventricular fibrillation or immediate ventricular fibrillation. In severe heart failure, sudden cardiac death also may occur due to bradyarrhythmias. Other dysrhythmias complicating heart failure include atrial and ventricular extrasystoles, atrial fibrillation (AF), and sustained and nonsustained ventricular tachyarrhythmias. The exact mechanism of the increased vulnerability to arrhythmias is not known. Depending on the etiology of heart failure, different preconditions, including ischemia or structural alterations such as fibrosis or myocardial scarring, may be prominent. Reentrant mechanisms around scar tissue, afterdepolarizations, and triggered activity due to changes in calcium metabolism significantly contribute to arrhythmogenesis. Furthermore, alterations in potassium currents leading to action potential prolongation and an increase in dispersion of repolarization play a significant role. Treatment of arrhythmias is necessary either because patients are symptomatic or to reduce the risk for sudden cardiac death. The individual history, left ventricular function, electrophysiologic testing, and the signal-averaged ECG give useful information for identifying patients at risk for sudden cardiac death. The implantable cardioverter defibrillator (ICD) has evolved as a promising therapy for life-threatening arrhythmias. A potential role may exist for antiarrhythmic drugs, mainly amiodarone. There is growing 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 because of AF or nonsustained VTs that may activate the device. Catheter ablation or map-guided endocardial resection are additional options in selected patients but seldom represent the only therapeutic strategy.
authors.affiliation: Department of Cardiology and Angiology and Institute for Arteriosclerosis Research, Hospital of the Westfälische Wilhelms-University, Münster, Germany. l.eckardt@uni-muenster.de
authors.forename: L
authors.initials: L
authors.lastname: Eckardt
authors.forename: W
authors.initials: W
authors.lastname: Haverkamp
authors.forename: R
authors.initials: R
authors.lastname: Johna
authors.forename: D
authors.initials: D
authors.lastname: Böcker
authors.forename: M C
authors.initials: MC
authors.lastname: Deng
authors.forename: G
authors.initials: G
authors.lastname: Breithardt
authors.forename: M
authors.initials: M
authors.lastname: Borggrefe
mesh_terms: D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000175:diagnosis / Q000209:etiology* / Q000628:therapy; D002303:Cardiac Output, Low / Q000150:complications* / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial; D002986:Clinical Trials as Topic; D006801:Humans
chemical_list: D000889:Anti-Arrhythmia Agents