title: Mechanisms underlying ventricular arrhythmias in idiopathic dilated cardiomyopathy: implications for management.
abstract: Ventricular arrhythmias (VA) have been associated with mortality in idiopathic dilated cardiomyopathy (IDCM). All 3 main mechanisms of arrhythmogenesis - reentry, trigger activity, and automatism - have been implicated. Arrhythmogenic substrates in IDCM favor these mechanisms and are often potentiated by electrolyte imbalance secondary to diuretic treatment, by antiarrhythmic drugs, or by bradycardia, leading to polymorphic ventricular tachycardia (VT). Myocardial macroreentry is the mechanism most frequently responsible for monomorphic VT in IDCM; however, focal activation and His-Purkinje macroreentry are often responsible and, especially in the latter case, are frequently unrecognized. Clinical suspicion and final recognition by electrophysiologic testing have important therapeutic consequences, because both focal activation and His-Purkinje macroreentry can be treated effectively by catheter ablation. On the other hand, the frequent recurrences of myocardial macroreentrant VT after ablation require this therapy to be used in combination with drugs or an implantable cardioverter defibrillator (ICD). beta-Adrenoceptor antagonists (beta-blockers) have a beneficial effect for primary prevention of VA in IDCM. Type III antiarrhythmics have a neutral effect on mortality and type I antiarrhythmics should be avoided. Treatment of nonsustained VT in IDCM is controversial because it often presents without symptoms and is linked more to overall mortality than to arrhythmic mortality. Empiric treatment with amiodarone or electrophysiologically guided sotalol are preferred to the use of other drugs for secondary prevention of sustained VA. ICDs should be implanted in patients who have been resuscitated from cardiac arrest due to VA, or in those with poorly tolerated VT and severe left ventricular dysfunction. Empiric treatment with amiodarone or electrophysiologically guided class III antiarrhythmics may also be alternatives for patients with IDCM and no severe left ventricular dysfunction, especially if VT is well tolerated.
authors.affiliation: Arrhythmia Unit, Department of Cardiology, Hospital La Paz, Universidad Autónoma, Madrid, Spain. jlmerino@jet.es
authors.forename: J L
authors.initials: JL
authors.lastname: Merino
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control*; D002311:Cardiomyopathy, Dilated / Q000150:complications* / Q000628:therapy; D017115:Catheter Ablation; D002986:Clinical Trials as Topic; D003645:Death, Sudden / Q000209:etiology / Q000517:prevention & control; D017147:Defibrillators, Implantable; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000889:Anti-Arrhythmia Agents