Pharmacological therapy in coronary heart disease: prevention of life-threatening ventricular tachyarrhythmias and sudden cardiac death.
Life-threatening ventricular tachyarrhythmias are the main reason for sudden cardiac death in coronary heart disease. In the majority of survivors of cardiac arrest, malignant tachyarrhythmias generate from a structurally fixed arrhythmogenic substrate following myocardial infarction without evidence of acute ischaemia. Thrombolysis in acute myocardial infarction improves the electrical stability as elucidated by electrophysiological studies and the signal averaged surface ECG. In post-infarction patients, beta-blockers provide significantly beneficial effects on arrhythmic outcome, particularly in the presence of impaired left ventricular function, whereas calcium antagonists and vasodilators are of no affect or may worsen the prognosis. In survivors of myocardial infarction, the prophylactic use of class I antiarrhythmic agents, which are able to suppress frequent single or complex premature ventricular contractions, cause worsening of the prognosis due to their proarrhythmic properties. However, arrhythmia suppression by antiarrhythmic agents selects patients who are at very low risk for arrhythmic death. Pilot trials using class III antiarrhythmic agents suggest beneficial effect on the reduction of sudden death mortality. As regards secondary prevention of malignant tachyarrhythmias in survivors of ventricular tachycardia or fibrillation, there is controversy about the importance of Holter monitoring or invasive electrophysiological testing in the evaluation of drug efficacy. In patients with severely impaired left ventricular function, pharmacological treatment is of limited efficacy. Even in cases of significant suppression of spontaneous or inducible tachyarrhythmias documented by Holter recording or programmed ventricular stimulation, the arrhythmic outcome is considerably poorer, but it could be influenced by implantable defibrillators. Amiodarone, as a potential alternative to class I antiarrhythmic agents, particularly in patients refractory to conventional antiarrhythmic drugs, shows only limited effects on long-term outcome, which is in part caused by the toxicity of this agent. There is substantial need for new drugs without proarrhythmic properties and particularly for those that correct abnormalities of the automatic nervous system.
Kochs
M
M
Department of Internal Medicine II (Cardiology, Angiology, Nephrology and Pneumonology), University of Ulm, Germany.
Eggeling
T
T
Hombach
V
V
D000200:Action Potentials; D000638:Amiodarone / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D002986:Clinical Trials as Topic; D016757:Death, Sudden, Cardiac / Q000209:etiology / Q000517:prevention & control*; D004599:Electric Stimulation Therapy; D015716:Electrocardiography, Ambulatory; D006801:Humans; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D012008:Recurrence; D017180:Tachycardia, Ventricular / Q000150:complications / Q000503:physiopathology / Q000517:prevention & control*; D015912:Thrombolytic Therapy
D000806:Angiotensin-Converting Enzyme Inhibitors; D000889:Anti-Arrhythmia Agents; D002121:Calcium Channel Blockers; D000638:Amiodarone