Mechanisms and control of ventricular tachyarrhythmias

Mechanisms of ventricular arrhythmias, identification of patients at risk, use of specific therapeutic endpoints in selecting and monitoring antiarrhythmic regimens, and the role of pacemaker therapy and surgery in the management of ventricular arrhythmias are reviewed. Ventricular arrhythmias are usually caused by either a disturbance in impulse formation (automaticity), a disturbance in impulse propagation (re-entry), or a combination of these. In identifying patients at risk, ventricular arrhythmias must be evaluated with consideration for individual patients' characteristics. The prognostic importance of complex ventricular ectopy in apparently healthy individuals is unknown, but, during the first four hours after an acute myocardial infarction, ventricular extra beats often precede sudden death. Lidocaine remains the antiarrhythmic of choice for initial short-term therapy following acute myocardial infarction, although i.v. bretylium is sometimes used. Beta-adrenergic antagonists should be considered for all post-MI patients within one to three weeks after infarction and continued for two to three years. Membrane-depressant agents (quinidine, procainamide, disopyramide) should be avoided in patients with prolonged QT syndrome, Romano-Ward syndrome, or torsade de pointes. Noninvasive (ambulatory ECG monitoring and exercise testing) and invasive (electro-physiologic studies) tests are sometimes useful in diagnosis and in selection of appropriate drug therapy. Nonpharmacologic treatment of ventricular tachyarrhythmias includes permanent pacemakers, internal defibrillation devices, and surgery. The ideal antiarrhythmic agent with predictable efficacy and minimal toxicity has yet to be identified. Future clinical trials with conventional and investigational antiarrhythmic agents may establish a more clear-cut role for the pharmacologic management of ventricular tachyarrhythmias.