Ventricular arrhythmias: medical therapy, device treatment, and indications for electrophysiologic study.
Sustained ventricular arrhythmias occur most frequently during the first several months following MI, although the risk of arrhythmia development continues for many years. The mechanism responsible for most of these arrhythmias is a re-entrant circuit located in the border zone between the normal and scarred subendocardium. Clinical factors that identify patients at greatest risk for developing sustained ventricular arrhythmias after MI include depressed left ventricular function, acute left ventricular aneurysm formation, electrical instability, new bundle branch blocks, and residual ischemia. Attempts to lower the arrhythmic risk of these patients is a major area of clinical investigation. Although frequent asymptomatic ventricular ectopy and nonsustained ventricular tachycardia are risk factors for sudden death after infarction, it has not been demonstrated that empiric treatment of these arrhythmias with antiarrhythmic agents improves survival. Electrophysiologic studies have significantly contributed to understanding the mechanisms responsible for sustained ventricular arrhythmias. Although the role of electrophysiologic studies in guiding therapy in patients with sustained ventricular tachycardia or sudden death after infarction has been well established, their utility to identify high risk subgroups after infarction has not been conclusively determined. New treatment modalities have resulted in an improved outcome in patients with malignant ventricular arrhythmias (Table 2). These strategies include new pharmacologic therapies, arrhythmia surgery, use of automatic implantable cardioverter defibrillators or antitachycardia pacemakers, and percutaneous catheter ablation of the re-entrant circuit responsible for these arrhythmias.
D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D004554:Electric Countershock / Q000295:instrumentation*; D004562:Electrocardiography; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D009203:Myocardial Infarction / Q000150:complications*; D010138:Pacemaker, Artificial; D013610:Tachycardia / Q000503:physiopathology / Q000628:therapy*; D014693:Ventricular Fibrillation / Q000503:physiopathology / Q000628:therapy*
D000889:Anti-Arrhythmia Agents