Programmed Ventricular Stimulation

Abstract

> How easy it is to make people believe a lie, and how hard it is to undo that work again! > > —Mark Twain, Mark Twain in Eruption 1 Medicine, like most other human endeavors, goes through fads. These fads are often initiated by persuasive, well-meaning people who have an incomplete grasp of fundamental pathophysiology. Because ideas underlying fads may sound plausible, the fad is perpetuated and accepted as gospel until a randomized, controlled trial or other well-designed study proves the concept faulty. One example of this phenomenon is seen in the evolution of efforts to prevent sudden cardiac death (SCD) in survivors of acute myocardial infarction (MI). Widespread study of SCD was aided by the development of technology permitting real-time ECG monitoring, resulting in proliferation of the cardiac care unit in the 1960s and 1970s. Patients who developed primary ventricular fibrillation with acute MI in the cardiac care unit were often observed to exhibit progressively frequent and “complex” ventricular ectopy in the minutes leading up to ventricular fibrillation. At the same time, randomized trials demonstrated that antiarrhythmic agents such as lidocaine, procainamide, and quinidine could reduce the occurrence of ventricular fibrillation in this setting. These observations then gave rise to the following assumptions: (1) SCD late after MI is due exclusively to ventricular fibrillation; (2) the presence of frequent ventricular ectopy and nonsustained ventricular tachycardia (VT) 2 to 4 weeks after the onset of acute infarction identifies patients at risk of SCD; and (3) suppression of ventricular ectopy by antiarrhythmic drugs prevents postinfarction SCD.2 As a result, it became common for physicians to perform a 24-hour ambulatory monitor in patients with recent MI and then to prescribe long-term antiarrhythmic drugs in patients with complex ectopy. This continued for 20 years until the Cardiac Arrhythmia Suppression Trial (CAST) proved that this …