But Does It Increase Survival Rate?

In the early 1960s, we used the few antiarrhythmic drugs available empirically, presuming that every premature ventricular contraction had to be suppressed. This presumption spurred ever greater effort, much of it going into antiarrhythmic drug development.' Throughout the 1980s, one new drug was being developed about every six months,2 and the number of antiarrhythmic prescriptions rose exponentially.3 However, with this widespread use also came troubling reports of the drugs' negative inotropic and proarrhythmic effects.4,5 Then CAST dealt a swift and decisive blow6: Class IC agents, which had previously been highly regarded, were worse than placebo in treating patients with prior myocardial infarction who had premature ventricular contractions. This overturned conventional wisdom, and we had to revise our thinking: Spontaneously occurring premature ventricular contractions in patients with relatively normal ventricular function need not be treated; Holter monitoring may not be a good tool to guide antiarrhythmic therapy in patients with ventricular tachyarrhythmias.7