The Riddle of Nonsustained Ventricular Tachycardia and Sudden Cardiac Death

The graveyard of cardiovascular therapeutics is littered with common-sense ideas. Premature ventricular contractions trigger episodes of ventricular fibrillation; therefore, suppression of premature ventricular contractions should lessen the risk of cardiac arrest and sudden death–and yet it has not.1–2 Sudden cardiac death (SCD), which is responsible for between 184 000 and 450 000 deaths in the United States per year,3–6 remains a conundrum, both in prevention and prediction of those at risk. The epidemiology of SCD presents challenges for clinical care; patients who are in the known highest-risk subgroups, such as those with abnormal systolic left ventricular function, account for the minority of events.7 Even among this high-risk subgroup with a mortality benefit afforded by implantable cardioverter defibrillator (ICD) placement, the majority of implanted patients never require therapy for arrhythmic events from the device.8–9 This actuality emphasizes the need to better identify those at highest risk, even within subpopulations in jeopardy of SCD.Article see p 455 In the prethrombolytic era of therapy for myocardial infarction (MI), ventricular ectopy and nonsustained ventricular tachycardia (NSVT) were known to predict increased mortality post MI.10–12 However, with reperfusion and use of β-blockers, NSVT after MI has not always been demonstrated to be an independent predictor of mortality, especially after ejection fraction (EF) is taken into account, and its prognostic significance is ambiguous.13–16 Moreover, whether NSVT is causative in the genesis of SCD or simply a marker of imperiled substrate or disordered autonomic regulation is unknown. In one of the most simultaneously enlightening and discouraging clinical trials, the Cardiac Arrhythmia Suppression Trial, not only did suppression of ventricular ectopy not result in a decreased risk of SCD, treatment with flecainide was associated with an increased risk of SCD, possibly due to proarrhythmia.1 Subsequent pharmacological trials also have demonstrated …