Despite the significant decline in coronary artery disease (CAD) mortality in the second half of the 20th century, 1 sudden cardiac death (SCD) continues to claim 250 000 to 300 000 US lives annually. 2 In North America and Europe the annual incidence of SCD ranges between 50 to 100 per 100 000 in the general population. 3–6 Because of the absence of emergency medical response systems in most world regions, worldwide estimates are currently not available. 7 However, even in the presence of advanced first responder systems for resuscitation of out-of-hospital cardiac arrest, the overall survival rate in a recent North American analysis was 4.6%. 8 SCD can manifest as ventricular tachycardia (VT), ventricular fibrillation (VF), pulseless electric activity (PEA), or asystole. In a significant proportion of patients, SCD can present without warning or a recognized triggering mechanism. The mean age of those affected is in the mid 60s, and at least 40% of patients will suffer SCD before the age of 65. 4 Consequently, enhancement of methodologies for prediction and prevention of SCD acquires a unique and critical importance for management of this significant public health issue. Prediction and prevention of SCD is an area of active investigation, but considerable challenges persist that limit the efficacy and cost-effectiveness of available methodologies. 7, 9, 10 It was recognized early on that optimization of SCD risk stratification will require integration of multi-disciplinary efforts at the bench and bedside, with studies in the general population. 11–13 This integration has yet to be effectively accomplished. There is also increasing awareness that more investigation needs to be directed toward identification of early predictors of SCD. 14 Significant advancements have occurred for risk prediction in the inherited channelopathies15–17 and other inherited conditions that predispose to SCD, such as hypertrophic cardiomyopathy, 18 but there is much to be accomplished in this regard for the more common complex phenotypes, such as SCD, among patients with CAD. Many cardiovascular treatments (eg, lipid lowering and antihypertensive agents, antiischemic interventions, and heart failure therapies) prevent or delay the progression of the cardiovascular diseases that are the most frequent cause of SCD. However, the current workshop focused specifically on risk prediction for arrhythmic death in cardiac populations rather than on the broader topics of prediction and prevention of cardiac diseases in general.

Unfortunately, specific pharmacological therapies directed at the electrophysiological substrate and mechanisms that cause arrhythmias have proven disappointing when applied to high or moderate risk patients without prior documented clinical arrhythmias. The implantable cardioverter-defibrillator (ICD) in combination with heart failure drug therapy remains the mainstay of SCD prevention19, 20 but is likely to benefit only the small population at high risk who can be identified before an SCD event. 5, 21