At the genome level, research has focused on the role of SCN5A gene mutations in arrhythmogenesis. Nevertheless, the investigators have recently described acquired defects in Na+ channel messenger RNA (mRNA) that result in reduced Na+ current and occur only in failing hearts. Three 3'-terminal SCN5A mRNA splicing variants were identified and characterized in failing human heart ventricles. Additional measurements suggested that the truncation mutants could cause electrical abnormalities severe enough to contribute to arrhythmic risk. Also, the investigators showed that lymphocytes process sodium channels similarly to cardiomyocytes. Thus, lymphocyte SCN5A mRNA processing may serve as a surrogate marker to assess SCN5A function at the cardiac level and may correlated with arrhythmic risk in high risk populations. This study will determine if SCN5A variant levels are predictive of appropriate ICD therapies in patients with a newly implanted ICD.