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Sudden cardiac death (SCD) is a major public health issue and ranks among the leading causes of mortality in the developed world. The mechanism of death is mostly malignant ventricular arrhythmia. The underlying etiology is primarily ischemic heart disease, although susceptibility to SCD is a complex process with multiple interactions between genes that regulate cardiac and vascular function and other physiological factors. A minority of cases of cardiac arrest or SCD occur in the context of hereditary channelopathies, without overt structural heart disease, such as Brugada syndrome, long QT syndrome, or catecholaminergic polymorphic VT. Prevention of SCD is hampered by our inability to predict who is at risk at an individual level, since the majority of cases occur as the index event without associated high-risk features. In patients with high-risk features for SCD, antiarrhythmic drugs do not reduce mortality and, in fact, can contribute to arrhythmic death, particularly in those with impaired left ventricular systolic function. The ICD is the only proven treatment for prevention of SCD. The advent of the ICD has been perceived as a panacea for SCD, although in reality the degree of residual risk is significant. Ongoing research into genetic susceptibilities and the development of complex computer modeling may provide us with a better understanding of this complex disease process in the future. Until such time, SCD is destined to remain a significant public health threat that requires further study.