Abstract

Sudden cardiac death (SCD), which is responsible for approximately 300 000 deaths in the United States, refers to an unexpected death from a cardiovascular cause in a person with or without preexisting heart disease. Most studies include cases that are associated with death occurring within 1 hour of an acute change in clinical status or an unexpected death that occurred within the previous 24 hours,1 but this definition is not specific for sudden arrhythmic death. The most common sequence of events leading to arrhythmic SCD is the degeneration of ventricular tachycardia (VT) into ventricular fibrillation (VF), often followed by asystole or pulseless electric activity. The transition of shockable rhythms (VT/VF) to more ominous rhythms such as asystole or pulseless electric activity depends on various factors, but is highly dependent on time; the longer the time interval, the more likely the VT/VF degenerates to pulseless electric activity or asystole. Although VF and VT together represent the initial rhythm in half of all outpatient cardiac arrests, data suggest that with each passing minute of untreated VF, the likelihood of survival is reduced by 7% to 10%.2 Preexisting coronary artery disease and its sequelae (eg, acute myocardial ischemia, scarring from previous myocardial infarction, heart failure) are manifest in 80% of SCDs.3 Dilated nonischemic and hypertrophic cardiomyopathies account for the second largest number of SCDs, whereas other cardiac disorders such as congenital heart disease and underlying genetically determined ion channel anomalies account for 5% to 10% of SCDs.3 Although the cascade of events triggering SCD are complex and are currently active areas of investigation, the general goals of reducing SCD are focused on (1) identifying and preventing sudden death in high-risk individuals by using efficacious therapies such as medications and implantable cardioverter defibrillators (ICDs), (2) organizing resuscitation services to improve …

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