Risk reduction strategies for sudden cardiac death in acute myocardial infarction

Abstract

Sudden cardiac death (SCD) resulting from an acute myocardial infarction (AMI) is the result of a chain of events beginning with the development of the atherosclerotic plaque and ending with the terminal event of an untreated lethal arrhythmia provoked by sudden ischemia. Out-of-hospital arrest has an extremely poor prognosis, thus prevention is critical. Certain risk factors for atherosclerosis are particularly associated with SCD, especially smoking, and smoking cessation is a critical element of prevention. Other cardiac findings such as left ventricular hypertrophy atrial fibrillation have also been associated with SCD. Most patients have a symptomatic prodrome and patients should be educated to heed this warning. Electrocardiogram (ECG) findings at screening are generally non-specific; nevertheless, an elongated QTc interval and signs of left ventricular hypertrophy are markers associated with SCD. There is a genetic component to SCD that is under intense study; patients tend to have a family history of sudden death. Monogenic disorders such as long QT predispose patients to SCD during AMI. Genome-wide association studies have implicated several sites as being associated with SCD in the general population; a single allele linked to SCN5A is found in African-Americans. Treatment with statins is beneficial; other treatments have yet to be proven in primary prevention. Automatic external defibrillators in public sites used promptly by minimally trained personal can be life-saving. Risk stratification is dynamic and should be periodically reassessed. © Touch Briefings 2011.