Prevention of sudden cardiac death: Need for a plaque stabilizer

Abstract

Prevention of sudden cardiac death due to cardiac arrhythmias, asystole, or electromechanical dissociation remains a major medical and epidemiologic problem. There are many potential causes of sudden cardiac death, including acute coronary occlusion, chronic coronary heart disease with myocardial scar from one or more prior myocardial infarctions, cardiomyopathy, a host of cardiac genetic disorders such as hypertrophic cardiomyopathy and long QT syndrome to name a few, and a spectrum of other cardiac conditions. It is well recognized that acute coronary-related events account for most of the sudden cardiac deaths in the adult population. Despite the current widespread use of effective cardiac therapy, including β-blockers, angiotensin-converting enzyme inhibitors, lipid-lowering statins, aspirin, and implantable cardiac defibrillator and cardiac resynchronization therapy devices in appropriately selected highrisk cardiac patients, sudden cardiac death remains a major public health problem. Epidemiologic studies that have focused on sudden cardiac death have identified the traditional coronary risk factors of hypercholesterolemia, hypertension, and cigarette smoking as being more frequent in those who die suddenly than in matched comparison patients without sudden death. Although these findings provide insight into the coronary vascular mechanism of sudden cardiac death, they are not sensitive or specific enough to permit selection of patients for truly effective preventive therapy as the risk of sudden cardiac death remains high in those with and without these risk factors despite aggressive drug and device therapy. We can reduce the risk of sudden cardiac death with appropriately tailored medical therapy in patients with established coronary heart disease, but from an epidemiologic perspective, we have made only a small dent in the rate of sudden cardiac death in the general population. Several community-based autopsy studies have investigated the underlying cardiac pathology in sudden cardiac death, including the report by Adabag et al in the current issue of the American Heart Journal. The Adabag autopsy study involved 71 sudden cardiac death victims aged 25 to 60 years, which occurred in Hennepin