Highly sensitive troponin assay and sudden cardiac death in the community: Unlocking the pathophysiology of sudden cardiac death one biomarker at a time

摘要

The current approach to prevention of SCD involves the placement of an implantable cardiac-defibrillator (ICD) in high-risk individuals. For such an approach to be effective, it needs to be applied to populations at elevated risk for SCD. However, identifying those at elevated risk has proven to be problematic (3). The best-known predictors of SCD are the degree of left ventricular systolic dysfunction and the severity of heart failure symptoms (5). In such patients, the use of ICD therapy has demonstrated clear survival benefits (6,7). Unfortunately, the use of these criteria to reduce SCD incidence in the general population has significant limitations. In fact, most SCD victims in the community do not have a pre-existing history of depressed ejection fraction or a clinical history of heart failure (8-10). As such, our current strategy fails to identify and affect the vast majority of individuals who suffer a SCD event.Significant efforts have been made to improve risk prediction models for SCD in the general population by incorporating additional clinical characteristics (11-13). Coronary artery disease (CAD) is the most common substrate underlying SCD, noted in up to 75% of cases (3). As such, it is not surprising that CAD and risk factors for CAD (hypertension, hypercholesterolemia, diabetes, kidney disease, obesity, and smoking) are also predictive of SCD (3). Unfortunately, these risk factors are also strongly associated with competing causes of cardiac death. As such, their ability to improve patient selection for device-based therapy is limited. ICD therapy specifically targets SCD events. The utilization of screening markers that are also associated with competing modes of death significantly limits the effectiveness of defibrillation therapy, which only targets SCD.