Abstract
Introduction: Sudden Cardiac Death (SCD) is a major cause of death (15%-20% of all mortality). Its high incidence led to consider it as a major public health problem worldwide. In the United State, it has been estimated that 360,000 death per year has resulted from SCD whether in emergency departments or even before reaching hospitals. The primary prevention of SCD is a public health challenge. This has resulted for many reasons: (a) the current management of SCD is directed toward a small percentage of the population at risk; (b) ineffectiveness of pharmaceutical strategies; (c) The device therapy (implantable cardioverter-defibrillator (ICD) is designed to rescue patients after the occurrence of the event. In addition, different approaches and combinations to risk stratification have failed to produce an acceptable positive predictive value. The presence of organic heart disease and decreased left ventricular ejection fraction (LVEF) were the main criteria to use ICD as primary prophylaxis against SCD. However, a lower LVEF could be a good indicator for total cardiac mortality but it is not specific for SCD; thus, this strategy has resulted in a significant redundancy and hence cost burden. Developing better criteria to use ICD as prophylaxis becomes a priority.
The aim of work: In this review, we will discuss Sudden cardiac death-causes and prevention
Methodology: We did a systematic search for sudden cardiac death-causes and prevention in the emergency department using PubMed search engine (http://www.ncbi.nlm.nih.gov/) and Google Scholar search engine (https://scholar.google.com). All relevant studies were retrieved and discussed. We only included full articles.
Conclusions: The future goals to risk stratification and management of SCD especially post-MI could be summarized as the following: (1) Identification of novel clinical, electrophysiological, biochemical, and genetic markers for SCD, this includes the assessment of functional consequences of sequence variants identified in human genetic studies as well as relevant environmental-genetic interactions; (2) Identification of a relatively limited number of incrementally low to intermediate cumulative risk variants and development of a "signature" combination of risk markers. (3) Reducing the redundancy and enhance the criteria for ICD implantation usage that is currently based on reduced LVEF. This should be done by identifying more eligible patients for ICD with either very low or a very high noninvasive clinical risk variable. (4) Development of novel pharmacological, non-pharmacological, and behavioral approaches for risk modification and prevention of SCD; (5) A wider collaboration among different academic and industrial institutions. This could be achieved by sharing research results as well as resources including clinical data, blood and other tissues from biorepository centers. The ultimate goal is not only to change the current management strategy of SCD by reducing the use of ICD, but by identifying novel methods for risk stratification, risk modification, and prevention of SCD that could be generalized.