Editorial: Sudden cardiac death - the challenge to cardiology

KYAMC Journal

Hellenic journal of cardiology : HJC = Hellēnikē kardiologikē epitheōrēsē

Cardiac Defibrillation, 2013

Annals of Medicine, 2008

Sudden cardiac death (SCD), also known as sudden arrest, is a major health problem worldwide. It is usually defined as an unexpected death from a cardiac cause occurring within a short time in a person with or without preexisting heart disease. The pathogenesis of SCD is complex and multifaceted. A dynamic triggering factor usually interacts with an underlying heart disease, either genetically determined or acquired, and the final outcome is the development of lethal tachyarrhythmias or, less frequently, bradycardia. It has increasingly been highlighted that a reliable clinical and diagnostic approach might be effective to unmask the most important genetic and environmental factors, allowing the construction of a rational personalized medicine framework that can be applied in both the preclinical and clinical settings of SCD. The aim of the present article is to provide a concise overview of prevalence, pathogenesis, clinical presentation, and diagnostic approach to this challenging disorder.

Circulation, 2010

Circulation research, 2015

Sudden cardiac death (SCD) from cardiac arrest is a major international public health problem accounting for an estimated 15%-20% of all deaths. Although resuscitation rates are generally improving throughout the world, the majority of individuals who experience a sudden cardiac arrest will not survive. SCD most often develops in older adults with acquired structural heart disease, but it also rarely occurs in the young, where it is more commonly because of inherited disorders. Coronary heart disease is known to be the most common pathology underlying SCD, followed by cardiomyopathies, inherited arrhythmia syndromes, and valvular heart disease. During the past 3 decades, declines in SCD rates have not been as steep as for other causes of coronary heart disease deaths, and there is a growing fraction of SCDs not due to coronary heart disease and ventricular arrhythmias, particularly among certain subsets of the population. The growing heterogeneity of the pathologies and mechanisms u...

Cardiac Electrophysiology Clinics, 2017

Electrophysiologic surrogates of sudden cardiac death Biomarkers of sudden cardiac death Genomics of sudden cardiac death Noninvasive variables of sudden cardiac death KEY POINTS Electrophysiological surrogates for sudden cardiac death in ischemic heart disease include measures of conduction disorders, dispersion of repolarization, and of autonomic system. Arrhythmic risk for sudden cardiac death in ischemic heart disease could be modified by specific biomarkers, genomics, and noninvasive variables. The ultimate goal of management of sudden cardiac death should go beyond optimal use of the ICD to primarily identify novel methods for risk stratification, risk modification, and prevention of sudden cardiac death that could be applied to the general public at large.

Circulation, 2008

S udden cardiac death (SCD) is the final common end point of multiple disease processes. It results from a complex interplay of structural, metabolic, and genetic determinants. Although epidemiological risk factors such as age, prior myocardial infarction, and low ejection fraction are well established, this syndrome also has a strong genetic component. An understanding of the genetic contributions to risk could add substantially to the prediction and prevention of SCD. In this review, we explore the epidemiology, heritability, and allelic architecture of SCD and provide a detailed overview of the genetics of inherited electrophysiological and structural heart diseases that are potent risk factors for SCD.

Journal of Arrhythmia, 2009

It is becoming increasingly appreciated that besides depressed left ventricular systolic function and the conventional risk stratification tools, new markers for plaque vulnerability, enhanced thrombogenesis, specific genetic alterations of the autonomic nervous system, cardiac sarcolemmal and contractile proteins, and familial clustering may better segregate patients with atherosclerotic coronary artery disease who are at high risk for SCD from those who may suffer from nonfatal ischemic events. Better understanding of pathophysiological processes, such as postmyocardial infarction remodeling, the transition from compensated hypertrophy to heart failure, and the increased cardiovascular risk of coronary artery disease in the presence of diabetes or even a prediabetic state will help to improve both risk stratification and management. The rapidly developing fields of microchips technology and proteomics may allow rapid and cost-effective mass screening of multiple risk factors for SCD. The ultimate goal is to identify novel methods for risk stratification, risk modification, and prevention of SCD that could be applied to the general public at large. (J Arrhythmia 2009; 25: 122-129)