E Z Golukhova, O I Gromova, R A Shomahov, N I Bulaeva, L A Bockeria
Bakoulev Centre for Cardiovascular Surgery, Rublevskoye sh. 135, 121552, Moscow, Russia.
Acta Naturae. 2016 Apr-Jun;8(2):62-74.
The abrupt cessation of effective cardiac function that is generally due to heart rhythm disorders can cause sudden and unexpected death at any age and is referred to as a syndrome called "sudden cardiac death" (SCD). Annually, about 400,000 cases of SCD occur in the United States alone. Less than 5% of the resuscitation techniques are effective. The prevalence of SCD in a population rises with age according to the prevalence of coronary artery disease, which is the most common cause of sudden cardiac arrest. However, there is a peak in SCD incidence for the age below 5 years, which is equal to 17 cases per 100,000 of the population. This peak is due to congenital monogenic arrhythmic canalopathies. Despite their relative rarity, these cases are obviously the most tragic. The immediate causes, or mechanisms, of SCD are comprehensive. Generally, it is arrhythmic death due to ventricular tachyarrythmias - sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). Bradyarrhythmias and pulseless electrical activity account for no more than 40% of all registered cardiac arrests, and they are more often the outcome of the abovementioned arrhythmias. Our current understanding of the mechanisms responsible for SCD has emerged from decades of basic science investigation into the normal electrophysiology of the heart, the molecular physiology of cardiac ion channels, the fundamental cellular and tissue events associated with cardiac arrhythmias, and the molecular genetics of monogenic disorders of the heart rhythm (for example, the long QT syndrome). This review presents an overview of the molecular and genetic basis of SCD in the long QT syndrome, Brugada syndrome, short QT syndrome, catecholaminergic polymorphic ventricular tachycardia and idiopathic ventricular fibrillation, and arrhythmogenic right ventricular dysplasia, and sudden cardiac death prevention strategies by modern techniques (including implantable cardioverter-defibrillator).
有效心脏功能的突然停止通常是由心律紊乱引起的,可在任何年龄导致突然和意外死亡,被称为“心源性猝死”(SCD)综合征。仅在美国,每年就发生约40万例心源性猝死。复苏技术的成功率不到5%。心源性猝死在人群中的患病率随着冠状动脉疾病患病率的上升而增加,冠状动脉疾病是心脏骤停最常见的原因。然而,5岁以下人群的心源性猝死发病率有一个高峰,每10万人中有17例。这个高峰是由先天性单基因心律失常通道病引起的。尽管这些病例相对罕见,但显然是最悲惨的。心源性猝死的直接原因或机制是综合性的。一般来说,是由于室性快速心律失常——持续性室性心动过速(VT)或室颤(VF)导致的心律失常性死亡。缓慢性心律失常和无脉性电活动在所有登记的心脏骤停病例中占比不超过40%,它们更常是上述心律失常的结果。我们目前对心源性猝死机制的理解来自于对心脏正常电生理学、心脏离子通道分子生理学、与心律失常相关的基本细胞和组织事件以及心律单基因疾病(例如长QT综合征)分子遗传学的数十年基础科学研究。本综述概述了长QT综合征、Brugada综合征、短QT综合征、儿茶酚胺能多形性室性心动过速和特发性室颤、致心律失常性右室心肌病中心源性猝死的分子和遗传基础,以及现代技术(包括植入式心脏复律除颤器)的心源性猝死预防策略。