Genetic aspects of arrhythmias.
Advances in the treatment and prevention of heart disease have led to consistently declining morbidity and mortality rates over the past 30 years. Despite these advances, therapy remains largely palliative. The development of curative therapies is limited by our lack of knowledge of the basic mechanisms of disease. In the next decade, we will probably change many of these current approaches from treating the crisis to preventing the disease. Molecular biology and genetics have elucidated several basic pathways. It is hoped that targeted therapies will prevent or arrest many of these cardiac diseases, in particular, arrhythmias and sudden death. With the discovery of the genes causing familial diseases like long QT, hypertrophic cardiomyopathy, and Brugada syndrome, we have identified several substrates responsible for triggering malignant arrhythmias.
Roberts
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Baylor College of Medicine, Houston, TX 77030-2717, USA. rroberts@bcm.tmc.edu
Brugada
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D000293:Adolescent; D000328:Adult; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000235:genetics*; D019571:Arrhythmogenic Right Ventricular Dysplasia / Q000235:genetics; D001210:Asia, Southeastern / Q000453:epidemiology; D001281:Atrial Fibrillation / Q000235:genetics; D002037:Bundle-Branch Block / Q000150:complications / Q000235:genetics; D002312:Cardiomyopathy, Hypertrophic / Q000453:epidemiology / Q000235:genetics / Q000503:physiopathology; D002648:Child; D002675:Child, Preschool; D002874:Chromosome Mapping; D002877:Chromosomes, Human / Q000235:genetics; D016757:Death, Sudden, Cardiac / Q000209:etiology; D005260:Female; D018740:Genetic Heterogeneity; D008040:Genetic Linkage; D005820:Genetic Testing; D015316:Genetic Therapy; D006330:Heart Defects, Congenital / Q000453:epidemiology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000235:genetics / Q000473:pathology; D015994:Incidence; D007223:Infant; D007231:Infant, Newborn; D007473:Ion Channels / Q000502:physiology; D017136:Ion Transport; D008133:Long QT Syndrome / Q000235:genetics; D008297:Male; D051379:Mice; D023421:Models, Animal; D009154:Mutation; D062554:NAV1.5 Voltage-Gated Sodium Channel; D010641:Phenotype; D015995:Prevalence; D011817:Rabbits; D012306:Risk; D015222:Sodium Channels / Q000235:genetics / Q000502:physiology; D013577:Syndrome
D007473:Ion Channels; D062554:NAV1.5 Voltage-Gated Sodium Channel; C568320:SCN5A protein, human; C568321:Scn5a protein, mouse; D015222:Sodium Channels