Reclassifying some channelopathies: Changes after a long wait
Abstract
Sudden cardiac death and malignant ventricular arrhythmias —in individuals without demonstrable structural heart disease by conventional methods—, have long been a subject of controversy. Primary electrical diseases became equivalent to purely electrical diseases, and the term “channelopathy” has undergone modifications because alterations in some interacting proteins are added to genetic mutations, and because there are structural abnormalities such as inflammation, fibrosis, adiposis, myocarditis, microaneurysms, increased collagen, mechanical dysfunction and others, evidenced by more sensitive diagnostic procedures: the heart is normal in appearance but the myocytes are not. In addition to the genetic basis (ion channel dysfunction) and the clinical presentation, structural alterations are integrated and Brugada, long QT and short QT syndromes are considered as organic-functional, electroanatomic diseases, requiring their reclassification, which is transcendental to stratify risk and adopt the most appropriate therapeutic approach.
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