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Brugada syndrome (BrS) is a genetic disorder in which the electrical activity of the heart is abnormal due to channelopathy. [2] It increases the risk of abnormal heart rhythms and sudden cardiac death. [2]
Rare diseases called ion channelopathies may play a role such as long QT syndrome (LQTS), Brugada syndrome (BrS), CPVT (catecholaminergic polymorphic ventricular tachycardia), progressive cardiac conduction defect (PCCD), early repolarization syndrome, mixed sodium channel disease, and short QT syndrome. [13]
Long QT syndrome, the most common form of cardiac channelopathy, is characterized by prolonged ventricular repolarization, predisposing to a high risk of ventricular tachyarrhythmias (e.g., torsade de pointes), syncope, and sudden cardiac death.
Long QT syndrome is estimated to affect 1 in 7,000 people. [6] Females are affected more often than males. [6] Most people with the condition develop symptoms before they are 40 years old. [6] It is a relatively common cause of sudden death along with Brugada syndrome and arrhythmogenic right ventricular dysplasia. [3]
This is a list of disorder codes in the Online Mendelian Inheritance in Man (OMIM) database. These are diseases that can be inherited via a Mendelian genetic mechanism. OMIM is one of the databases housed in the U.S. National Center for Biotechnology Information.
Brugada syndrome is a genetic disease that can result in mutations in the sodium ion channel (gene SCN5A) of the myocytes in the heart. [12] Brugada syndrome can result in ventricular fibrillation and potentially death. It is a major cause of sudden unexpected cardiac death in young, otherwise healthy people. [13]
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The resting 12-lead ECG is a useful test to differentiate CPVT from other electrical diseases of the heart that can cause similar abnormal heart rhythms. Unlike conditions such as long QT syndrome and Brugada syndrome, the resting 12-lead ECG in those with CPVT is generally normal. [8]