Those diagnosed with<unk>  are usually advised to avoid drugs that can prolong the<unk>  interval further or lower the threshold for TDP, lists of which can be found in public access online databases. In addition to this, two intervention options are known for individuals with<unk> : arrhythmia prevention and arrhythmia termination. Arrhythmia prevention Arrhythmia suppression involves the use of medications or surgical procedures that attack the underlying cause of the arrhythmias associated with<unk> . Since the cause of arrhythmias in<unk>  is early afterdepolarizations (EADs), and they are increased in states of adrenergic stimulation, steps can be taken to blunt adrenergic stimulation in these individuals. These include administration of beta receptor blocking agents, which decreases the risk of stress-induced arrhythmias. Nadolol, a powerful non-selective beta blocker, has been shown to reduce the arrhythmic risk in all three main genotypes <unk> 1,<unk> 2, and<unk> 3). Genotype and<unk>  interval duration are independent predictors of recurrence of life-threatening events during beta-blocker therapy. To be specific, the presence of<unk> c >500 ms and<unk> 2 and<unk> 3 genotype are associated with the highest incidence of recurrence. In these patients, primary prevention with use of implantable cardioverter-defibrillators can be considered. * Potassium supplementation: If the potassium content in the blood rises, the action potential shortens, so increasing potassium concentration could minimize the occurrence of arrhythmias. It should work best in<unk> 2, since the hERG channel is especially sensitive to potassium concentration, but the use is experimental and not evidence-based. * Sodium channel blocking drugs such as mexiletine have been used to prevent arrhythmias in<unk> . While the most compelling indication is for those whose<unk>  is caused by defective sodium channels producing a sustained late current <unk> 3), mexiletine also shortens the<unk>  interval in other forms of<unk>  including<unk> 1,<unk> 2 and<unk> 8. As the predominant action of mexiletine is on the early peak sodium current, there are theoretical reasons why drugs which preferentially suppress the late sodium current such as ranolazine may be more effective, although evidence that this is the case in practice is limited. * Amputation of the cervical sympathetic chain (left stellectomy). This therapy is typically reserved for<unk>  caused by JLNS, but may be used as an add-on therapy to beta blockers in certain cases. In most cases, modern therapy favors ICD implantation if beta blocker therapy fails. * In patients considered at high risk of life-threatening arrhythmic events, ICD implantation may be considered as a preventive step. Arrhythmia termination Arrhythmia termination involves stopping a life-threatening arrhythmia once it has already occurred. One effective form of arrhythmia termination in individuals with<unk>  is placement of an implantable cardioverter-defibrillator (ICD). Also, external defibrillation can be used to restore sinus rhythm. ICDs are commonly used in patients with fainting episodes despite beta blocker therapy, and in patients having experienced a cardiac arrest. As mentioned earlier, ICDs may be used also in patients considered at high risk of life-threatening arrhythmic events. With better knowledge of the genetics underlying<unk> , more precise treatments hopefully will become available.
Long QT syndrome
Brugada syndrome
Short QT syndrome
Arrhythmogenic cardiomyopathy
Catecholaminergic polymorphic ventricular tachycardia
Opitz G/BBB syndrome
Jervell and Lange-Nielsen syndrome
Familial atrial fibrillation