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September 25, 2018 Circulation. 2018;138:e272–e391. DOI: 10.1161/CIR.0000000000000549 e342

CLINICAL STATEMENTS AND GUIDELINES Digoxin concentration monitoring is unreliable after antidigoxin antibody administration. 2.	 Monitoring high-risk patients during initiation of QT-prolonging antiarrhythmic medications and recognition of the syndrome when it occurs are the first steps. Temporary pacing is highly effective in managing torsades de pointes that is recurrent after potassium and magnesium supplementation.S10.7-3 Isoproterenol can also be used to increase heart rate and abolish postectopic pauses.S10.7-3

3.	 Intravenous magnesium can suppress episodes of torsades de pointes without necessarily shortening QT, even when serum magnesium is normal.S10.7-4,S10.7-5 Repeated doses may be needed, titrated to suppress ectopy and nonsustained VT episodes while precipitating factors are corrected.S10.7-4 Magnesium toxicity (areflexia progressing to respiratory depression) can occur at high serum concentrations, but this risk is very small with the doses usually used to treat torsades de pointes, 1 to 2 g intravenously.S10.7-14 Allelic variants in clinical long QT disease genes have been identified in patients with medicationinduced torsades de pointes.S10.7-7,S10.7-15–S10.7-18 Further, whole exome sequencing implicates an increased burden of rare potassium channel variants in the risk of medication-induced torsades de pointes.S10.7-17,S10.7-19 These findings do not yet support general genetic screening for prediction of medication-induced torsades de pointes. In long QT syndrome, genetic testing may be performed in the index case who experienced medicationinduced torsades de pointes and, if he/she did not survive that event, electrocardiographic screening of first-degree relatives may be performed. 4.	 Maintaining serum potassium between 4.5 mEq/L and 5 mEq/L shortens QT and may reduce the chance of recurrent torsades de pointes.S10.7-6,S10.7-7 5.	 In large clinical trials, sodium channel blockers increased mortality among patients convalescing from MI,S10.7-20 but similar trends were also seen with earlier trials of mexiletineS10.7-21 and disopyramide.S10.7-22 Based on CAST, flecainide is contraindicated in patients with ischemia, prior MI, and is avoided in patients with other structural heart diseases.S10.7-20

Sodium channel blockers increase defibrillation energy requirement and pacing thresholdsS10.7-8,S10.7-9; as a consequence, patients may require reprogramming or revision of pacing or ICD systems or changes in their medication regimens (although modern pacing systems that provide automatic pacing threshold testing and adjustment of pacing output have mitigated the risk of loss of capture). Sodium channel blockers can “convert” AF to slow atrial flutter, which can show 1:1 atrioventricular conduction with wide QRS complexes that can be confused with VT.S10.7-23 Sodium channel blockers, like procainamide and flecainide, can occasionally precipitate the typical Brugada syndrome ECG.S10.7-24,S10.7-25 This has been reported not only with antiarrhythmic medications but also with tricyclic antidepressantsS10.7-26 and cocaineS10.7-27 (www.brugadadrugs.org).S10.7-28 Whether this represents unmasking individuals with clinically unapparent Brugada syndrome (see Section 7.9.1.3) or one end of a broad spectrum of responses to sodium channel blockers is unknown.

In the setting of sodium-channel blocker toxicity, limited animal data suggest that administration of sodium, as sodium chloride or sodium bicarbonate, may improve conduction slowing or suppress frequent or cardioversion-resistant VT.S10.7-29 Successful treatment with beta blockersS10.7-30 and intravenous fat emulsion and/or extracorporeal membrane oxygenation has also been reported.S10.7-31 6.	QT-prolonging medications (www.crediblemeds. org)S10.7-32 are not used in patients with congenital or acquired long QT syndrome unless there is no suitable alternative or the benefit greatly exceeds the risk. Episodes of torsades de pointes can be precipitated by exposure to a QT-prolonging medication, and underlying prolongation of the QT (from genetic and clinical risk factors) increases this risk.S10.7-10 Medications implicated in torsades de pointes are found in several medication classes, including antiarrhythmics, antihistamines, antibiotics, antifungals, antidepressants, antipsychotics, opiates, and anticancer agentsS10.7-10 (Table 10).

10.8 Adult Congenital Heart Disease

Recommendations for Adult Congenital Heart Disease References that support the recommendations are summarized in Online Data Supplement 54.

COR LOE Recommendations

I B-NR 1. Adult patients with repaired complex congenital heart disease presenting with frequent, complex, or sustained VA, or unexplained syncope should undergo evaluation for potential residual anatomic or coronary abnormalities.S10.8-1–S10.8-6

I B-NR 2. In patients with adult congenital heart disease and complex or sustained VA in the presence of important residual hemodynamic lesions, treatment of hemodynamic abnormalities with catheter or surgical intervention as feasible is indicated prior to consideration of ablation or an ICD.S10.8-3,S10.8-7–S10.8-12

I B-NR 3. In patients with adult congenital heart disease and hemodynamically unstable VT, an ICD is recommended after evaluation and appropriate treatment for residual lesions/ ventricular dysfunction if meaningful survival of greater than 1 year is expected.S10.8-13–S10.8-17

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