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September 25, 2018 Circulation. 2018;138:e272–e391. DOI: 10.1161/CIR.0000000000000549 e294

CLINICAL STATEMENTS AND GUIDELINES discontinuance of the medication.S5.1.5.2-26 For this reason, chronic treatment of young patients with amiodarone should be reserved as a bridge to more definitive treatment options such as catheter ablation. Baseline evaluation of patients may include ECG, liver function tests, thyroid function tests, chest x-ray, and pulmonary function tests (including diffusing capacity of the lungs  for carbon monoxide). Monitoring for toxicity generally includes periodic history and physical examination, as well as evaluation of the ECG, chest x-ray, and thyroid, liver, and lung function. High-resolution chest CT is generally reserved for suspected pulmonary toxicity.S5.1.5.2-30

Although sotalol has some efficacy in suppressing VA, it has significant proarrhythmic effects and has not been shown to improve survival.S5.1.5.2-31 D-sotalol was shown in the SWORD (Survival With Oral d-Sotalol) trial to increase the risk of death in patients with heart failure.S5.1.5.2-32 Unlike amiodarone and many other antiarrhythmic agents, sotalol appears to reduce the defibrillation threshold.S5.1.5.2-33 Also, sotalol may lead to HF decompensation, and so its use in patients with an LVEF <20% is generally avoided.

5.1.4 Calcium Channel Blockers

For the treatment of most VA, nondihydropyridines calcium channel blockers have no role. In fact, intravenous verapamil given for sustained VT has been associated with hemodynamic collapse, especially in patients with prior MI.S5.1.5.2-34,S5.1.5.2-35 For patients with a structurally normal hearts, verapamil or diltiazem can suppress some outflow tract origin.S5.1.5.2-35–S5.1.5.2-39 Oral and intravenous verapamil are effective in treating idiopathic interfascicular reentrant LVT.S5.1.5.2-38 Calcium channel bloickers should not be given to patients with VT in the settin of HFrEF. 5.1.5. Nonantiarrhythmic Medications and Therapies 5.1.5.1. Electrolytes Administration of potassium and magnesium has been proposed as helpful adjuncts in the prevention of VA.S5.1.5.2-40,S5.1.5.2-41 Hypokalemia and hypomagnesemia are common consequences of diuretic therapy in HF, both have been associated with VA during an acute MI,S5.1.5.2-41,S5.1.5.2-42 and can increase the risk of torsades de pointes in patients on medications or with conditions known to prolong the QT interval.S5.1.5.2-43 In fact, in patients with torsades de pointes, intravenous magnesium is first-line therapy.S5.1.5.2-44 In patients who are deficient in both magnesium and potassium, magnesium should be repleted to facilitate replacement of the potassium.S5.1.5.2-45 In the case of potassium, some recommend keeping the potassium level between 4.5 mmol/L and 5 mmol/L to prevent VA and SCD.S5.1.5.2-46,S5.1.5.2-47 A large observational study of patients with an acute MI found that the lowest rates of death were seen in patients with serum potassium concentrations between 3.5 mmol/L and <4.5 mmol/ L.S5.1.5.2-48 Interestingly, the rates of VA did not rise unless the potassium was <3 mmol/L or ≥5 mmol/L. Likewise, a large randomized, double-blind trial of intravenous magnesium in the post-MI period demonstrated no benefit in 30-day mortality.S5.1.5.2-40 It remains quite reasonable to monitor potassium and magnesium during aggressive diuresis and in the post-MI period.

5.1.5.2. n-3 Fatty Acids and Lipids Both n-3 poly-unsaturated fatty acids and statin therapies may have a role in the prevention of SCD, thought to be due to a stabilization of the bilipid myocyte membrane involved in maintaining electrolyte gradients.S5.1.5.2-49 Early data were promising regarding the effects of n-3 polyunsaturated fatty acids on the reduction of cardiovascular events and SCD. In 2006, a large metaanalysis of 19 observational and RCTs demonstrated a significant association between the consumption of n-3 polyunsaturated fatty acids and prevention of SCD.S5.1.5.2-50 The randomized GISSI (Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto)-Prevenzione trial in people with recent MI, found that fish oil 1 g/d reduced mortality, due to fewer SCD.S5.1.5.2-51 However, subsequent RCTs have not replicated these benefits and have shown n-3 polyunsaturated fatty acids to be ineffective.S5.1.5.2-52–S5.1.5.2-56 Because studies showed a consistent lack of harm from n-3 polyunsaturated fatty acids, patients can be reassured of their safety. Longerterm data will hopefully clarify the conflicting results. In contrast, statin medications clearly reduce mortality and appear to reduce the risk of SCD related to ischemic heart disease.S5.1.5.2-57 The predominant mechanism remains uncertain. Prevention of coronary plaque rupture or a direct cardioprotective effect reducing VA has been suggested. Experimental ischemia/reperfusion models demonstrate a cardioprotective effect of statins, and a large observational analysis observed this effect in humans.S5.1.5.2-42,S5.1.5.2-56–S5.1.5.2-58 This was explored further in HF in several secondary analyses of patients on statins in ICD prevention trials, including the MADIT-CRT (Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy), SCD-HeFT, AVID (Antiarrhythmics versus Implantable Defibrillators),S5.1.5.2-59 and DEFINITE (DEFibrillators In Non-Ischemic Cardiomyopathy Treatment Evaluation) trials that showed less SCD risk among the patients on statins.S5.1.5.2-58,S5.1.5.2-60–S5.1.5.2-62 However, this general effect in HF was not confirmed in 2 prospective RCTs of rosuvastatin in HF; the CORONA (Controlled Rosuvastatin Multinational Trial in Heart Failure) and GISSI- HF (Gruppo Italiano per lo Studio della Sopravvivenza nell'Insufficienza Cardiaca-Heart Failure).S5.1.5.2-63,S5.1.5.2-64 It appears that the beneficial effects of statins are con-

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