p.22 抽出テキスト

Circulation. 2018;138:e272–e391. DOI: 10.1161/CIR.0000000000000549 September 25, 2018 e293 CLINICAL STATEMENTS AND GUIDELINES

ICD without a history of documented VT/VF and with one of the following conditions: BUN ≥26 mg/dL, QRS >120 msec, atrial fibrillation, or NSVT or >500 VPBs on 24-hour Holter recording; 2) having a primary prevention ICD with a history of documented VT/VF appropriately treated with ICD therapy or untreated NSVT; or 3) having a secondary prevention ICD after documented VT/VF or cardiac arrest. Ranolazine did not significantly reduce the primary endpoint of VT/VF requiring appropriate ICD therapy or death. In a prespecified secondary analysis, ranolazine was associated with a significant reduction in VT events treated with anti-tachycardia pacing.S5.1.5.2-9

5.1.2 Beta Blockers

Because of their excellent safety profile and effectiveness in treating VA and reducing the risk of SCD, beta blockers are often first-line antiarrhythmic therapy.S5.1.5.2-10,S5.1.5.2-11 Their antiarrhythmic efficacy is related to the effects of adrenergic-receptor blockade on sympathetically mediated triggering mechanisms, slowing of the sinus rate, and possibly inhibition of excess calcium release by the ryanodine receptor.S5.1.5.2-12 Beta blockers reduce all-cause mortality and SCD in patients with HF with reduced EF (HFrEF).S5.1.5.2-13–S5.1.5.2-15 Although beta blockers have long been proven to reduce mortality after MI,S5.1.5.2-16 registry data confirm that early beta blocker use in patients with MI and risk factors for shock (>70 years of age, symptoms  <12 hours [ST-elevation MI patients], systolic blood pressure <120 mm Hg, and heart rate >110 beat/min on presentation) is associated with an increased risk of shock or death.S5.1.5.2-17 In the setting of polymorphic VT after MI, beta blockers reduce mortality.S5.1.5.2-18 Beta blockers suppress VA in some patients with structurally normal hearts.S5.1.5.2-19 When used in combination with membrane-stabilizing antiarrhythmic medications, beta blockers can enhance antiarrhythmic efficacy.S5.1.5.2-20 Beta blockers (eg, nadolol, propranolol) are also first- line therapy for some cardiac channelopathies (eg, long QT syndrome, catecholaminergic polymorphic ventricular tachycardia).

5.1.3 Amiodarone and Sotalol

Amiodarone possesses a wide spectrum of actions that include blockade of beta receptors and sodium, calcium and potassium currents (ie, a multichannel blocker). Its overall long-term effect on survival is controversial, with most studies showing no clear advantage over placebo. A few studies and a meta-analysis of several large studies have shown a reduction in SCD using amiodarone in patients with LV dysfunction due to prior MI and NICM,S5.1.5.2-21–S5.1.5.2-23 but SCD-HeFT showed no survival benefit from amiodarone compared with placebo.S5.1.5.2-24 A secondary analysis of the SCD-HeFT showed increased risk of mortality with amiodarone in patients with New York Heart Association (NYHA) class III symptoms.S5.1.5.2-25 A systematic review of the literature in high-risk patients (LVEF <40%, with or without coronary disease), concluded that, for primary prevention, amiodarone, compared with no treatment or placebo, decreased the risk of SCD (Risk ratio: 0.76; 95% CI: 0.66–0.88) and all-cause mortality (Risk ratio: 0.88; 95% CI: 0.78–1.00), but the quality of the supporting evidence was very low.S5.1.5.2-26 For secondary prevention of SCD, the same systematic review identified neither risk nor benefit with amiodarone.S5.1.5.2-26 Compared with beta-blocker therapy and other antiarrhythmic medications (including sotalol), amiodarone appears to reduce the risk of SCD and all-cause mortality.S5.1.5.2-26 Intravenous amiodarone has a role in reducing recurrent VF/VF during resuscitation.S5.1.5.2-3,S5.1.5.2-27–S5.1.5.2-29 Chronic administration of amiodarone is associated with complex medication interactions and a host of adverse effects involving the lung, liver, thyroid, skin, and nervous system. As a general rule, the longer the therapy and the higher dose of amiodarone, the greater the likelihood of adverse effects that will require

Verapamil (IV) IV: 2.5–5 mg q 15–30 min Sustained release PO: 240–480 mg/d VT (specifically RVOT, verapamilsensitive idiopathic LVT) ICa-L Sinus rate slowed

PR prolonged AV nodal conduction slowed t1/2: 3–7 h

Metab: H Excr: U Cardiac: Hypotension, edema, HF, AVB, bradycardia, exacerbation of HFrEF

Other: Headache, rash, gingival hyperplasia, constipation, dyspepsia

*Although up to 800 mg every 8 h might be used, higher doses of amiodarone are associated with a higher risk of adverse events. Modified from Shleifer JW, et al.S5.1.5.2-2 Alpha indicates alpha-adrenergic receptor; ARVC, arrhythmogenic right ventricular cardiomyopathy; AV, atrioventricular; AVB, atrioventricular block; Beta, betaadrenergic receptor; HF, heart failure; CPVT, catecholaminergic polymorphic ventricular tachycardia; DFT, defibrillation threshold; F, feces; H, hepatic; ICa, L-type calcium channel current; IK1, inward rectifier potassium channel; IKACh, muscarinic receptor-gated potassium channel; IKATP, adenosine-activated potassium channel; IKr, rapid delayed rectifier potassium current; IKs, slow delayed rectifier potassium current; IKur, ultra-rapid delayed rectifier potassium current; INa, fast inward sodium current; Ito, transient outward potassium current; LQTS, long QT syndrome; LVT, left ventricular tachycardia; M, muscarinic; Metab, metabolism; NAPA, n-acetyl procainamide; PVC, premature ventricular complex; QTc, corrected QT interval; t1/2, half-life; RVOT, right ventricular outflow tract; T3, triiodothyronine; TdP, torsades de pointes; U, urine; VT, ventricular tachycardia; and VF, ventricular fibrillation.

Table 7.  Continued

Antiarrhythmic Medication (Class) and Dose Uses in VA/SCA Target Electrophysiological

Effects Pharmacological

Characteristics Common Adverse Effects

Downloaded from http://ahajournals.org by on October 7, 2026