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Circulation. 2018;138:e272–e391. DOI: 10.1161/CIR.0000000000000549 September 25, 2018 e295 CLINICAL STATEMENTS AND GUIDELINES

fined to the population with or at risk for atherosclerotic cardiovascular disease and/or ischemia, and not HF generally.

5.2 Preventing SCD With HF

Medications

Recommendation for Pharmacological Prevention of SCD References that support the recommendation are summarized in Online Data Supplement 10.

COR LOE Recommendation

I A 1. In patients with HFrEF (LVEF ≤40%), treatment with a beta blocker, a mineralocorticoid receptor antagonist and either an angiotensin-converting enzyme inhibitor, an angiotensin-receptor blocker, or an angiotensin receptor-neprilysin inhibitor is recommended to reduce SCD and all-cause mortality.S5.2-1–S5.2-8

Recommendation-Specific Supportive Text

1.	For patients with HF and depressed LV function, appropriate medical therapy is important to reduce SCD. These therapies have various beneficial effects on arrhythmia mechanisms. Beta blockers reduce myocardial oxygen demand and electrical excitability, and counter arrhythmogenic effects of sympathetic stimulation. Angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers decrease preload and afterload, decreasing myocardial oxygen demand, blocking the formation of angiotensin II, and slowing the progression of ventricular remodeling and fibrosis. Mineralocorticoid receptor antagonists limit potassium loss, decrease fibrosis, and increase the myocardial uptake of norepinephrine.S5.2-7 RCTs in patients with HFrEF have consistently demonstrated that chronic therapy with beta blockers reduces all-cause mortality, VA, and SCD.S5.2-2,S5.2-4,S5.2-5,S5.2-9 Three beta blockers (ie, bisoprolol, carvedilol, sustained-release metoprolol succinate) have been proven to reduce mortality in patients with current or prior symptoms of HFrEF without beta-blocker contraindications. Angiotensinconverting enzyme inhibition also reduces mortality and SCD.S5.2-3 Angiotensin-receptor blockers added to angiotensin-converting enzyme inhibitor showed additional benefit to angiotensin-converting enzyme inhibitors in someS5.2-10 but not other RCTs.S5.2-8,S5.2-11 Therapy with the mineralocorticoid-receptor antagonists, spironolactone and eplerenone, have also demonstrated reductions in both all-cause mortality and SCD.S5.2-6,S5.2-12,S5.2-13 Recent studies of the angiotensin receptor-neprilysin inhibitor (sacubitril/valsartan) versus angiotensin-converting enzyme inhibitor demonstrated a reduction in SCD and cardiac mortality.S5.2-14

5.3 Defibrillators for Treatment of VA

and SCD

See Sections 7, 10.2, 10.3, 10.8, and 10.9. Defibrillation is highly effective in terminating lifethreatening VA. This therapy can be delivered by a transvenous ICD, a subcutaneous implantable cardioverter-defibrillator, a wearable cardioverter-defibrillator or an external defibrillator. These devices monitor the heart rhythm continuously and deliver therapy in response to a tachycardia that meets preprogrammed detection rates and arrhythmia duration. The vast majority of transvenous ICDs are implanted in the subclavicular area under fluoroscopy guidance. subcutaneous implantable cardioverter-defibrillators are implanted in the left side of the chest over the sixth rib between the left midaxillary and left anterior axillary lines. ICDs with epicardial sensing and pacing leads are still being implanted in some patients especially those with certain forms of congenital heart disease. The transvenous ICD has been in clinical use for >3 decades, and robust data from high-quality RCTs support its use in various patient populations including survivors of cardiac arrest, patients with VT and structural heart disease, and patients with significant LV dysfunction.

5.4 Catheter Ablation

5.4.1 General Considerations

Catheter ablation is an important treatment option for patients with VA when antiarrhythmic medications are ineffective, not tolerated, or not desired by the patient. Monomorphic VA usually have an origin or substrate that can be targeted for ablation. Ablation is an option for selected patients with polymorphic VT/VF only if an initiating PVC focus or substrate can be identified. The ablation strategy, risks and outcomes are related to the mechanism and location of the VA. Most VA originate close to the subendocardium and are approached through a transvenous (for the right ventricle) or transaortic/transeptal (for the left ventricle) catheterization. Some diseases give rise to VA from the subepicardium, which may be approached by epicardial mapping and ablation. Pericardial access is usually achieved by a percutaneous subxiphoid puncture. The catheter ablation procedure usually involves attempts to induce VT by programmed electrical stimulation to confirm the diagnosis and guide ablation. Problems limiting success include inability to induce an arrhythmia for mapping (common with idiopathic VA), or origin of the arrhythmia from an inaccessible location in the myocardium (common in some cardiomyopathies).

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