The risk is increased irrespective of HFrEF SCD makes up a greater proportion of deaths in patients with milder HF symptoms and lesser proportion in those with moderate/severe HF The reported incidence of SCD varies depending on the definition used and the population studied. Although many deaths, classified as sudden, are indeed due to lethal VA, others may be due to bradyarrhythmias, pulseless electrical activity, and sud- den hemodynamic deterioration.S7.7.1-7 S7.7.1-9 Medical therapy with neurohormonal agents de- creases the risk of SCD by reducing both the incidence of VA and disease progression.S7.7.1-7,S7.7.1-10 S7.7.1-12 De- spite GDMT for HFrEF, some patients remain at risk for SCD, and an ICD may be helpful. See Sections 7.1 and 7.2 for the indications on ICDs in patients with reduced LVEF. CRT, in appropriate patients, has also been shown to reduce the incidence of SCD.S7.7.1-13 The pathophysiology of SCD in HF is complex, re- sulting from interactions between both functional and structural changes that occur in patients with HFrEF that result in increased susceptibility to SCD.S7.7.1-14 Although many of the risk factors are shared among HFrEF patients, the reason that SCD strikes a particular individual is usually unknown; however, some individu- als may have a genetic susceptibility.S7.7.1-15 Varying de- grees of myocardial fibrosis, neurohormonal activation, and increased wall stress alter the electrophysiological properties with changes in cell coupling, ionic currents (electrical remodeling), and calcium handling that likely contribute to the development of lethal VA.S7.7.1-16 Con- tributing factors extrinsic to the heart include electro- lyte abnormalities related to volume shifts and diuretic use, sympathetic activation, hemodynamic stress, and hypoxia. Recommendation-Specific Supportive Text 1. Many patients with advanced HF listed for heart transplant would not otherwise qualify for ICD given the severity of illness including NYHA class IV status and/or use of inotropic infusion. 