Gaps in Non-pharmacological Therapy
Coronary artery disease (CAD) is the most common aetiology of HFrEF.35 While revascularisation with concurrent use of viability studies in severe ischaemic cardiomyopathy is logically sound, recent studies have challenged this dictum. The Surgical Treatment for Ischemic Heart Failure (STICH) trial showed no mortality benefit with coronary artery bypass grafting (CABG) when compared to medical therapy in patients with EF <35 %.36 Though notably, after taking into account patient crossover from the medical therapy arm, the ‘as-treated’ analysis showed decreased mortality with CABG (HR 0.70, 95 % CI 0.58–0.84). An imaging substudy of STICH showed that viability assessment by single-photon emission computed tomography (SPECT) or dobutamine echocardiography did not identify patients who would benefit from CABG.7 Cardiac magnetic resonance and position emission tomography imaging promise improved sensitivities and specificities in identifying viable myocardium, but their impact on clinical outcomes has not been rigorously tested.38 Thus the roles of viability testing and revascularisation in patients with CAD and severely reduced EF remain debatable. The ESC Guideline gives a viability testing Class IIa/LOE C recommendation and recommends against revascularisation in patients without viable myocardium (Class III/LOE C). The ACCF/AHA Guideline gives viability testing and revascularisation in patients with LVEF <35 % a Class IIa/ LOE B recommendation.
Though sodium and fluid restriction in patients with HF appears intuitive, its role is controversial. Even though sodium restriction is endorsed by many guidelines, small RCTs have shown worse neurohormonal profiles and increase in HF admissions for patients with HFrEF assigned to low-sodium diet.39–41 Similarly, other small trials have shown no significant benefit with fluid restriction in patients with HF.42,43 More recently, one RCT showed New York Heart Association (NYHA) class improvement in patients with chronic HF randomised to modest sodium and fluid restriction,44 while another RCT showed no clinical benefit with aggressive sodium and fluid restriction in hospitalised patients with ADHF.45 Despite conflicting data, the ACCF/ AHA Guideline gives sodium restriction and fluid restriction Class IIa/ LOE C recommendation, and the ESC Guideline gives only a general recommendation supporting sodium restriction and fluid restriction for symptomatic HF. Well-powered outcome trials are needed. Given the complexity of sodium and fluid homeostasis, perhaps the answer may be individualised targets based on the patient’s clinical status.
Other non-pharmacological interventions, such as self-management counselling, telephone support and home visitation have been advocated. However, there is no definitive evidence supporting an individual approach.46 While intensive multidisciplinary programmes have been found to reduce mortality and hospitalisation, the resources required to maintain this strategy have limited its ability to reach a wide spectrum of patients.47