April 2021 at a glance: focus on systolic function, quality of life and treatment in heart failure.

Abstract

Left ventricular (LV) systolic ejection time is a prognostic marker in patients with heart failure (HF) and reduced ejection fraction (HFrEF).1, 2 Alhakak et al.3 reviewed the definition and methods of measurement of LV ejection time, the mechanisms behind its shortening in HFrEF, its role as a prognostic marker and in the assessment of the response to medical treatment. Left ventricular ejection fraction (LVEF) remains the landmark parameter of LV systolic function. It is a major prognostic marker both in acute and chronic HF.4, 5 Strange et al.5, 6 furthered their previous findings showing in a large cohort of 117 275 subjects followed up by echocardiography that even modest LVEF changes over time, i.e. at least 6 months, have a significant prognostic impact. Five-year all-cause mortality increased from 12% to 29% among subjects with the smallest to the largest decrease in LVEF (from <5 units to >30 units). Health-related quality of life (QoL) scores are clinically relevant in patients with HF.7-9 In a recent analysis of BIOSTAT-CHF, Ravera et al.10 reported worse QoL scores in women with HFrEF as compared with men, both when assessed with the Kansas City Cardiomyopathy Questionnaire (KCCQ) overall score (median 44 vs. 53; P < 0.001) and the EuroQol 5 dimensions utility score (median 0.62 vs. 0.73; P < 0.001). Of note, QoL was independently associated with subsequent outcome both in women and men. Turgeon et al.11 synthetized evidence regarding the impact of HFrEF pharmacotherapy on QoL in a comprehensive systematic review and meta-analysis. QoL was improved by angiotensin receptor blockers, angiotensin receptor–neprilysin inhibitor, sodium–glucose co-transporter 2 inhibitors, ivabradine, hydralazine–nitrate, and intravenous iron whereas findings were inconclusive for angiotensin-converting enzyme inhibitors, beta-blockers, digoxin, and oral iron. Sodium–glucose co-transporter 2 inhibitors have a pivotal role in the treatment of patients with HFrEF.12-14 Their cost-effectiveness has also been shown.15 Despite differences in the pathophysiology of ischaemic and non-ischaemic HF,16 dapagliflozin had similar effects on the risk of worsening HF or cardiovascular death as well as on symptoms and QoL in patients with HFrEF of ischaemic and non-ischaemic aetiology in DAPA-HF.17 Comorbidities have a major role in patients with HF, including those enrolled in clinical trials.18 Two analyses from DAPA-HF reported that patients with concomitant anaemia or chronic obstructive pulmonary disease had poorer outcomes. However, the benefit of dapagliflozin on cardiovascular events was independent of their presence.19, 20 Rivaroxaban 2.5 mg twice daily may be considered among treatment options for patients with HF, coronary artery disease and LVEF >30%.14 An analysis of COMMANDER-HF demonstrated that high plasma D-dimer levels (>515 ng/mL) identify patients at high risk of stroke who can benefit from rivaroxaban administration.21 Iron deficiency is a major therapeutic target in HF.9, 14, 22 In a non-randomized, open-label, prospective pilot study, oral sucrosomial iron improved exercise capacity and QoL in patients with HFrEF and Iron deficiency, with significant improvement in 6-min walk distance and KCCQ at 3 and 6 months (all adjusted P-values <0.01).23 The MSC-HF trial reported a positive effect of intramyocardial injection of autologous bone marrow-derived mesenchymal stromal cells (MSCs) in patients with ischaemic HF.24 The Phase II CONCERT-HF trial demonstrated that the combination of MSCs and c-kit positive cardiac cells was associated with further improvement in clinical outcome and QoL.25