Highlights in heart failure

Abstract

Heart failure (HF) remains a major cause of mortality, morbidity, and poor quality of life. It is an area of active research. This article is aimed to give an update on recent advances in all aspects of this syndrome. Major changes occurred in drug treatment of HF with reduced ejection fraction (HFrEF). Sacubitril/valsartan is indicated as a substitute to ACEi/ARBs after PARADIGM-HF (hazard ratio [HR], 0.80; 95% confidence interval [CI], 0.73 to 0.87 for sacubitril/valsartan vs. enalapril for the primary endpoint and Wei, Lin and Weissfeld HR 0.79, 95% CI 0.71-0.89 for recurrent events). Its initiation was then shown as safe and potentially useful in recent studies in patients hospitalized for acute HF. More recently, dapagliflozin and prevention of adverse-outcomes in DAPA-HF trial showed the beneficial effects of the sodium-glucose transporter type 2 inhibitor dapaglifozin vs. placebo, added to optimal standard therapy [HR, 0.74; 95% CI, 0.65 to 0.85;0.74; 95% CI, 0.65 to 0.85 for the primary endpoint]. Trials with other SGLT 2 inhibitors and in other patients, such as those with HF with preserved ejection fraction (HFpEF) or with recent decompensation, are ongoing. Multiple studies showed the unfavourable prognostic significance of abnormalities in serum potassium levels. Potassium lowering agents may allow initiation and titration of mineralocorticoid antagonists in a larger proportion of patients. Meta-analyses suggest better outcomes with ferric carboxymaltose in patients with iron deficiency. Drugs effective in HFrEF may be useful also in HF with mid-range ejection fraction. Better diagnosis and phenotype characterization seem warranted in HF with preserved ejection fraction. These and other burning aspects of HF research are summarized and reviewed in this article.

Keywords: HFmrEF; HFpEF; HFrEF; acute heart failure; heart failure; treatment.

Figure 1

Effect of sacubitril/valsartan vs. ACE inhibitors on recurrent events. Cumulative rate of heart failure hospitalizations (A) and the primary composite endpoint (B). From reference 41.

Figure 2

Potential pathways linking empagliflozin with heart failure outcome improvement. CV, cardiovascular; HF, heart failure; HHF, hospitalization for heart failure; MI, myocardial infarction; REG, removal of excess glucose; SGLT2i, sodium–glucose co‐transporter 2 inhibitors. UNa, urinary sodium. From reference 63

Figure 3

Comparison of hard endpoints from MITRA‐FR and COAPT. COAPT, Cardiovascular Outcomes Assessment of the MitraClip Percutaneous Therapy for Heart Failure Patients with Functional Mitral Regurgitation; GDMT, guideline‐directed medical therapy; MITRA‐FR, Percutaneous Repair with the MitraClip Device for Severe Functional/Secondary Mitral Regurgitation. From reference 71

Figure 4

Effects of ferric carboxymaltose on cardiovascular hospitalizations and cardiovascular mortality in iron‐deficient heart failure patients. Relative risks of cardiovascular hospitalizations and cardiovascular mortality. Individual randomized controlled trials meta‐analysis. CI, confidence interval; FCM, ferric carboxymaltose. Frome reference 108

Figure 5

Effect of candesartan on the primary outcome by ejection fraction category. Kaplan–Meier time to event rates for candesartan vs. placebo for the primary composite outcome: time to cardiovascular death or first heart failure hospitalization in the three ejection fraction categories. Large graphs show y‐axis up to 1.0; inserted graphs show y‐axis up to 0.4. HFmrEF, heart failure with mid‐range ejection fraction; HFpEF, heart failure with preserved ejection fraction; HFrEF, heart failure with reduced ejection fraction; HR, hazard ratio. From reference 181