Aims Significant recovery of left ventricular ejection fraction (LVEF) occurs in a proportion of patients with heart failure (HF) and reduced ejection fraction (HFrEF). We analysed outcomes, including mortality [all‐cause, cardiovascular (CV), HF‐related, and sudden death], and HF‐related hospitalizations in this HF‐recovered group. The primary endpoint was a composite of CV death or HF hospitalization. Methods and results LVEF was assessed at baseline and at 1 year in 1057 consecutive HF patients. Patients were classified into three groups: (i) HF‐recovered: LVEF <45% at baseline and ≥45% at 1 year (n = 233); (ii) HF with preserved EF (HFpEF): LVEF ≥45% throughout follow‐up (n = 117); and (iii) HFrEF: LVEF <45% throughout follow‐up (n = 707). Mean follow‐up was 5.6 ± 3.1 years. HF‐recovered patients differed from HFrEF and HFpEF groups in demographic and clinical characteristics. The mean LVEF increase was 21.1 ± 10 points in HF‐recovered patients. Using the HF‐recovered group as a reference, the risks for the primary composite endpoint (n = 376), with non‐CV death as competing risk, for HFpEF and HFrEF groups were: hazard ratio (HR) 2.33 [95% confidence interval (CI) 1.60–3.39], P < 0.001 and HR 1.99 (95% CI 1.50–2.65), P < 0.001, respectively. All‐cause (n = 429), CV (n = 245), HF‐related (n = 127), and sudden death (n = 60) were significantly lower in HF‐recovered subjects relative to HFrEF (all P < 0.01). HF‐recovered patients also experienced less recurrent HF hospitalizations (P < 0.001). Conclusion One in four treated patients with HFrEF showed recovery of systolic function. HF‐recovered patients had significantly improved mortality and morbidity relative to HFpEF and HFrEF subjects. Further research is needed to identify optimal medications and device indications for HF‐recovered patients.

LVEF trajectories vary in HF depending on a number of disease modifiers, but an inverted U-shaped pattern with lower LVEF at both ends of the distribution emerged. A declining LVEF in the preceding period was associated with higher mortality.

BackgroundPatients with diabetes mellitus (DM) have an increased risk of developing heart failure (HF). Further, DM is associated with poor prognosis in patients with HF. Our aim was to determine whether DM has any impact on the predictive value of a multi-biomarker panel in patients with HF.MethodsWe included 1069 consecutive ambulatory HF patients in the study: age 66.2 ± 12.8 years, 33.5 ± 13.3 left ventricular ejection fraction, 36% diabetic patients. We measured serum concentrations of N-terminal pro-brain natriuretic peptide (NT-proBNP), high-sensitivity troponin T (hs-TnT), ST2, galectin-3, high-sensitivity C reactive protein (hs-CRP), cystatin-C, soluble transferrin receptor (sTfR), and neprilysin and followed patients for 4.9 ± 2.8 years. Primary endpoints were all-cause and cardiovascular death.ResultsDuring follow-up, 534 patients died; 283 died of cardiovascular causes. Diabetic subjects had higher mortality (57.7 vs. 45.6%, p < 0.001). NTproBNP (p = 0.07), hs-TnT (p < 0.001), galectin-3 (p < 0.001), and cystatin-C (p = 0.001) concentrations were higher in diabetic patients, whereas sTfR levels were lower (p = 0.005). There were no interactions between DM and NTproBNP, hs-TnT, galectin-3, hs-CRP, cystatin-C, sTfR, and neprilysin relative to risk prediction for all-cause or cardiovascular death. By contrast, ST2 significantly interacted with DM for all-cause (p = 0.02) and cardiovascular (p = 0.03) death. In diabetic patients, HRs for ST2 were 1.27 (95% CI 1.16–1.40, p < 0.001) and 1.23 (95% CI 1.09–1.39, p = 0.001) for all-cause and cardiovascular death, respectively. In nondiabetic patients, HRs for ST2 were 1.53 (95% CI 1.35–1.73, p < 0.001) and 1.64 (95% CI 1.31–2.05, p < 0.001) for all-cause and cardiovascular death, respectively. The multivariable Cox regression analysis showed that hs-TnT and ST2 were the only markers that were independently associated with both all-cause and cardiovascular mortality in patients with HF and diabetes. Moreover, in these patients, the combination of these two markers significantly increased discrimination as assessed by the area under the curve.ConclusionsBiomarkers used in the general population to predict the clinical course of heart failure are also useful in patients with diabetes. In these patients, among all the biomarkers analysed only hs-TnT and ST2 were independently associated with both all-cause and cardiovascular mortality.

AimsBetter management of heart failure (HF) over the past two decades has improved survival, mainly by reducing the incidence of death due to cardiovascular (CV) causes. Deaths due to non-CV causes, particularly cancer, may be increasing. This study explored the modes of death of consecutive patients who attended a HF clinic over A total of 935 deaths were ascertained from 2002 to 2018 among 1876 patients (mean age 65.8 ± 12.5 years, 75% men, left ventricular ejection fraction < 50%) admitted to our HF clinic. Median follow-up was 4.2 years [1.9-7.8].Mode of death was curated from patient health records and verified by the Catalan and Spanish health system databases. Trends for every mode of death were assessed by polynomial regression. Two trends were observed: a significant reduction in sudden death (P = 0.03) without changes in HF progression as mode of death (P = 0.26), and a significant increase in non-CV modes of death (P < 0.001). Non-CV deaths accounted for 17.4% of deaths in 2002 and 65.8% of deaths in 2018. A total 138 deaths were due to cancer (37% of non-CV deaths). A significant trend was observed towards a progressive increase in cancer deaths over time (P = 0.002).

Background: Long-term trajectories of left ventricular ejection fraction (LVEF) in heart failure (HF) patients with preserved EF (HFpEF) remain unclear. Our objective was to assess long-term longitudinal trajectories in consecutive HFpEF patients and the prognostic impact of LVEF dynamic changes over time. Methods and Results: Consecutive ambulatory HFpEF patients admitted to a multidisciplinary HF Unit were prospectively evaluated by 2-dimensional echocardiography at baseline and at 1, 3, 5, 7, 9, and 11 years of follow-up. Exclusion criteria were patients having a previous known LVEF <50%, patients undergoing only 1 echocardiogram study, and those with a diagnosis of dilated, noncompaction, alcoholic, or toxic cardiomyopathy. One hundred twenty-six patients (age, 71±13 years; 63% women) were included. The main pathogeneses were valvular disease (36%) and hypertension (28%). Atrial fibrillation was present in 67 patients (53%). The mean number of echocardiographies performed was 3±1.2 per patient. Locally weighted error sum of squares curves showed a smooth decrease of LVEF during the 11-year follow-up that was statistically significant in linear mixed-effects modeling ( P =0.01). Ischemic patients showed a higher decrease than nonischemics. The great majority (88.9%) of patients remained in the HFpEF category during follow-up; 9.5% evolved toward HF with midrange LVEF, and only 1.6% dropped to HF with reduced LVEF. No significant relationship was found between LVEF dynamics in the immediate preceding period and mortality. Conclusions: LVEF remained ≥50% in the majority of patients with HFpEF for ≤11 years. Only 1.6% of patients evolved to HF with reduced LVEF. Dynamic LVEF changes were not associated with mortality.

Both BMI and survival after a mean follow-up of 4.3 ± 3.0 years (up to 10 years) were assessed for 2527 ambulatory patients (66.3% men; mean age 69 ± 12.3 years). A total of 1102 (43.6%) patients had T2D and ischaemic aetiology of HF was present in 47.8%; mean left ventricular ejection fraction was 38 ± 16%. Based on BMI scores, patients were categorized as either underweight, normal, overweight, or obese. A significant survival interaction was observed between BMI and T2D. Smooth spline curves for the estimation of risk of all-cause and cardiovascular death showed the classic obesity paradox, with reduced mortality as BMI increased in non-diabetics; for T2D patients this pattern was lost. After adjustment for age and sex, hazard ratios for low-weight and obesity were: 2.04 [95% confidence intervals (CI) 1.50-2.78, P < 0.001] and 0.76 (95% CI 0.58-0.99, P = 0.04), respectively, for non-T2D patients; and 1.30 (95% CI 0.77-2.19, P = 0.32) and 0.99 (95% CI 0.78-1.26, P = 0.95), respectively, for T2D patients. Multivariate analyses for mortality (including BMI as a continuous variable) were significant for non-diabetic patients only.

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Background In heart failure ( HF ), weight loss ( WL ) has been associated with an adverse prognosis whereas obesity has been linked to lower mortality (the obesity paradox). The impact of WL in obese patients with HF is incompletely understood. Our objective was to explore the prevalence of WL and its impact on long‐term mortality, with an emphasis on obese patients, in a cohort of patients with chronic HF . Methods and Results Weight at first visit and the 1‐year follow‐up and vital status after 3 years were assessed in 1000 consecutive ambulatory, chronic HF patients (72.7% men; mean age 65.8±12.1 years). Significant WL was defined as a loss of ≥5% weight between baseline and 1 year. Obesity was defined as body mass index ≥30 kg/m 2 (N=272). Of the 1000 patients included, 170 experienced significant WL during the first year of follow‐up. Mortality was significantly higher in patients with significant WL (27.6% versus 15.3%, P <0.001). In univariable Cox regression analysis, patients with significant WL had 2‐fold higher mortality (hazard ratio 1.95 [95% CI 1.39–2.72], P <0.001). In multivariable analysis, adjusting for age, sex, body mass index, New York Heart Association functional class, left ventricular ejection fraction, HF duration, ischemic etiology, diabetes, and treatment, significant WL remained independently associated with higher mortality (hazard ratio 1.89 [95% CI 1.32–2.68], P <0.001). Among obese patients with HF , significant WL was associated with an even more ominous prognosis (adjusted hazard ratio for death of 2.38 [95% CI 1.31–4.32], P =0.004) than that observed in nonobese patients (adjusted hazard ratio 1.83 [95% CI 1.16–2.89], P =0.01). Conclusions Weight loss ≥5% in patients with chronic HF was associated with high long‐term mortality, particularly among obese patients with HF .