AimsLung ultrasound (LUS) is a useful tool with which to assess subclinical pulmonary congestion and to stratify the prognosis of patients with heart failure (HF). The aim of this study was to evaluate whether an LUS‐guided follow‐up protocol improves the outcomes of patients with HF.Methods and resultsIn this single‐blind clinical trial, 123 patients admitted for HF were randomized to either a standard follow‐up (n = 62, control group) or a LUS‐guided follow‐up (n = 61, LUS group). The primary endpoint was a composite of urgent visit, hospitalization for worsening HF and death during follow‐up. Visits were scheduled at 14, 30, 90 and 180 days after discharge. Treating physicians were encouraged to modify diuretic therapy in accordance with the number of B‐lines recorded by LUS. The mean ± standard deviation (SD) age of the patients was 69 ± 12 years and 72% were male. The mean ± SD left ventricular ejection fraction was 39 ± 14%. The hazard ratio for the primary outcome in the LUS group was 0.518 [95% confidence interval (CI) 0.268–0.998; P = 0.049], mainly resulting from a decrease in the number of urgent visits for worsening HF. The number of patients needed to treat to avoid an event was 5 (95% CI 3–62). Other secondary endpoints such as N‐terminal pro‐B‐type natriuretic peptide reduction were not achieved. The safety parameters were similar in the two groups. Patients in the LUS group received more loop diuretics [51 (91%) vs. 42 (75%); P = 0.02] and showed an improvement in the distance achieved in the 6‐min walking test [60 m (interquartile range: 29–125 m) vs. 37 m (interquartile range: 5–70 m); P = 0.023].ConclusionsTailored LUS‐guided diuretic treatment of pulmonary congestion in this proof‐of‐concept study reduced the number of decompensations and improved walking capacity in patients with HF. LUS is a non‐invasive, safe and easy‐to‐use technique with potential clinical applicability to guide pulmonary congestion treatment in patients with HF.

Recently published studies have found an impaired immune response after SARS‐CoV‐2 vaccination in solid organ recipients. However, most of these studies have not assessed immune cellular responses in liver and heart transplant recipients. We prospectively studied heart and liver transplant recipients eligible for SARS‐CoV‐2 vaccination. Patients with past history of SARS‐CoV‐2 infection or SARS‐CoV‐2 detectable antibodies (IgM or IgG) were excluded. We assessed IgM/IgG antibodies and ELISpot against the S protein 4 weeks after receiving the second dose of the mRNA‐1273 (Moderna) vaccine. Side effects, troponin I, liver tests and anti‐HLA donor‐specific antibodies (DSA) were also assessed. A total of 58 liver and 46 heart recipients received two doses of mRNA‐1273 vaccine. Median time from transplantation to vaccination was 5.4 years (IQR 0.3–27). Sixty‐four percent of the patients developed SARS‐CoV‐2 IgM/IgG antibodies and 79% S‐ELISpot positivity. Ninety percent of recipients developed either humoral or cellular response (87% in heart recipients and 93% in liver recipients). Factors associated with vaccine unresponsiveness were hypogammaglobulinemia and vaccination during the first year after transplantation. Local and systemic side effects were mild or moderate, and none presented DSA or graft dysfunction after vaccination. Ninety percent of our patients did develop humoral or cellular responses to mRNA‐1273 vaccine. Factors associated with vaccine unresponsiveness were hypogammaglobulinemia and vaccination during the first year after transplantation, highlighting the need to further protect these patients.

ObjectivesThe aim of this study was to analyse baseline characteristics and outcome of patients with heart failure and mid-range left ventricular ejection fraction (HFmrEF, left ventricular ejection fraction (LVEF) 40%–49%) and the effect of 1-year change in LVEF in this group.SettingMulticentre prospective observational study of ambulatory patients with HF followed up at four university hospitals with dedicated HF units.ParticipantsFourteen per cent (n=504) of the 3580 patients included had HFmrEF.InterventionsBaseline characteristics, 1-year LVEF and outcomes were collected. All-cause death, HF hospitalisation and the composite end-point were the primary outcomes.ResultsMedian follow-up was 3.66 (1.69–6.04) years. All-cause death, HF hospitalisation and the composite end-point were 47%, 35% and 59%, respectively. Outcomes were worse in HF with preserved ejection fraction (HFpEF) (LVEF>50%), without differences between HF with reduced ejection fraction (HFrEF) (LVEF<40%) and HFmrEF (all-cause mortality 52.6% vs 45.8% and 43.8%, respectively, P=0.001). After multivariable Cox regression analyses, no differences in all-cause death and the composite end-point were seen between the three groups. HF hospitalisation and cardiovascular death were not statistically different between patients with HFmrEF and HFrEF. At 1-year follow-up, 62% of patients with HFmrEF had LVEF measured: 24% had LVEF<40%, 43% maintained LVEF 40%–49% and 33% had LVEF>50%. While change in LVEF as continuous variable was not associated with better outcomes, those patients who evolved from HFmrEF to HFpEF did have a better outcome. Those who remained in the HFmrEF and HFrEF groups had higher all-cause mortality after adjustment for age, sex and baseline LVEF (HR 1.96 (95% CI 1.08 to 3.54, P=0.027) and HR 2.01 (95% CI 1.04 to 3.86, P=0.037), respectively).ConclusionsPatients with HFmrEF have a clinical profile in-between HFpEF and HFrEF, without differences in all-cause mortality and the composite end-point between the three groups. At 1 year, patients with HFmrEF exhibited the greatest variability in LVEF and this change was associated with survival.