Background: High-flow nasal cannula oxygen therapy (HFNC) has been shown to be a useful therapy in the treatment of patients with Acute Respiratory Distress Syndrome (ARDS), but its efficacy is still unknown in patients with COVID-19. Our objective is to describe its utility as therapy for the treatment of ARDS caused by SARS-CoV-2. Methods: A retrospective, observational study was performed at a single centre, evaluating patients with ARDS secondary to COVID-19 treated with HFNC. The main outcome was the intubation rate at day 30, which defined failure of therapy. We also analysed the role of the ROX index to predict the need for intubation.Results: In the study period, 196 patients with bilateral pneumonia were admitted to our pulmonology unit, 40 of whom were treated with HFNC due to the presence of ARDS. The intubation rate at day 30 was 52.5%, and overall mortality was 22.5%. After initiating HFNC, the SpO2/FiO2 ratio was significantly better in the group that did not require intubation (113.4±6.6 vs 93.7±6.7, p=0.020), as was the ROX index (5.0±1.6 vs 4.0±1.0, p=0.018). A ROX index less than 4.94 measured 2 to 6 h after the start of therapy was associated with increased risk of intubation (HR 4.03 [95% CI 1.18 – 13.7]; p=0.026).Conclusion: High-flow therapy is a useful treatment in ARDS in order to avoid intubation or as a bridge therapy, and no increased mortality was observed secondary to the delay in intubation. After initiating HFNC, a ROX index below 4.94 predicts the need for intubation.

Heart transplantation from donors after the circulatory determination of death (DCDD) is expanding worldwide. Thoraco-abdominal normothermic regional perfusion (TA-NRP) allows the validation and recovery of the DCDD heart, but there is limited evidence on the results of heart transplants performed with this approach. This multicenter, nationwide, prospective study describes the short-term outcomes of adult patients receiving a DCDD heart transplant obtained via TA-NRP followed by static cold storage in Spain. Recipients of hearts from donors after the neurological determination of death (DNDD) were used as controls. The primary outcome was a composite of 1-year all-cause death or severe primary graft failure (PGF). During 2020-2023, 98 adult DCDD and 347 DNDD heart transplants were performed across 11 centers. The primary outcome was met by 21 (21.4%) and 77 (22.2%) patients, respectively (p=0.87). Thirty-day and 1-year survival were 94.9% and 88.8% in the DCDD vs 93.7% and 87.3% in the DNDD group (p=0.70). Severe PGF was observed in 13 (13.3%) vs 52 (15.0%) patients (p=0.67). By inverse probability weighting, the DCDD heart was not associated with the primary outcome (HR 0.97;95%CI 0.58-1.62;p=0.91). In conclusion, adult DCDD heart transplantation based on TA-NRP and static cold storage provides similar short-term outcomes than DNDD heart transplants.

Background: Poor natriuresis has been associated with a poorer response to diuretic treatment and worse prognosis in acute heart failure. Recommendations on how and when to measure urinary sodium (UNa) are lacking. We aim to evaluate UNa quantification after a furosemide stress test (FST) capacity to predict appropriate decongestion during acute heart failure hospitalization. Methods: Patients underwent an FST on day-1 of admission, and UNa was measured 2 hours after, dividing patients into low or high UNa based on the sample median value. A semiquantitative composite congestive score (CCS; 0–9) and NT pro-BNP (N-terminal pro-B-type natriuretic peptide) quantification were assessed before the FST and at day 5 after the FST. Results: Median UNa after FST in the 65 patients included was 113 (97–122) mmol/L. At day 5, a lower proportion of patients with a low UNa reached a 30% decrease in NT-proBNP levels (21 [66%] for low UNa versus 31 [94%] for high UNa; P =0.005) and an appropriate grade of decongestion (CCS<3) (20 [62%] for low UNa versus 32 [97%] for high UNa; P 83 mmol/L 2 hours after FST had a 96% sensitivity to predict an NT-proBNP reduction ≥30% and 95% to predict a CCS<3 at day 5. Low UNa patients presented a lower cumulative diuresis and weight loss and presented more often with prolonged hospitalization, worsening heart failure, and readmission because of acute heart failure or death at 6 months. Conclusions: Low natriuresis after an FST identified patients at a higher risk of an inadequate diuretic response and an inappropriate decongestion. FST-guided diuretic treatment might help to improve decongestion, shorten hospitalizations, and to reduce adverse outcomes.

Aims The outpatient diuretic dose is a marker of diuretic resistance and prognosis in chronic heart failure (HF). Still, the impact of the preadmission dose on diuretic efficiency (DE) and prognosis in acute HF is not fully known. Methods and results We conducted an observational and prospective study. All patients admitted for acute HF treated with intravenous diuretic and at least one criterion of congestion on admission were evaluated. Decongestion [physical examination, hemoconcentration, N-terminal pro-brain natriuretic peptide (NT-proBNP) change, and lung ultrasound], DE (weight loss and urine output per unit of 40 mg furosemide), and urinary sodium were monitored on the fifth day of admission. DE was dichotomized into high–low based on the median value. A multivariate Cox regression analysis was conducted to find predictors of HF readmission or mortality. A total of 105 patients were included between July 2017 and July 2019. Mean age was 74.5 ± 12.0 years, 64.8% were male, 33.3% had de novo HF, and mean left ventricular ejection fraction was 46 ± 17%. Median follow-up was 26 [15–35] months. Low DE based on weight loss was associated with a higher previous dose of furosemide (odds ratio [OR] 1.01 [1.00–1.02]), thiazide treatment before admission (OR 9.37 [2.19–40.14]), and lower diastolic blood pressure (OR 0.95 [0.91–0.98]) in the multivariate regression model. Only previous dose of furosemide (OR 1.01 [1.00–1.02]) and haemoglobin at admission (OR 0.76 [0.58–0.99]) were associated with low DE based on urine output in the multivariate analysis. The correlation between the previous dose of furosemide and DE based on weight loss was poor (r = −0.12; P = 0.209) and with DE based on urine output was weak to moderate (r = −0.33; P < 0.001). Low DE based on weight loss and urine output was associated with lesser decongestion measured by NT-proBNP (P = 0.011; P = 0.007), hemoconcentration (P = 0.006; P = 0.044), and lung ultrasound (P = 0.034; P = 0.029), but not by physical examination (P = 0.506; P = 0.560). Survival and event-free survival in acute decompensated HF (ADHF) were lower than in de novo HF; a preadmission dose of furosemide > 80 mg in ADHF identified patients with particularly poor prognosis (log-rank < 0.001). In ADHF, the preadmission dose of furosemide (hazard ratio [HR] 1.34 [1.08–1.67] per 40 mg) and NT-proBNP at admission (HR 1.03 [1.01–1.06] per 1000 pg/mL) were independently associated with mortality or HF readmission in the multivariate Cox regression analysis. Conclusions The outpatient dose of furosemide before acute HF admission predicts DE and must be taken into account when deciding on the initial diuretic dose. In ADHF, the outpatient dose of furosemide can predict long-term prognosis better than DE during hospitalization.

Background/Objectives: Heart failure (HF) is a leading cause of morbidity and mortality worldwide, with a higher prevalence among older adults. Iron deficiency (ID), affecting up to 50% of HF patients, is closely linked to chronic inflammation, exacerbating HF outcomes. This review aims to explore the interplay between inflammation, ID, and HF, focusing on older patients, and to identify therapeutic gaps and emerging treatment strategies. Methods: A comprehensive review of the literature was conducted, emphasizing the pathophysiological mechanisms of inflammation and ID in HF, the challenges of current diagnostic criteria, and the limitations of available treatments. Emerging pharmacological and diagnostic approaches were analyzed. Results: Chronic inflammation in HF, particularly in older adults, promotes functional ID through elevated hepcidin levels, impairing iron availability and worsening anemia. Current diagnostic criteria, relying heavily on ferritin, often misclassify ID due to inflammation. Intravenous (IV) iron therapy shows clinical benefits in patients with <50% left ventricular ejection fraction (LVEF), but the evidence is limited in heart failure with preserved ejection fraction (HFpEF). Emerging therapies, such as Sodium-Glucose Cotransporter-2 inhibitors (SGLT2is) and prolyl hydroxylase inhibitors like Roxadustat, offer promising avenues to improve iron metabolism and outcomes. Conclusions: ID and inflammation significantly impact HF progression, particularly inolder adults. Refining diagnostic criteria and exploring innovative therapies are critical to addressing these challenges. Future research should prioritize personalized approaches targeting inflammation and ID, especially in underrepresented populations, such as HFpEF and elderly patients.

Telemonitoring through multiple variables measured on cardiac devices has the potential to improve the follow-up of patients with heart failure. The HeartLogic algorithm (Boston Scientific), implemented in some implantable cardiac defibrillators and cardiac resynchronisation therapy, allows monitoring of the nocturnal heart rate, respiratory movements, thoracic impedance, physical activity and the intensity of heart tones, with the aim of predicting major clinical events. Although HeartLogic has demonstrated high sensitivity for the detection of heart failure decompensations, its effects on hospitalisation and mortality in randomised clinical trials has not yet been corroborated. This review details how the HeartLogic algorithm works, compiles available evidence from clinical studies, and discusses its application in daily clinical practice.