Aim: Patients with advanced heart failure (AHF) who are not candidates to advanced therapies have poor prognosis. Some trials have shown that intermittent levosimendan can reduce HF hospitalizations in AHF in the short term. In this real-life registry, we describe the patterns of use, safety and factors related to the response to intermittent levosimendan infusions in AHF patients not candidates to advanced therapies. Methods and results: Multicentre retrospective study of patients diagnosed with advanced heart failure, not HT or LVAD candidates. Patients needed to be on the optimal medical therapy according to their treating physician. Patients with de novo heart failure or who underwent any procedure that could improve prognosis were not included in the registry. Four hundred three patients were included; 77.9% needed at least one admission the year before levosimendan was first administered because of heart failure. Death rate at 1 year was 26.8% and median survival was 24.7 [95% CI: 20.4–26.9] months, and 43.7% of patients fulfilled the criteria for being considered a responder lo levosimendan (no death, heart failure admission or unplanned HF visit at 1 year after first levosimendan administration). Compared with the year before there was a significant reduction in HF admissions (38.7% vs. 77.9%; P < 0.0001), unplanned HF visits (22.7% vs. 43.7%; P < 0.0001) or the combined event including deaths (56.3% vs. 81.4%; P < 0.0001) during the year after. We created a score that helps predicting the responder status at 1 year after levosimendan, resulting in a score summatory of five variables: TEER (+2), treatment with beta-blockers (+1.5), Haemoglobin >12 g/dL (+1.5), amiodarone use (−1.5) HF visit 1 year before levosimendan (−1.5) and heart rate >70 b.p.m. (−2). Patients with a score less than −1 had a very low probability of response (21.5% free of death or HF event at 1 year) meanwhile those with a score over 1.5 had the better chance of response (68.4% free of death or HF event at 1 year). LEVO-D score performed well in the ROC analysis. Conclusion: In this large real-life series of AHF patients treated with levosimendan as destination therapy, we show a significant decrease of heart failure events during the year after the first administration. The simple LEVO-D Score could be of help when deciding about futile therapy in this population.

The treatment of congestion in heart failure (HF) is a challenge despite the therapeutic arsenal available. The aim was to analyze the different combinations of diuretics used to resolve congestion in patients admitted for decompensated HF and to define clinical profiles according to these treatments. Single-centre study of 1,559 patients admitted for decompensated HF between 2016 and 2020. Patients were grouped according to the diuretic combination that led to clinical stabilisation and discharge from the hospital: 1) Loop diuretic. 2)Loop diuretic+distal tubule (antialdosterone±thiazides). 3) Loop diuretic+distal+proximal tubule (acetazolamide±SGLT2 inhibitor). 4) Loop diuretic+distal tubule+collecting duct (tolvaptan). 5) Loop diuretic+distal+proximal+collecting duct. Based on these diuretic combinations, profiles with clinical, analytical and echocardiographic differences were established. There were more previous hospitalizations in groups 4 and 5 (p=0.001) with a predominance of pulmonary congestion in profiles 1 and 2 and systemic congestion in 3, 4, and 5. Creatinine and CA125 were higher in profiles 4 and 5 (p=0.01 and p=0.0001), with no differences in NT-proBNP. Profiles 4 and 5 had a higher proportion of dilatation and depression of right ventricular (p=0.0001) and left ventricular (p=0.003) function. Diuretic therapy-defined groups then proved to also differ in clinical characteristics. The diuretic treatment used identifies 5 clinical profiles according to the degree of congestion, renal function, CA125, and right ventricular functionality. These profiles would guide the best diuretic treatment on admission.

This study aims to analyze whether NT-proBNP at admission and discharge in de novo heart failure (HF) with reduced ejection fraction (HFrEF) is associated with myocardial recovery. This is a prospective observational study in two centers. Patients admitted with de novo HFrEF between 2021 and 2023 were included. HF with improved ejection fraction (HFimpEF) was defined as an improvement of at least 10 points with an ejection fraction >40%. Of the 248 patients who were included, 63.3% met HFimpEF criteria at follow-up, with no differences in age or gender. There were no differences in NT-proBNP at admission, but there were at discharge, where its value was inversely associated with myocardial recovery (OR 0.99 for each increase in the square root of NT-proBNP, 95% CI 0.98–0.99, p = 0.048). An NT-proBNP > 10,000 pg/mL at discharge was independently associated with reduced ventricular recovery (OR 0.28, 95% CI 0.07–0.94, p = 0.043). A smaller reduction in NT-proBNP during admission decreased the probability of recovery (OR 0.13, 95% CI 0.03–0.61, p = 0.010). In conclusion, in admissions for de novo HFrEF, NT-proBNP at discharge is inversely associated with myocardial recovery; a level > 10,000 pg/mL is an independent predictor for a lack of recovery, while a greater reduction increases the likelihood of recovery.

This study aims to analyze the factors associated with the lack of carbohydrate antigen 125 (CA-125) elevation in cases of acute heart failure (HF) decompensation. This retrospective study was conducted on 3167 consecutive patients admitted for acute HF in the cardiology department of a referral hospital (June 2019 to June 2024). Admissions from outpatient clinics (n: 1018) and transfers from other hospitals (n: 752) were excluded. The variables of interest included clinical, echocardiographic, therapeutic, and analytical factors. Low CA-125 levels were defined as values ≤ 50 U/mL. A total of 1397 patients were included, of whom 515 had normal CA-125 levels and 882 had elevated levels. Clinically, independent predictors of low CA-125 were sinus rhythm on electrocardiogram (OR: 1.42, 95% CI: 1.12–1.64; p: 0.003) and sleep apnea–hyponpnea syndrome (OR: 1.76, 95% CI: 1.15–2.70; p: 0.009). Echocardiographically, inferior vena cava collapse greater than 50% with inspiration was associated with low CA-125 (OR: 1.78, 95% CI: 1.19–2.69; p = 0.005), as well as with non-severe right ventricular dysfunction. (OR: 2.42; IC95%: 1.39–4.20; p: 0.002). Analytically, elevated NT-proBNP levels were associated with elevated CA-125 levels (OR: 0.99; IC95%: 0.99–0.99; p: 0.006). Survival was higher in the group with CA-125 ≤ 50 U/mL (p: 0.019). Conversely, as CA-125 values increased, mortality also rose. In conclusion, the absence of CA-125 elevation in patients admitted for acute HF is associated with sinus rhythm, sleep apnea–hyponpnea syndrome, low NT-proBNP levels, and inferior vena cava collapse greater than 50% with inspiration.

Background/Objectives: Patients diagnosed with decompensated congestive heart failure (HF) often have elevated CA-125 levels, attributed to systemic congestion. However, a subgroup of patients presents with normal CA-125 levels. The primary objective of this study was to characterize the clinical, analytical, and echocardiographic profiles of patients admitted for decompensated congestive HF according to their CA-125 levels. The secondary objective was to analyze mortality after discharge. Methods: We conducted a retrospective study of patients hospitalized for a decompensated congestive HF episode. Recruitment was consecutive over more than 4 years (December 2019–June 2024), with 3151 patients recruited. Scheduled admissions, transfers from other hospitals, pulmonary congestion patterns, mixed patterns, and low output were the exclusion criteria. The final number of patients included was 166, all with an isolated systemic congestion pattern: CA-125 ≤ 50 U/mL: 38, and CA-125 > 50 U/mL: 128. Results: The comparative analysis between the groups showed that patients with CA-125 ≤ 50 U/mL were more often women (p < 0.05). They also had lower bilirubin and GOT/AST levels (p < 0.05). The percentage of patients with a preserved left ventricular ejection fraction (≥50%) was higher in the CA-125 ≤ 50 U/mL group (p < 0.05). The right ventricular (RV) size and inferior vena cava (IVC) were enlarged in both groups but with no significant differences (p < 0.05). However, the degree of RV dysfunction was greater in the CA-125 > 50 U/mL group, while the proportion of patients with inspiratory collapse of the IVC was higher in the CA-125 ≤ 50 U/mL group (p < 0.05). Survival curves differed from the first month and throughout the follow-up, with higher mortality in the CA-125 > 50 U/mL group. Thus, the probability of being alive at the end of the follow-up was over 50% in the CA-125 ≤ 50 U/mL group, while in the CA-125 > 50 U/mL group, it was around 25% (p < 0.05). Conclusions: The proportion of patients with decompensated congestive HF and systemic congestion who present with a low CA-125 level is close to 25%. These patients are mostly women with a preserved ejection fraction and inspiratory collapse of the IVC of >50%. Moreover, they have a higher survival rate, so a low CA-125 could help identify a subgroup of patients with a better prognosis.

Background. This study aims to determine whether the administration of ferric carboxymaltose (FCM) in patients with acute heart failure (AHF) and iron deficiency (ID) improves morbidity and mortality. Methods. We studied 890 consecutive patients admitted for AHF. Patients were divided into six groups according to reduced left ventricular ejection fraction (HFrEF) or preserved (HFpEF), presence of ID, and administration of FCM. Emergency visits, re-admissions, and all-cause mortality were assessed at 6 months. Results. The overall prevalence of ID was 91.2%. In the HFrEF group, no differences were found in isolated events when patients with untreated vs. treated ID were compared, while differences were found in the combined event rate (p = 0.049). The risk calculation showed an absolute risk reduction (ARR) of 10% and relative risk reduction (RRR) of 18%. In HFpEF there was a positive trend with regard to the combined event (p = 0.107), with an ARR of 9% and an RRR of 15%. The number of patients we needed to treat to prevent a combined event was 10.5 in HFrEF and 10.8 in HFpEF. Conclusions. FCM in AHF reduced the combined event rate of emergency visits, re-admission, and all-cause death at 6 months in HF with left ventricular ejection fraction <50%, and showed a positive trend in HFpEF.