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The prediction of sudden cardiac death (SCD) in heart failure (HF) remains an unmet need. The aim of our study was to assess the prevalence of SCD over 20 years in HF outpatients managed in a Mediterranean multidisciplinary HF Clinic, and to compare the proportion of SCD (SCD/all-cause death) to the expected proportional occurrence based on the validated Seattle Proportional Risk Model (SPRM) score.This prospective observational registry study included 2,772 HF outpatients admitted between August 2001 and May 2021. Patients were included when the cause of death was known and SPRM score was available.Over the 20-year study period, 1,351 (48.7%) patients died during a median follow-up period of 3.8 years (interquartile range 1.6-7.6). Among these patients, the proportion of SCD out of the total of deaths was 13.6%, while the predicted by SPRM was 39.6%. This lower proportion of SCD was observed independently of left ventricular ejection fraction, ischemic etiology, and the presence of an implantable cardiac defibrillator.In a Mediterranean cohort of HF outpatients, the proportion of SCD was lower than expected based on the SPRM score. Future studies should investigate to what extend epidemiological and guideline-directed medical therapy patterns influence SCD.

Myocardial fibrosis may increase vulnerability to poor prognosis in patients with heart failure (HF), even in those patients exhibiting left ventricular reverse remodeling (LVRR) after guideline-based therapies.This study sought to characterize fibrosis at baseline in patients with HF with left ventricular ejection fraction (LVEF)50% by determining serum collagen type I-derived peptides (procollagen type I C-terminal propeptide [PICP] and ratio of collagen type I C-terminal telopeptide to matrix metalloproteinase-1) and to evaluate their association with LVRR and prognosis.Peptides were determined in 1,034 patients with HF at baseline. One-year echocardiography was available in 665 patients. Associations of peptides with 1-year changes in echocardiographic variables were analyzed by multivariable linear mixed models. LVEF was considered improved if it increased by ≥15% or to ≥50% or if it increased by ≥10% to40% in patients with LVEF ≤40%. Cardiovascular death and HF-related outcomes were analyzed in all patients randomized to derivation (n = 648) and validation (n = 386) cohorts.Continuous associations with echocardiographic changes were observed only for PICP. Compared with high-PICP (≥108.1 ng/mL) patients, low-PICP (108.1 ng/mL) patients exhibited enhanced LVRR and a lower risk of HF-related outcomes (P ≤ 0.018), with women and nonischemic patients with HF showing a stronger LVEF increase (interaction P ≤ 0.010). LVEF increase was associated with a better prognosis, particularly in low-PICP patients (interaction P ≤ 0.029). Only patients with both low PICP and improved LVEF exhibited a better clinical evolution than patients with nonimproved LVEF (P 0.001).Phenotyping with PICP, a peptide associated with myocardial fibrosis, may be useful to differentiate patients with HF who are more likely to experience clinical myocardial recovery from those with partial myocardial improvement.

INTRODUCTION AND OBJECTIVES Advanced lipoprotein phenotyping is a better predictor of atherosclerotic cardiovascular risk than cholesterol concentration alone. Lipoprotein profiling in heart failure (HF) is incompletely characterized. We aimed to describe the lipoprotein profile in patients with chronic HF compared with a matched control population. METHODS This cross-sectional study was performed from May 2006 to April 2014 and included ambulatory patients with chronic HF. Lipid concentrations and the size of main lipoprotein fractions (high-density lipoprotein [HDL], low-density lipoprotein [LDL], and very low-density lipoprotein) and the particle concentration of their 3 subfractions (large, medium and small) were assessed using 1H magnetic resonance spectroscopy. RESULTS The 429 included patients with chronic HF were compared with 428 matched controls. Patients with chronic HF had lower total cholesterol and lower mean LDL (1115 vs 1352 nmol/L; P

Background: Real-time remote monitoring of pulmonary artery pressures has previously shown to reduce heart failure (HF) related hospitalisations and to improve quality of life of selected HF patients. The value of CardioMEMS in Southern Europe, where healthcare costs are significantly lower, remains uncertain. Objective: To evaluate the cost-effectiveness of the CardioMEMS HF system in the Spanish healthcare setting. Methodology: This single-centre study included 35 HF patients with a CardioMEMS device (treatment group) and compared them with similar patients receiving standard HF treatment (control group). The Propensity Score Matching method was used and the comparators were found using the variables age, sex, New York Heart Association class, left ventricular ejection fraction, and diabetes mellitus. Cost-effectiveness was measured as the incremental cost per quality-adjusted life year gained. Results: The CardioMEMS HF system outperformed usual management with a net monetary value difference of 2,731€ per patient at 1 year. The incremental cost per quality-adjusted life year gained was 15,896€. Results were consistent in the sensitivity analyses performed. Conclusion: This analysis suggests that remote monitoring of pulmonary artery pressure with CardioMEMS HF system is a cost-effective strategy in the Spanish healthcare setting.

The Nancy team is supported by the RHU Fight-HF, a public grant overseen by the French National Research Agency (ANR) as part of the second 'Investissements d'Avenir' programme (reference: ANR-15-RHUS-0004), by the French PIA project 'Lorraine Université d'Excellence' (reference: ANR-15-IDEX-04-LUE), the ANR FOCUS-MR (reference: ANR-15-CE14-0032-01), ERA-CVD EXPERT (reference: ANR-16-ECVD-0002-02), the Contrat de Plan Etat Lorraine IT2MP, and FEDER Lorraine. Aims: In ambulatory patients with chronic heart failure (HF), congestion and decongestion assessment may be challenging. The aim of this study is to assess the value of lung ultrasound (LUS) in outpatients with HF in characterizing decompensation and recompensation, and in outcomes prediction. Methods and results: Heart failure outpatients attended to establish HF decompensation were included. LUS was blindly performed at baseline (LUS1) and at clinical recompensation (LUS2). B-lines were counted in eight scanned areas. Diagnosis of no HF decompensation vs. right-sided, left-sided, or global HF decompensation, and patients' management were performed by physicians blinded to LUS1. Outcome was the composite of all-cause death or HF-related hospitalization. Two hundred and thirty-three suspicions of HF decompensation were included in 187 patients (71.4 ± 11.3 years, 66.8% men). Mean B-line (LUS1) was 17.6 ± 11.2 vs. 3.7 ± 4.5 for episodes with and without HF decompensation, respectively (P < 0.001). Global HF decompensation showed the highest number of B-lines (20.6 ± 11), followed by left-sided (19.7 ± 11.6) and right-sided (13.5 ± 9.8). B-lines declined to 6.9 ± 6.7 (LUS2) (P < 0.001 vs. LUS1) after treatment, within a mean time of 24.2 ± 23.7 days [median 13.5 days (interquartile range 6-40)]. B-lines were significantly associated with the composite endpoint at 30 days (hazard ratio [HR] 1.04 [95% confidence interval 1.01-1.07], P = 0.02), but not at 60 (P = 0.22) or 180 days (P = 0.54). In multivariable analysis, B-line number remained as an independent predictor of the composite endpoint at 30 days, [HR 1.04 (1.01-1.07), P = 0.014], with a 4% increase risk per B-line added. B-lines correlated significantly with CA125 (R = 0.30, P = 0.001). Conclusions: Lung ultrasound supports the diagnostic work-up of congestion and decongestion in chronic HF outpatients and identifies patients at high risk of short-term events.

Resumen Introduccion y objetivos La utilidad de la ecografia pulmonar (EP) en la insuficiencia cardiaca (IC) aguda esta bien definida, pero no asi en la IC cronica. Este estudio investigo el valor pronostico de la EP en pacientes estables con IC cronica. Metodos Se incluyo a pacientes ambulatorios consecutivos con visita programada en una unidad de IC. La EP se realizo in situ, con los datos clinicos enmascarados, y evaluo 8 areas toracicas. La suma de lineas B en todas las areas pulmonares y los cuartiles de dicha adicion se utilizaron para los analisis de regresion lineal y de Cox. Los objetivos principales fueron el compuesto de muerte por cualquier causa u hospitalizacion por IC y mortalidad por cualquier causa. Resultados Se incluyo a 577 individuos (edad, 69 ± 12 anos; el 72% varones). La media de lineas B fue de 5 ± 6. Durante un seguimiento de 31 ± 7 meses, en 157 pacientes se produjo el resultado compuesto y 111 fallecieron. Tener ≥ 8 lineas B (Q4) doblo el riesgo de padecer el evento compuesto (p Conclusiones La EP identifico a pacientes con IC cronica estable y alto riesgo de muerte u hospitalizacion por IC.

There is an urgent need for cost-effective strategies to promote quality of life in patients with heart failure (HF). Several studies reported benefits in HF prognosis for marine omega-3 fatty acids and plant-based dietary patterns.The aim of this study was to explore whether dietary alpha-linolenic acid (ALA), the main plant omega-3, relates to a better HF prognosis.ALA was determined in serum phospholipids (which reflect long-term dietary ALA intake and metabolism) by gas chromatography in 905 ambulatory patients with HF caused by different etiologies.After a median follow-up of 2.4 years (range: 0.02-3 years), 140 all-cause deaths, 85 cardiovascular (CV) deaths, and 141 first HF hospitalizations (composite of all-cause death and first HF hospitalization, n = 238) were documented. Using Cox regression analyses, we observed that, compared with patients at the lowest quartile of ALA in serum phospholipids (Q1), those at the 3 upper quartiles (Q2-Q4) exhibited a reduction in the risk of composite of all-cause death and first HF hospitalization (HR: 0.61; 95% CI: 0.46-0.81). Statistically significant reductions were observed for all-cause death (HR: 0.58; 95% CI: 0.41-0.82), CV death (HR: 0.51; 95% CI: 0.32-0.80), first HF hospitalization (HR: 0.58; 95% CI: 0.40-0.84), and the composite of CV death and HF hospitalization (HR: 0.58; 95% CI: 0.42-0.79).HF patients with bottom 25% ALA levels in serum phospholipids had a worse prognosis during a mid-term follow-up compared with those with the highest levels. This might be a target population in whom to test dietary ALA-rich interventions to promote quality of life.

Aims: Bendopnea is a clinical symptom of advanced heart failure with uncertain prognostic value. We aimed to evaluate whether bendopnea and the change in oxygen saturation when bending forward (bending oxygen saturation index [BOSI]) are associated with adverse outcomes in ambulatory chronic heart failure (CHF) patients.Methods and results: We prospectively evaluated 440 subjects with symptomatic CHF. BOSI was defined as the difference between sitting and bending oxygen saturation (SpO2). The endpoint was the total number of worsening heart failure (WHF) events (heart failure hospitalization or urgent heart failure visit requiring parenteral diuretic therapy). The mean age was 74 ± 10 years, 257 (58.6%) were male, and 226 (51.4%) had a left ventricular ejection fraction 2 when bending (BOSI 0%), those with BOSI ≥−3% showed an increased risk of WHF events (incidence rate ratio [IRR] 2.16, 95% confidence interval [CI] 1.67–2.79; p < 0.001). In contrast, bendopnea was not associated with the risk of total WHF episodes (IRR 1.04, 95% CI 0.83–1.31; p = 0.705).Conclusions: In ambulatory and stable CHF patients, BOSI ≥−3% and not bendopnea was independently associated with an increased risk of total (first and recurrent) WHF episodes. Awareness of SpO2 while assessing bendopnea may be a useful tool for predicting heart failure decompensations.

The impact of increasing temperatures on renal function in heart failure (HF) outpatients has never been specifically analyzed.We retrieved creatinine and estimated glomerular filtration rate (eGFR) values of all HF outpatients followed at a HF clinic and temperature data from 2002 to 2021. For each patient and each year we averaged values of creatinine, eGFR and monthly temperatures during summer and the rest of the year.The study cohort included 2167 HF patients undergoing 25,865 elective visits, with a median of 14 visits for each patient (interquartile range 7-23). At the first visit, patients (70% men) had an age of 67 ± 13 years, and a left ventricular ejection fraction of 35 ± 14%. Creatinine was 1.25 ± 0.51 mg/dL, and eGFR was 65 ± 25 mL/min/1.73 mThe magnitude of temperature elevation during summer has increased over 20 years. This elevation correlates with the decline in renal function during summer. This might be an example of how global warming is affecting human health.

The role of inflammation in heart failure (HF) has been extensively described, but it is uncertain whether inflammation exerts a different prognostic influence according to etiology. We aimed to examine the inflammatory state in chronic HF by measuring N-acetylglucosamine/galactosamine (GlycA) and sialic acid (GlycB), evolving proton nuclear magnetic resonance biomarkers of systemic inflammation, and explore their prognostic value in patients with chronic HF. The primary end point was a composite of all-cause death and HF readmission. A total of 429 patients were included. GlycB correlated with interleukin-1 receptor-like 1 in the whole cohort (r

Summary Background & aims Nutritional status is an important prognostic factor in patients with heart failure (HF). In a pilot study we previously observed that the Mini Nutritional Assessment Short Form tool (MNA-SF) was the best approach for the screening of nutritional status in HF outpatients over other screening tools. The current study aimed to determine whether the MNA-SF has prognostic value in outpatients with HF and whether the impact of malnutrition differs depending on left ventricular ejection fraction (LVEF). Methods Prospective study performed in outpatients attending a HF clinic at a university hospital. All subjects completed the MNA-SF at study entry. The primary endpoint was all-cause mortality. Secondary end-points were the number of recurrent HF-related hospitalizations and the composite end-point of all-cause death or HF-related hospitalizations. Patients with malnutrition and at risk of malnutrition were merged and considered as having abnormal nutritional status for statistical analysis. Results From October 2016 to November 2017, 555 patients were included (age 69 ± 11.5 years, 71% male, LVEF 44.6 ± 13.2). Abnormal nutritional status was identified in 103 (18.6%) subjects. HF patients with preserved LVEF had a higher proportion of abnormal nutritional status (23%) than patients with HF and mid-range LVEF (HFmrEF) (16.4%) or those with HF with reduced LVEF (HFrEF) (15.9%.). During a mean follow-up of 23.8 ± 6.6 months, 99 patients died (17.8%), 74 were hospitalized due to HF (13.3%) and the composite end-point was observed in 181 (32.6%). In the univariate analysis, abnormal nutritional status was significantly associated with all-cause mortality (p = 0.02) and the composite end-point (p = 0.02) in the total cohort. However, in the multivariate analysis including age, sex, NYHA functional class, BMI, ischemic aetiology, diabetes, hypertension and HF duration, abnormal nutritional status remained significantly associated with all-cause mortality (HR 3.32 [95%CI 1.47–7.52], p = 0.004), and the composite end-point (HR 2.53 [95%CI 1.30–4.94], p = 0.006) only in HFmrEF patients. Patients with abnormal nutritional status suffered double the crude number of recurrent HF-related hospitalizations (16.4 vs. 8.4 per 100 patients-years, p Conclusions The implementation of MNA-SF as a routine screening tool allowed the detection of abnormal nutritional status in almost one out of five ambulatory HF patients. Nutritional status assessed by the MNA-SF was an independent predictor of all-cause death and the composite end-point of all-cause death or HF-related hospitalization in outpatients with HFmrEF. Furthermore, abnormal nutritional status was significantly related to recurrent hospitalizations across the HF spectrum.

Aims Systolic pulmonary artery pressure (SPAP), tricuspid annular plane systolic excursion (TAPSE), and TAPSE/SPAP ratio trajectories are not fully characterized in chronic heart failure (HF). We assessed very long-term longitudinal SPAP, TAPSE and TAPSE/SPAP trajectories in HF patients, and their dynamic changes in outcomes. Methods and results Prospective, consecutive, observational registry of real-life HF patients, performing echocardiography studies at baseline and according to a prospectively structured schedule after 1 year, and then every 2 years, up to 15 years. Pulmonary hypertension (PH) was defined as SPAP ≥40 mmHg; right ventricular dysfunction (RVD) was defined at TAPSE ≤16 mm; and TAPSE/SPAP ratio was dichotomized at 0.36 mm/mmHg. The clinical endpoints were all-cause death, the composite endpoint of mortality or HF hospitalization and the number of recurrent HF hospitalizations. The study cohort included 1557 patients. Long-term SPAP trajectory Loess curves were U-shaped with a nadir at 7 years. TAPSE Loess curves showed a marked rise during the first year, with stabilization thereafter. TAPSE/SPAP ratio Loess splines were similar to the later with a smooth decline towards the end. Patients who died had higher SPAP, lower TAPSE and lower TAPSE/SPAP ratio in the preceding period than survivors. Baseline PH and/or RVD were independently associated with mortality and HF-related hospitalizations, and the persistence of one or both entities at 1 year conferred a worse long-term prognosis. Conclusions Long-term trajectories for SPAP, TAPSE and TAPSE/SPAP ratio are reported in patients with chronic HF. An increasing SPAP and declining TAPSE and TAPSE/SPAP ratio in the preceding period is associated with higher mortality.

We assessed differences in long-term all-cause and cardiovascular (CV) mortality in heart failure (HF) outpatients based on the etiology of HF. Consecutive patients admitted to the HF Clinic from August 2001 to September 2019 (N = 2587) were considered for inclusion. HF etiology was divided into ischemic heart disease (IHD), dilated cardiomyopathy (DCM), hypertensive heart disease, alcoholic cardiomyopathy, drug-induced cardiomyopathy (DICM), valvular heart disease, and hypertrophic cardiomyopathy. All-cause death and CV death were the primary end points. Among 2387 patients included in the analysis (mean age 66.5 ± 12.5 years, 71.3% men), 1317 deaths were recorded (731 from CV cause) over a maximum follow-up of 18 years (median 4.1 years, interquartile range (IQR) 2–7.8). Considering IHD as the reference, only DCM had a lower risk of all-cause death (adjusted hazard ratio (aHR) 0.68, 95% confidence interval (CI) 0.56–0.83, p < 0.001), and only DICM had a higher risk of all-cause death (aHR 1.47, 95% CI 1.02–2.11, p = 0.04). However, almost all etiologies had a significantly lower risk of CV death than IHD. Among the studied HF etiologies, DCM and DICM have the lowest and highest risk of all-cause death, respectively, whereas IHD has the highest adjusted risk of CV death.

Introduction: Although small-sample size studies have shown that basal alterations of estimated glomerular filtration rate (eGFR) are related to short- and mid-term higher mortality in acute heart failure (AHF), there is scarce information on the influence of an altered eGFR on long-term mortality and readmissions. Therefore, this multicenter study sought to investigate the relationship between eGFR on admission for AHF and both long-term mortality and readmissions in a large sample of patients. Methods: We retrospectively evaluated 4,595 patients consecutively discharged after admission for AHF at three tertiary-care hospitals from January 1, 2008, to January 1, 2020. To investigate the effect of eGFR on admission with long-term morbimortality, we stratified the patients according to four eGFR categories: −1·1.73 m−2 (G4 and G5 patients, n = 534), 30–44 mL·min−1·1.73 m−2 (G3b patients, n = 882), 45–59 mL·min−1·1.73 m−2 (G3a patients, n = 1,080), and ≥60 mL·min−1·1.73 m−2 (G1 and G2 patients, n = 2,099). eGFR was calculated by the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation within the first 24 h following admission. Results: At a median follow-up of 2.20 years, multivariate analyses revealed that compared to G1 and G2 patients, G4 and G5 patients exhibited a higher risk of all-cause (HR = 1.15, 95% CI: 01.02–1.30, p = 0.020) and cardiovascular (CV) (HR = 1.20, 95% CI: 1.04–1.39, p = 0.013) mortality. Similarly, multivariate analyses also showed that the lower the eGFR, the higher the risk of readmissions. In fact, compared to G1 and G2 patients, G4 and G5 patients displayed significantly increased incident rate ratios of total all-cause (28%), CV (26%), and HF-related (30%) readmissions. Conclusion: Data from this large study provide evidence that an eGFR below 30 mL·min−1·1.73 m−2 on admission could be an independent predictor for long-term mortality and readmissions in patients with AHF.

This report presents the clinical characteristics, outcomes and complications of all consecutive patients implanted with a long-term mechanical circulatory support device in Spain between 2007 and 2020.Analysis of the Spanish Registry of durable ventricular assist devices (REGALAD) including data form Spanish centers with a mechanical circulatory support program.During the study period, 263 ventricular assist devices were implanted in 22 hospitals. The implanted device was an isolated continuous-flow left ventricular assist device in 182 patients (69%), a pulsatile-flow device (58 isolated left ventricular and 21 biventricular) in 79 (30%), and a total artificial heart in 2 patients (1%). The strategy of the implant was as bridge to heart transplant in 78 patients (30%), bridge to candidacy in 110 (42%), bridge to recovery in 3 (1%) and destination therapy in 72 patients (27%). Overall survival at 6, 12 and 24 months was 79%, 74% and 69%, respectively, and was better in continuous-flow left ventricular assist devices (84%, 80%, and 75%). The main adverse events related to this therapy were infections (37% of patients), bleeding (35%), neurological (29%), and device malfunction (17%).Durable ventricular assist devices have emerged in Spain in the last few years as a useful therapy for patients with advanced heart failure. As in other international registries, the current trend is to use continuous-flow intracorporeal left ventricular devices, which are associated with better results. Adverse events continue to be frequent and severe.

Background Real-life clinical practice has confirmed the value of pulmonary artery (PA) pressure-guided therapy in patients with heart failure (HF) and history of repeated HF hospitalizations (HFH), to greater extent to that reported in the pivotal clinical trial CHAMPION-HF. The value of hemodynamic monitoring in a population of patients with HF and elevated natriuretic peptides, but without recent HFH, is unknown. Objective To assess N-terminal-pro-brain natriuretic peptide (NTproBNP) dynamics before and 6 months after PA pressure sensor implantation. Methods Ten patients managed in a multidisciplinary HF clinic implanted with the CardioMEMS PA pressure sensor were consecutively included from June 2019 to July 2020. Mean age was 63.1±23.5 years, 30% were women, 40% had HF with reduced EF (EF Results Mean daily pressure transmission rate was 92.4±5.1%. During the six-month study period 90% of patients had a change in medication related to PA pressure, with an average of 0.21 [0.17–0.66] changes per patient per month. Mean PA pressure at baseline was 28.5±9.5 mmHg, and decreased by 5.5 mmHg at 6 months (p=0.01) (Figure 1). NTproBNP was also significantly lower six months post CardioMEMS implantation; decreasing from 1696 pg/ml [976–2930] at baseline to 1046 pg/ml [616–2076] after six months (p=0.04) (Figure 2). There was a weak correlation between the change in NTproBNP and the change in mean PA pressure (R2=0.22, p=0.17). Conclusions NTproBNP values were significantly lower 6-months following implantation of a PA pressure sensor to guide HF management. Mean PA pressures were also significantly reduced. Funding Acknowledgement Type of funding sources: Public hospital(s). Main funding source(s): Hospital Universitari Germans Trias i Pujol Figure 1. Change in mean PA pressure over time.Figure 2. Change in NTproBNP after PAP monitoring.

Background Heart failure (HF) is the final stage of many cardiac disorders. Mortality in heart HF remains challenging despite improvement in outcomes proved in clinical trials in HF with reduced ejection fraction and it can be influenced by the aetiology of HF. Purpose To assess differences in long-term mortality (up to 18 years) in a real-life cohort of HF outpatients according to the aetiology of HF. Methods Consecutive patients with HF admitted at the HF Clinic from August 2001 to September 2019 were included. Follow-up was closed at 30.9.2020. HF aetiology was divided into ischemic heart disease (IHD), dilated cardiomyopathy (CM) –including non-compaction CM–, hypertensive CM, alcohol-derived CM, drug-derived CM, valvular disease, hypertrophic CM and others. For the present analysis, this latter group was excluded due to the big heterogeneity and limited number of patients in each subtype of aetiology. All-cause death and cardiovascular death were the primary end-points. Fine & Gray method for competing risk was used for cardiovascular mortality analysis. Results Out of 2387 patients included (age 66.5±12.5 years, 71.3% men, LVEF 35.4%±14.2, mainly in NYHA class II [65.5%] and III [26.5%]), 1317 deaths were recorded (731 from cardiovascular cause) during a maximum follow-up of 18 years (median 4.1 years [IQR 2–7.8] for the total cohort, 5.3 years [IQR 2.6–9.7] for survivors). Figure 1 shows Cox regression multivariable analysis for all-cause death and cardiovascular mortality. Considering IHD aetiology as reference, only dilated CM showed significantly lower risk of all-cause death, and only drug-induced CM showed higher risk of all-cause death. However, when cardiovascular mortality was considered almost all aetiologies showed significant lower risk of cardiovascular death than IHD. Figure 2 shows adjusted survival curves (A) and adjusted incidence curves of cardiovascular death (B) based on HF aetiology. Conclusions After adjusting for multiple prognostic factors among the studied HF aetiologies, dilated CM and drug-related CM showed the lowest and the highest risk of all-cause death, respectively. Patients with IHD showed the highest adjusted risk of cardiovascular death. Funding Acknowledgement Type of funding sources: None.

Background Heart failure (HF) is characterized by alterations in kidney function that are associated with poor prognosis and can be related to the evolution of the disease or induced by medical treatment. High temperatures during summer may result in some degree of dehydration, especially in patients treated with diuretics, and may contribute to transient glomerular filtration rate (eGFR) reduction. Objective To assess creatinine and eGFR changes during summer in ambulatory heart failure patients. Methods Consecutive patients with HF admitted at our HF Clinic (Spain) from August 2001 to December 2020 were included. eGFR was calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula. We included in the analysis creatinine and eGFR values that were assessed at planned visits only, discarding urgent renal function assessments. Creatinine and eGFR values were grouped according to the period of the year (summer [from June to September, both included] vs. the rest of the year). Changes in creatinine and eGFR between the rest of the year and summer for each patient were evaluated using paired samples t-test. Results Out of 37360 creatinine and eGFR values, 25458 were included in the analysis for a total of 2423 patients (median number of observations for each patient: 8, IQR 4–15). Mean creatinine and eGFR were 1.4±1.0 mg/dl and 63.0±27.7 ml/min, respectively. Table 1 shows baseline patient characteristics. Creatinine increased significantly during summer (1.44±0.9 mg/dl vs. 1.48±1.1 mg/dl, p Conclusions In ambulatory HF patients in a Mediterranean area, we found significant worsening of renal function during summer, likely related to an imbalance between water intake and fluid loss. To prevent summer-driven kidney stress, diuretic treatment should be carefully adjusted during the hottest months of the year. Funding Acknowledgement Type of funding sources: None. Table 1

Severe tricuspid regurgitation remains a challenging heart-valve disease to effectively treat with high morbidity and mortality at mid-term. Currently guideline-directed medical treatment is limited to escalating dose of diuretics, and the rationale and timing of open-heart surgery remains controversial. Emerging percutaneous therapies for severe tricuspid regurgitation continue to show promising results in early feasibility studies. However, randomized trial data is lacking. Additionally, many patients are deemed unsuitable for these emerging therapies due to anatomical or imaging constraints. Given the technical simplicity of the bicaval valve implantation (CAVI) technique compared to other transcatheter devices, CAVI is postulated as a suitable alternative for a wide variety of patients affected with severe+ tricuspid regurgitation. In this review we illustrate the current evidence and ongoing uncertainties of CAVI, focusing on the novel CAVI-specific devices.

Background N-terminal pro-brain natriuretic peptide (NT-proBNP) predicts mortality and the development of heart failure (HF) in hypertrophic cardiomyopathy (HCM), however, evidence regarding soluble interleukin-1 receptor-like 1 (ST2) in this population is lacking. Purpose To assess the ST2 and NT-proBNP significance for risk stratification of patients with HCM during long-term follow-up. Methods We prospectively enrolled a cohort of consecutive patients with HCM admitted to an ambulatory HF Unit in a Tertiary University Hospital. All patients had clinical and echocardiographic evaluation and measurement of NT-proBNP and ST2 at inclusion. The primary endpoint was the composite of all-cause death or HF-related hospitalization. Results 103 patients were enrolled, 68% (n=70) males with a median (IQR) age of 60 (50–71) years. The median (IQR) of ST2 was 31.5 (IQR: 24.5 – 40.7) pg/mL. During a median follow-up of 2.5 years, 17 patients had the primary endpoint. Both, NT-proBNP and ST2 (both log-transformed) were associated with the primary endpoint in the univariable analyses (p Conclusions ST2 appears to be a valuable biomarker for the prediction of death and heart failure related hospitalization in patients with HCM, outperforming the prognostic value of NT-proBNP. Future research should delve into this association. Funding Acknowledgement Type of funding sources: None.

Background Right ventricular-pulmonary circulation coupling (RVPAC), which can be measured by the relation between tricuspid annular plane systolic excursion (TAPSE) and systolic pulmonary artery pressure (SPAP) by echocardiography, has been postulated as an independent prognostic factor of hospitalizations and mortality in heart failure (HF) patients. Purpose Our aim was to know the predictors of RVPAC improvement in a chronic HF cohort. Methods Retrospective analysis of a prospectively studied cohort of HF outpatients of different aetiologies attended in a multidisciplinary HF Unit. Prospectively scheduled echo-Doppler studies were performed at first visit and 1 year. A TAPSE/SPAP ratio Results From August 2001 to July 2017, 554 patients with TAPSE and SPAP data in the initial visit were included. Mean follow-up time was 4.6±3.7 years. At first visit 252 (45.5%) patients had RVPAC Conclusions Atrial fibrillation/flutter, increasing SPAP and female gender hamper RVPAC improvement at 1 year in HF patients with baseline TAPSE/SPAP ratio Funding Acknowledgement Type of funding sources: None. Multivariate regression analysis

Rationale The use of sodium-glucose co-transporter 2 inhibitors (SGLT2i) to treat heart failure with preserved ejection fraction (HFpEF) is under investigation in ongoing clinical trials, but the exact mechanism of action is unclear. Here we aimed to use artificial intelligence (AI) to characterize the mechanism of action of empagliflozin in HFpEF at the molecular level. Methods We retrieved information regarding HFpEF pathophysiological motifs and differentially expressed genes/proteins, together with empagliflozin target information and bioflags, from specialized publicly available databases. Artificial neural networks and deep learning AI were used to model the molecular effects of empagliflozin in HFpEF. Results The model predicted that empagliflozin could reverse 59% of the protein alterations found in HFpEF. The effects of empagliflozin in HFpEF appeared to be predominantly mediated by inhibition of NHE1 (Na+/H+ exchanger 1), with SGLT2 playing a less prominent role. The elucidated molecular mechanism of action had an accuracy of 94%. Empagliflozin's pharmacological action mainly affected cardiomyocyte oxidative stress modulation, and greatly influenced cardiomyocyte stiffness, myocardial extracellular matrix remodelling, heart concentric hypertrophy, and systemic inflammation. Validation of these in silico data was performed in vivo in patients with HFpEF by measuring the declining plasma concentrations of NOS2, the NLPR3 inflammasome, and TGF-β1 during 12 months of empagliflozin treatment. Conclusion Using AI modelling, we identified that the main effect of empagliflozin in HFpEF treatment is exerted via NHE1 and is focused on cardiomyocyte oxidative stress modulation. These results support the potential use of empagliflozin in HFpEF. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Instituto de Salud Carlos IIICentro de investigaciόn biomédica en red cardiovascular (CIBERCV) Summary figureTable 1

Altres ajuts: acords transformatius de la UAB Aims: Several heart failure (HF) web-based risk scores are currently used in clinical practice. Currently, we lack head-to-head comparison of the accuracy of risk scores. This study aimed to assess correlation and mortality prediction performance of Meta-Analysis Global Group in Chronic Heart Failure (MAGGIC-HF) risk score, which includes clinical variables + medications; Seattle Heart Failure Model (SHFM), which includes clinical variables + treatments + analytes; PARADIGM Risk of Events and Death in the Contemporary Treatment of Heart Failure (PREDICT-HF) and Barcelona Bio-Heart Failure (BCN-Bio-HF) risk calculator, which also include biomarkers, like N-terminal pro B-type natriuretic peptide (NT-proBNP). Methods and results: A total of 1166 consecutive patients with HF from different aetiologies that had NT-proBNP measurement at first visit were included. Discrimination for all-cause mortality was compared by Harrell's C-statistic from 1 to 5 years, when possible. Calibration was assessed by calibration plots and Hosmer-Lemeshow test and global performance by Nagelkerke's R. Correlation between scores was assessed by Spearman rank test. Correlation between the scores was relatively poor (rho value from 0.66 to 0.79). Discrimination analyses showed better results for 1-year mortality than for longer follow-up (SHFM 0.817, MAGGIC-HF 0.801, PREDICT-HF 0.799, BCN-Bio-HF 0.830). MAGGIC-HF showed the best calibration, BCN-Bio-HF overestimated risk while SHFM and PREDICT-HF underestimated it. BCN-Bio-HF provided the best discrimination and overall performance at every time-point. Conclusions: None of the contemporary risk scores examined showed a clear superiority over the rest. BCN-Bio-HF calculator provided the best discrimination and overall performance with overestimation of risk. MAGGIC-HF showed the best calibration, and SHFM and PREDICT-HF tended to underestimate risk. Regular updating and recalibration of online web calculators seems necessary to improve their accuracy as HF management evolves at unprecedented pace.

Introduction The CardioMEMS device is inserted into the pulmonary artery and allows monitorization of pulmonary artery pressure in heart failure patients. Previous studies have shown a reduction in hospitalizations for heart failure and an improvement in quality of life in the group of patients monitored with the device. Patients and methods Eleven patients managed in a multidisciplinary heart failure clinic implanted with the sensor were consecutively included from June 2019 to February 2020. This is the first experience with a cardioMEMS device published in Spain. Results The device was successfully implanted in all cases without severe complications or sensor failures, allowing precise adjustment of medical treatment that led to very few heart failure readmissions. Discussion Wireless pulmonary artery pressure monitoring will probably become an essential component in the management of selected HF patients.

The use of sodium-glucose co-transporter 2 inhibitors to treat heart failure with preserved ejection fraction (HFpEF) is under investigation in ongoing clinical trials, but the exact mechanism of action is unclear. Here we aimed to use artificial intelligence (AI) to characterize the mechanism of action of empagliflozin in HFpEF at the molecular level. We retrieved information regarding HFpEF pathophysiological motifs and differentially expressed genes/proteins, together with empagliflozin target information and bioflags, from specialized publicly available databases. Artificial neural networks and deep learning AI were used to model the molecular effects of empagliflozin in HFpEF. The model predicted that empagliflozin could reverse 59% of the protein alterations found in HFpEF. The effects of empagliflozin in HFpEF appeared to be predominantly mediated by inhibition of NHE1 (Na+/H+ exchanger 1), with SGLT2 playing a less prominent role. The elucidated molecular mechanism of action had an accuracy of 94%. Empagliflozin's pharmacological action mainly affected cardiomyocyte oxidative stress modulation, and greatly influenced cardiomyocyte stiffness, myocardial extracellular matrix remodelling, heart concentric hypertrophy, and systemic inflammation. Validation of these in silico data was performed in vivo in patients with HFpEF by measuring the declining plasma concentrations of NOS2, the NLPR3 inflammasome, and TGF-beta1 during 12months of empagliflozin treatment. Using AI modelling, we identified that the main effect of empagliflozin in HFpEF treatment is exerted via NHE1 and is focused on cardiomyocyte oxidative stress modulation. These results support the potential use of empagliflozin in HFpEF.