ESC Heart Failure最新文献

Introduction: To externally validate an FDA-approved artificial intelligence (AI) tool for detecting heart failure with preserved ejection fraction (HFpEF) using echocardiographic video clips, comparing its performance to invasive haemodynamic criteria in a real-world referral cohort with unexplained dyspnoea.

Methods: We retrospectively analysed 47 patients who underwent transthoracic echocardiography (TTE) and right heart catheterization (RHC), including 28 with both rest and exercise haemodynamics. The AI model evaluated apical 4-chamber video data and classified outputs as HFpEF, no HFpEF, or non-diagnostic, without any other clinical data. The primary outcome was invasively defined HFpEF: pulmonary capillary wedge pressure (PCWP) ≥15 mmHg at rest or ≥25 mmHg with exercise. Secondary analysis used a PCWP/cardiac output (CO) slope >2 mmHg/L/min. We assessed sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV).

Results: Among patients with exercise RHC (n = 28), 71% met haemodynamic HFpEF criteria. The AI tool demonstrated sensitivity of 30%, specificity of 88%, PPV of 86%, and NPV of 33%. Using the PCWP/CO slope (n = 25), specificity and PPV were 100%, sensitivity 27%, and NPV 16%. AI-positive patients had significantly higher resting PCWP (20 vs 15 mmHg, P = .029), mean PA pressure (29 vs 24 mmHg, P = .02), and PVR (2.1 vs 1.3 WU, P = .002). In patients with indeterminate H2FPEF scores (n = 25), the AI correctly identified 80% of those with invasively confirmed HFpEF. Model performance was consistent across TTE-RHC intervals <365 and <90 days.

Conclusions: This AI model demonstrated high specificity and positive predictive value (PPV) for detecting HFpEF, reliably identifying patients with more advanced haemodynamic abnormalities. Its performance remained robust across variable intervals between transthoracic echocardiography (TTE) and right heart catheterization (RHC), and in patients with indeterminate clinical scores. Due to limited sensitivity, the tool is best utilized to enrich identification of patients with clearly abnormal haemodynamics rather than to exclude HFpEF, particularly in early or borderline cases. While broader use as a screening tool is promising, prospective validation studies are necessary to confirm its utility in general populations.

It has become increasingly recognized that heart failure with a preserved ejection fraction (HFpEF) results from an inflammatory process, congestion, and metabolic dysbiosis rather than an intrinsic structural heart abnormality. Recent studies have highlighted the close link between the heart, the liver, and the pancreas, which are organically connected via the same inflammatory processes and pathways. Liver congestion and fibrosis are responsible for the inflammatory process and the lack of metabolic adaptation, whereas pancreatic ischaemia and insufficiency of the exocrine glands aggravate malnutrition and cachexia, worsening the heart condition. Acute pancreatitis may cause heart failure and arrhythmia through injury and systemic inflammatory response syndrome (SIRS), an inflammatory process mediated by the cytokines released during the injury process. Recognition of this hepato-pancreato-cardiac axis offers a paradigm shift towards integrated management of HFpEF, emphasizing anti-inflammatory, metabolic, and haemodynamic interventions. Future research integrating multi-organ imaging, inflammatory biomarkers, and therapeutic trials such as GLP-1 receptor agonists, SGLT2 inhibitors, and cytokine blockers will be critical to disrupt this tri-organ inflammatory circuit and improve outcomes in HFpEF.

Aims: Cardiogenic shock (CS) represents an ominous complication of acute myocardial infarction (AMI) with a mortality rate exceeding 50%. The aim of the study was to evaluate current management, outcomes, and risk factors of mortality of AMI-related CS.

Methods: This snapshot registry evaluated all patients with AMI-related CS hospitalized in 9 cardiology centres across Poland between January and December 2023. The inclusion criteria involved CS defined as prolonged (>20 min) hypotension with signs of peripheral hypoperfusion and a diagnosis of AMI qualified for urgent coronary angiography. The primary endpoint was in-hospital mortality.

Results: The study comprised 141 patients (72.3% men; mean age was 69.2 [14] years). The majority of patients were in Society for Cardiovascular Angiography and Interventions class C (n = 71, 50.4%), followed by class D (n = 46, 32.6%) and class E (n = 24, 17.0%). Percutaneous coronary intervention was performed in 133 cases (94.3%) while coronary artery bypass graft in 5 (3.5%). Mechanical circulatory support (MCS) was used in 33 patients (23.4%) and involved intra-aortic balloon pump (n = 26, 18.4%), Impella CP (n = 6, 4.3%), Impella 5.5 (n = 2, 1.4%), and veno-arterial extracorporeal membrane oxygenation (n = 10, 7.1%). In-hospital mortality rate was 47.5% (n = 67), while 30-day mortality was 51.8% (n = 73). Cox proportional hazards model showed that non-ST-elevation AMI (HR = 2.38, 95%CI: 1.19-4.75), lack of the need for antibiotic therapy (HR = 2.61, 95%CI: 1.26-5.39), elevated lactates (unit HR per 1 mmol/l = 1.19, 95%CI: 1.11-1.27) and age (unit HR = 1.05; 95%CI: 1.02-1.07) were independent predictors of in-hospital mortality.

Conclusions: Short-term mortality rate of AMI-related CS still amounts to 50%, which advocates in favour of further research evaluating the true role of MCS in this population.

Introduction: Left ventricular assist device (LVAD) therapy is an established treatment modality for patients with advanced heart failure with reduced ejection fraction (HFrEF). This study aimed to evaluate the long-term outcomes of patients implanted with a Heartmate 3 LVAD.

Methods: We included 176 patients who were implanted with a HeartMate 3 LVAD at the University Medical Center Groningen (UMCG) between 2016 and 2025. The primary outcome of interest was on device survival. Secondary outcomes were major adverse events (including device dysfunction, major bleeding, device-related infections, ventricular tachycardia, cerebrovascular events and heart failure hospitalizations) stratified according to LVAD treatment strategy.

Results: Mean age at implantation was 56 ± 11 years, and 26% were female. The initial device strategy was bridge to transplant (BTT) in 24%, destination therapy (DT) in 34%, and bridge to decision (BTD) in 42%. Overall survival was 87%, 82% and 61% at 1, 2 and 5 years respectively. Kaplan-Meier analysis suggested longer on-device survival in BTT compared with DT patients, although interpretation is limited by differential censoring due to transplantation. Device-related infections and heart failure hospitalizations were the most common major adverse events, occurring 0.29 and 0.18 events per patient-year at risk, respectively. Device dysfunction and cerebrovascular events were rare, with incidence rates of 0.04 and 0.02 events per patient-year at risk, respectively. No LVAD pump thrombosis events were recorded during this time period.

Conclusion: Long-term survival on HeartMate 3 LVAD support exceeded 60% at 5 years in this single-centre cohort. While adverse events such as device related infections and heart failure hospitalizations continue to pose a substantial clinical challenge, the incidence of thrombotic complications was low, underscoring improvement in clinical outcomes with current generation centrifugal LVAD devices.

Polypharmacy is highly prevalent among patients with heart failure (HF), due to multimorbidity and guideline-directed pharmacotherapy. While polypharmacy aims to optimize management, it can increase the risk of drug-drug interactions and adverse drug events, which may compromise clinical outcomes. However, the evidence regarding the relationship between polypharmacy and cardiovascular (CV) outcomes in HF populations remains limited. The aim of this study was to determine the association between polypharmacy and adverse CV outcomes among patients with HF. A systematic review and meta-analysis were conducted to evaluate the association between polypharmacy and adverse CV outcomes in HF. Relevant studies were identified through searches of PubMed, Embase, and Web of Science. The primary outcomes included a composite CV endpoint and its individual components. Effect estimates, based on comparisons between the highest and lowest levels of polypharmacy, were pooled using random-effects models. Ten studies including 30 115 patients with HF were analyzed. Compared with those without polypharmacy, patients with polypharmacy had a significantly increased risk of the composite CV endpoint (HR: 1.27; 95% CI: 1.15-1.39). Notably, polypharmacy was linked to a higher risk of HF hospitalization (HR: 1.42; 95% CI: 1.28-1.56). No significant associations were found for CV death (HR: 1.07; 95% CI: 0.81-1.41) or all-cause mortality (HR: 1.05; 95% CI: 0.88-1.25). Polypharmacy in patients with HF was associated with increased risk of composite CV outcome and HF hospitalization, reflecting the complexity of managing multiple medications. These findings underscore the need for individualized medication reviews to minimize inappropriate prescribing and ensure continued delivery of evidence-based therapies. PROSPERO Registration Number CRD420251110556.

Introduction: Greater sodium avidity in acute heart failure (AHF) is associated with worse outcomes, but whether kidney tubule injury is associated with sodium avidity and impaired diuretic responsiveness remains underexplored.

Methods: We evaluated 339 participants from the ROSE-AHF trial, which enrolled patients hospitalized for AHF with kidney dysfunction and randomized them to the dopamine, nesiritide, or placebo group. Urinary kidney injury molecule-1 (KIM-1), N-acetyl-β-D-glucosaminidase (NAG), and neutrophil gelatinase-associated lipocalin (NGAL) were measured at enrolment. Associations between these biomarkers and urinary sodium (uNa) concentration at baseline, fractional excretion of sodium (FeNa), as well as total uNa output and urine output over 72-h were assessed using multivariable regression models.

Results: Higher KIM-1 and NAG values at baseline were associated with lower uNa concentration at baseline [-6.1% (-8.5%, -3.7%), P < 0.001 and -5.9% (-9.2%, -2.6%), P & .001, respectively, per two-fold increase in each biomarker]. Higher baseline KIM-1 and NAG were also associated with lower FeNa [-6.1% (-8.5%, -3.6%), P < .001 and -5.2% (-8.6%, -3.6%), P = 0 .001, respectively, per two-fold increase in each biomarker]. Higher baseline KIM-1 was associated with lower total uNa excretion over 72-h [-3.6% (-6.8%, -0.2%), P = 0.037 per two-fold increase]. None of the biomarkers were associated with urine output over 72-h.

Conclusion: Kidney tubular injury, as assessed by urine KIM-1 and NAG, is associated with greater sodium avidity and higher KIM-1 is associated with impaired diuretic responsiveness in AHF.