ESC Heart Failure最新文献

Aims: Cardiac implantable electrical devices such as cardiac resynchronization therapy with defibrillator (CRT-Ds) or cardiac contractility modulation (CCMs) are therapy options for patients with symptomatic heart failure (HF) and reduced left ventricular ejection fraction (LVEF) despite optimal medical treatment. As yet, a comparison between both devices has not been performed.

Methods and results: The Mannheim Cardiac Resynchronization Therapy Registry (MARACANA) and the Mannheim Cardiac Contractility Modulation Observational Study (MAINTAINED) included all patients who received CRTs or CCMs in our medical centre between 2012 and 2021. For the present analysis, we retrospectively compared patients provided with either CRT-Ds (n = 220) or CCMs with additional defibrillators (n = 105) regarding New York Heart Association classification (NYHA), LVEF, tricuspid annular plane systolic excursion (TAPSE), QRS-width and other HF modification aspects after 12 months. Before implantation, CCM patients presented with lower LVEF (23.6 ± 6.2 vs. 26.3 ± 6.5%) and worse NYHA (3.03 ± 0.47 vs. 2.81 ± 0.48, both P < 0.05), compared with CRT-D patients. Follow-up improvements in NYHA (2.43 ± 0.67 vs. 2.28 ± 0.72), LVEF (30.5 ± 10.7 vs. 35.2 ± 10.5%) and TAPSE (17.2 ± 5.2 vs. 17.1 ± 4.8 to 18.9 ± 3.4 vs. 17.3 ± 3.6 mm, each P < 0.05) were comparable. The intrinsic QRS-width was stable with CCM (109.1 ± 18 vs. 111.7 ± 19.7 ms, P > 0.05), while the paced QRS-width with CRT-D after 12 months was lower than intrinsic values at baseline (157.5 ± 16.5 vs. 139.2 ± 16 ms, P < 0.05). HF hospitalizations occurred more often for CCM than CRT-D patients (45.7 vs. 16.8%/patient years, odds ratio 4.2, P < 0.001).

Conclusions: Chronic heart failure patients could experience comparable 12-month improvements in functional status and ventricular reverse remodelling, with appropriately implanted CCMs and CRT-Ds. Differences in HF hospitalization rates may be due to the more advanced HF of CCM patients at implantation.

Aims: Sodium excretion is a well-defined marker used to assess diuretic response in acute heart failure (AHF). Despite a strong pathophysiological background, the role of urine chloride excretion has not been described and established yet. We aimed to evaluate chloride trajectory during intensive diuretic treatment in AHF patients and examine its potential role in predicting poor diuretic response.

Methods: The study was conducted on 50 AHF patients. Participants were included within the first 36 h of hospitalization. They received furosemide dose adjusted for body weight (half in bolus, half in 2 h infusion). Post-diuretic hourly urine collection with biochemical analysis was performed.

Results: In general, the concentrations of urine chloride (uCl^-) and sodium (uNa⁺) at the baseline samples exhibited a comparable level (71 ± 39 vs. 70 ± 44 mmol/L, respectively; P = 0.99), but across all post-furosemide study timepoints, uCl^- remained significantly higher than uNa⁺ since 1 to 6 h of the study. In this course, both ions (uCl^- and uNa⁺) reached peak values in 2 h (114 ± 28 vs. 97 ± 34 mmol/L, respectively; P < 0.01). The pattern of uCl^- dominance over uNa⁺ concentration was also observed in separate analyses of patients naïve to furosemide and those chronically exposed to furosemide. Regardless of these patterns, naïve to furosemide individuals excreted more ions (both uCl^- and uNa⁺) than chronically exposed patients at all timepoints. Additionally, a strong, linear correlation between uCl^- and uNa⁺ was observed in each post-furosemide timepoint (the strongest in 1 h r = 0.87; P < 0.001). Both interdependent ions concentration was almost parallel when analysed in chronic furosemide users and those naïve to furosemide separately [uCl^- = 0.85 * uNa⁺ + 28.82, P < 0.001, R² = 0.83 for chronic furosemide users, and uCl^- = 0.72 * uNa⁺ + 41.55, P < 0.001, R² = 0.65 for naïves to furosemide (linear regression model)]. Moreover, uCl^- (with cutoff point: 72 mmol/L) was a satisfactory predictive factor for poor diuretic response (<100 mL/h in 6 h since the beginning of furosemide infusion) [odds ratio (OR) 95% confidence interval (CI): 39.0 (3.8-405.00)]. It presented those properties also after adjusting for urine creatinine [cutoff point: 0.296 mmol/mg-OR (95% CI): 81.0 (8.0-816.0)].

Conclusions: Urine chloride and sodium are highly interrelated during decongestion of AHF patients. The uCl^- (cutoff 72 mmol/L) exhibits better prognostic abilities to identify poor diuretic response than uNa⁺.

Aims: We aimed to determine the use of sodium-glucose cotransporter 2 inhibitors (SGLT2is) and to identify clinical factors associated with their use in patients with heart failure (HF) in a real-life setting.

Methods: Real-world data on Empagliflozin and Dapagliflozin use in patients with HEART failure: The RED-HEART study is a multicentre, cross-sectional and observational study that included HF patients in the outpatient setting regardless of ejection fraction from 19 cardiology centres between August 2023 and December 2023.

Results: The study population consisted of 1923 patients with HF, predominantly men (61.2%), with a median age of 66 (range: 19-101) years. Overall, 925 patients (48.1%) were receiving SGLT2is. Among the study population, 22.1% had HF with preserved ejection fraction, 21.5% had HF with mildly reduced ejection fraction, 56.4% had HF with reduced ejection fraction and the use of SGLT2is was 42.0%, 47.9% and 50.6% in each group, respectively (P = 0.012). The use of SGLT2is was 76.6% in patients with HF and diabetes, 19.8% in patients with HF and chronic kidney disease and 26.8% in patients without diabetes and chronic kidney disease (P < 0.001). Higher education level [odds ratio (OR): 1.80; 95% confidence interval (CI): 1.06-3.05; P = 0.027], higher household income (OR: 3.46; 95% CI: 1.27-9.42; P = 0.015), New York Heart Association functional class IV (OR: 2.72; 95% CI: 1.16-6.35; P = 0.021), diabetes (OR: 9.42; 95% CI: 6.72-13.20; P < 0.001), the use of angiotensin receptor-neprilysin inhibitors (ARNis) (OR: 4.09; 95% CI: 2.39-7.01; P < 0.001), the use of mineralocorticoid receptor antagonists (MRAs) (OR: 2.02; 95% CI: 1.49-2.75; P < 0.001), the use of loop diuretics (OR: 1.62; 95% CI: 1.18-2.22; P = 0.003) and the use of thiazide diuretics (OR: 1.72; 95% CI: 1.30-2.29; P < 0.001) were independently associated with the use of SGLT2is. Conversely, atrial fibrillation (OR: 0.63; 95% CI: 0.45-0.88; P = 0.008), chronic kidney disease (OR: 0.53; 95% CI: 0.37-0.76; P = 0.001), the use of dihydropyridine calcium channel blockers (OR: 0.68; 95% CI: 0.48-0.98; P = 0.042) and the use of statins (OR: 0.67; 95% CI: 0.49-0.91; P = 0.010) were independently associated with the non-use of SGLT2is.

Conclusions: The RED-HEART study provided comprehensive real-world data about implementing SGLT2is in patients with HF. These results suggest that there is a need for organized action and close collaboration between healthcare providers to improve the implementation of SGLT2is, especially in patients with HF with preserved ejection fraction and chronic kidney disease.

Aims: Heart failure (HF) is characterized by a heightened risk of melanoma, which often metastasizes to the heart. The overlap pathology between HF and melanoma includes chronic low-grade inflammation and dysregulation of inflammatory cancer-associated fibroblasts (iCAFs). The impact of HF on iCAF-driven tumour inflammation remains obscure.

Methods and results: To identify critical genes for HF development, transcriptomic data (GSE57338) containing 313 clinical HF samples [136 healthy controls, 95 ischaemia (ISCH) and 82 dilated cardiomyopathy (DCM)] were analysed to screen differentially expressed genes (DEGs) and perform enrichment analysis. Fifty-one DEGs in ISCH and 62 DEGs in DCM were identified with log₂|fold change (FC)| ≥ 1 and P value ≤0.05. All these genes are involved in extracellular matrix organization, immune/inflammatory responses and Wnt signalling pathways. Then, the overall survival curves and prognostic models of DEGs in melanoma were evaluated. The correlation of gene expression with lymphocyte infiltration levels was assessed. Only aldehyde oxidase 1 (AOX1) and amphiregulin (AREG) maintained the same trend in melanoma as in HF, negatively affecting prognosis by regulating lymphocyte infiltration (log-rank P value = 0.0017 and 0.0019). The potential drug molecules were screened, and the binding energies were calculated via molecular docking. Eniluracil, a known AOX1 targeting drug, was found to stably bind with AREG (hydrogen bond binding energies: -65.633, -63.592 and -62.813 kcal/mol).

Conclusions: The increased prevalence of melanoma in HF patients and its propensity for cardiac metastasis may be due to AREG-mediated systemic low-grade inflammation. Eniluracil holds promise as a therapeutic agent that may block AREG signalling, inhibiting the activation of iCAF mediated by regulatory T cell (Treg) and neutrophil.

Aims: Impella malrotation-inlet orientation away from the left ventricular (LV) apex with normal console waveforms and proper device depth-is commonly observed and possibly associated worse haemodynamics. This study aimed to characterize the haemodynamic consequences of Impella malrotation in cardiogenic shock (CS) patients.

Methods and results: We included 100 CS patients (60 ± 12 years; 79.0% males) with available echocardiography during Impella support and pulmonary artery catheter assessment before and during (at 48 h) Impella support. Impella malrotation was identified in 36%. At 48 h, malrotation patients had higher pulmonary artery wedge pressure (PAWP, 16.0 ± 8.2 vs. 13.0 ± 4.6 mmHg; P = 0.033), higher systolic pulmonary artery pressure (PAP, 35.0 ± 11.3 vs. 29.5 ± 9.0 mmHg; P = 0.015), higher diastolic-PAP (19.3 ± 8.1 vs. 15.1 ± 6.1 mmHg; P = 0.007), higher mean-PAP (25.7 ± 9.1 vs. 20.8 ± 6.8 mmHg; P = 0.005), higher right atrial pressure (10.3 ± 4.8 vs. 7.7 ± 4.3 mmHg; P = 0.009), higher pulmonary vascular resistance index (4.78 ± 2.75 vs. 3.49 ± 1.94 WUm²; P = 0.020) and higher pulmonary artery elastance (0.91 ± 0.60 vs. 0.67 ± 0.40 mmHg/mL; P = 0.045). Serum lactate at 48 h was higher in malrotation patients (6.63 ± 6.25 vs. 3.60 ± 4.21 mmol/L; P = 0.004). Malrotation patients presented larger LVEDD during support (52 ± 10 vs. 46 ± 11 mm; P = 0.006), higher rates of aortic regurgitation (AR, 86 vs. 56%; P = 0.004) and higher increase in AR severity (+0.94 ± 0.92 vs. + 0.46 ± 0.95; P = 0.016). No significant differences were found in major adverse outcomes.

Conclusions: In CS patients, Impella malrotation is associated with suboptimal unloading of the LV, worse pulmonary haemodynamics and worse indexes of right ventricular afterload.

Aims: The mechanisms underlying the acute decompensation of heart failure (HF) remain unclear. The present study examined intracardiac dynamics during decompensated HF using echo-vector flow mapping.

Methods and results: Fifty patients admitted for decompensated HF were prospectively enrolled, and intracardiac energy loss (EL) was assessed by echo-vector flow mapping at admission (decompensated HF) and discharge (compensated HF). Outcome measures were average EL in the left ventricle (LV) in decompensated and compensated HF and were compared with those in 40 stable non-HF patients with cardiovascular diseases. The mean age of HF patients was 80.8 ± 12.4 years. The prevalence of both females and atrial fibrillation was 48.0%. The prevalence of HF with a reduced ejection fraction (<40%) (HFrEF) was 34.0%. The prevalence of decompensated HF classified into clinical scenario 1 was 33.3%. Blood pressure and NT-proBNP were significantly higher in decompensated HF than in compensated HF, while the ejection fraction (EF) was significantly lower. Average EL was significantly higher in compensated HF patients than in non-HF patients (40 mW/m·L vs. 26 mW/m·L, P = 0.047). A multivariable analysis identified age, systolic blood pressure, LVEF, and the absence of chronic obstructive pulmonary disease as independent risk factors for high LV-EL regardless of the presence of HF. Furthermore, average EL in HF patients was significantly higher under acute decompensated conditions than under compensated conditions (55 mE/m·L vs. 40 mE/m·L, [+18 mE/m·L, P = 0.03]). Higher EL under decompensated HF conditions was significant in non-HFrEF (+19 mW/m·L, P = 0.009) and clinical scenario 1 (+23 mW/m·L, P = 0.008). The multivariable analysis identified eGFR as an independent risk factor for a decrease in average LV-EL under decompensated conditions.

Conclusions: Energy inefficiency in LV was apparent even in stable HF patients and significant under acute decompensated conditions, particularly in HF with preserved EF and clinical scenario 1.