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Aims: Red blood cell distribution width-to-albumin ratio (RAR), an innovate biomarker of inflammation, can independently predict adverse cardiovascular outcomes. However, the association between RAR and prognosis in patients with non-ischaemic heart failure (NIHF) remains unclear., Methods and Results: A total of 2077 NIHF patients admitted to the Heart Failure Care Unit, Fuwai Hospital, were consecutively enrolled from December 2006 to October 2017 in this retrospective study. The primary endpoint was a composite outcome of all-cause mortality and heart transplantation. The correlation between RAR and the composite outcome was assessed by the Kaplan-Meier survival analysis and the Cox regression analysis. Incremental predictive values and the clinical performance of RAR for all-cause mortality or heart transplantation were also assessed based on a 12-variable traditional risk model. The median follow-up time in this study was 1433 (1341, 1525) days. As the gender no longer satisfied the Cox proportional risk assumption after 1150 days, we set 1095 days as the follow-up time for analysis. A total of 500 patients reached the composite outcome. Multivariable Cox regression showed that per log 2 increase of RAR was significantly associated with a 132.9% [hazard ratio 2.329, 95% confidence interval (CI) 1.677-3.237, P < 0.001] increased risk of all-cause mortality or heart transplantation. Better model discrimination [concordance index: 0.766 (95% CI 0.754-0.778) vs. 0.758 (95% CI 0.746-0.770), P < 0.001], calibration (Akaike information criterion: 1487.3 vs. 1495.74; Bayesian information criterion: 1566.25 vs. 1569.43; Brier score: 1569.43 vs. 1569.43; likelihood ratio test P < 0.001), and reclassification (integrated discrimination improvement: 1.35%, 95% CI 0.63-2.07%, P < 0.001; net reclassification improvement: 13.73%, 95% CI 2.05-27.18%, P = 0.034) were improved after adding RAR to the traditional model (P < 0.001 for all). A higher overall net benefit was also obtained in the threshold risk probability of 20-55%., Conclusions: High level of RAR was an independent risk factor of poor outcome in NIHF., (© 2024 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

The aim of this study was to investigate the clinical characteristics and prognosis of patients hospitalized with heart failure with preserved ejection fraction (HFpEF) and low N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels. Seven hundred ninety consecutive patients hospitalized with HFpEF from 2006 to 2017 were enrolled. Clinical characteristics and outcomes were compared between low NT-proBNP group (<300 ng/L) and elevated NT-proBNP group (≥300 ng/L). 108 HFpEF patients (13.7%) presented with low NT-proBNP levels. Age, body mass index, atrial fibrillation, New York Heart Association functional class, and albumin were independent predictors of low NT-proBNP levels in HFpEF patients. During the median follow-up duration of 1103 days, 11 patients (10.2%) in low NT-proBNP group suffered from primary endpoint event. Elevated NT-proBNP group had a higher risk of all-cause death or heart transplantation than low NT-proBNP group (adjusted HR [95%CI]: 2.36 [1.24,4.49], P = .009). Stratified analyses showed that the association between NT-proBNP (elevated NT-proBNP group vs low NT-proBNP group) and risk of all-cause death or heart transplantation was stronger in non-atrial fibrillation patients than in atrial fibrillation patients (P value for interaction = .025). Furthermore, the associations between NT-proBNP and risk of all-cause death or heart transplantation were stronger in younger and male patients than in older and female patients. However, both subgroups only reached borderline significant (P values for interaction = .062 and .084, respectively). Our findings suggest that low NT-proBNP levels were common in patients hospitalized with HFpEF. Patients with HFpEF and low NT-proBNP levels had a better prognosis than those with elevated NT-proBNP levels, particularly in younger, male, and non-atrial fibrillation patients., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc.)

Objective: Previous reports on the epidemiology, influencing factors, and the prognostic value of the components of PR interval in hospitalized heart failure patients were limited., Methods: This study retrospectively enrolled 1182 patients hospitalized with heart failure from 2014 to 2017. Multiple linear regression analysis was used to explore the association between the components of PR interval and the baseline parameters. The primary outcome was all-cause death or heart transplantation. Multivariable-adjusted Cox proportional hazard regression models were constructed to explore the predictive value of the components of PR interval for the primary outcome., Results: In multiple linear regression analysis, higher height (for every 10 cm increase in height: regression coefficient 4.83, P < 0.001) as well as larger atrial and ventricular size were associated with larger P wave duration but not with PR segment. The primary outcome occurred in 310 patients after an average follow-up of 2.39 years. Cox regression analyses revealed that the increase in PR segment was an independent predictor of the primary outcome (every 10 ms increase: hazard ratio 1.041, 95% confidence interval [CI] 1.010-1.083, P = 0.023), whereas the P wave duration did not show significant correlation. When adding the PR segment to an initial prognostic prediction model, the likelihood ratio test and categorical net reclassification index (NRI) showed a significant improvement, but the increase in C-index was not significant. In subgroup analysis, increased PR segment was an independent predictor of the primary endpoint in patients taller than 170 cm (each 10 ms increase: hazard ratio 1.153, 95% CI 1.085-1.225, P < 0.001) but not the shorter group (P for interaction = 0.006)., Conclusions: In hospitalized patients with heart failure, longer PR segment was an independent predictor of the composite endpoint of all-cause death and heart transplantation, especially in the taller group, but it had limited significance in improving the prognostic risk stratification of this population., (© 2023. The Author(s).)

Objective: To compare the hemodynamic effects of domestic levosimendan versus dobutamine on patients with acute decompensated heart failure (ADHF)., Methods: A total of 78 ADHF patients with pulmonary capillary wedge pressure (PCWP) ≥ 15 mm Hg and cardiac index (CI) ≤ 2.5 L×min(-1)×m(-2) were enrolled into this blind, positive-controlled, randomized and multicenter study to receive 24 h intravenous levosimendan or dobutamine therapy. They were randomized into 2 groups: levosimendan and dobutamine (n = 39 each)., Results: In the levosimendan group, the PCWP 24 h decreased significantly ((14.2 ± 7.6) vs (23.1 ± 8.1) mm Hg, P < 0.01)and CI increased significantly versus the baseline levels ((2.8 ± 0.7) L×min(-1)×m(-2) vs (2.0 ± 0.4) L×min(-1)×m(-2), P < 0.01). As compared with the dobutamine group, the change percentages versus baseline in PCWP, pulmonary arterial mean pressure (PAMP), systemic vascular resistance (SVR) at 24 h (median) decreased or increased significantly in the levosimendan group 45.5% vs 22.1% (P < 0.05); 20.8% vs 15.0% (P < 0.05); 34.5% vs 12.7% (P < 0.01); CI increased 39.8% vs 13.5% (P < 0.01). As compared with the baseline level, LVEF increased at 24 h in the levosimendan group (27.4% ± 6.1% vs 32.5% ± 8.7%, P < 0.05). Both PCWP and CI at 24 h correlated significantly with NT-proBNP at Day 3 (r = 0.31, P < 0.01; r = -0.29, P < 0.05). Dyspnea improved greatly at 24 h in the levosimendan group than that in the dobutamine group., Conclusion: As compared with dobutamine, domestic levosimendan may bring about better outcomes of hemodynamics and dyspnea.

Objective: To compare the plasma concentrations of N-terminal brain natriuretic peptide precursor (NT-proBNP) in patients with heart failure due to various heart diseases and analyze the influencing factors., Methods: We enrolled a total of 804 heart failure patients due to various heart diseases, including valvular heart disease (VHD), dilated cardiomyopathy (DCM), ischemic heart diseases (IHD), restrictive cardiomyopathy (RCM), hypertensive heart disease (HHD), hypertrophic cardiomyopathy (HCM), pulmonary heart disease (PHD) and adult congenital heart disease (CHD). The plasma concentration of NT-proBNP was measured by enzyme-linked immunosorbent assay (ELISA). Multiple linear regression analysis was used to detect the influencing factors for the plasma concentration of NT-proBNP., Results: The plasma concentration of NT-proBNP had no significant difference between patients with VHD, DCM, IHD, RCM, HCM, PHD, HHD and CHD. The median (25 percent, 75 percent) values were 1866 (803 - 3973), 2247 (1087 - 3865), 2400 (1182 - 4242), 2456 (1385 - 5839), 2204 (1053 - 3186), 2285 (1155 - 3424), 2313 (655 - 3850) and 2768 (795 - 4371) pmol/L respectively (P > 0.05). It increased with New York Heart Association (NYHA) class from II through III to IV. The median (25 percent, 75 percent) values were 646 (447 - 1015), 2160 (1118 - 3750) and 3342 (1549 - 5455) pmol/L respectively (P < 0.01). The patients with a body mass index (BMI) of ≥ 25 kg/cm(2) had a lower NT-proBNP concentration than those with a BMI of < 25 kg/cm(2). The median (25 percent, 75 percent) values were 1468 (784 - 3177) and 2424 (1090 - 4213) pmol/L respectively (P < 0.01). Patients with a serum creatinine concentration of ≥ 107 µmol/L had a higher NT-proBNP concentration than those < 107 µmol/L. The median (25 percent, 75 percent) values were 3337 (1470 - 5380) and 1644 (781 - 3375) pmol/L respectively (P < 0.01). Multiple linear regression analysis demonstrated that NYHA class, creatinine, BMI, hepatic damage and diastolic pressure were independently associated with the plasma concentration of NT-proBNP (all P < 0.01)., Conclusion: The plasma concentration of NT-proBNP has no significant difference between heart failure patients due to various heart diseases. Its level may be affected by NYHA class, serum creatinine, BMI, hepatic damage and diastolic pressure.

Objective: To detect the occurring and developing patterns of multiple organ damage in patients dying from acute decompensated heart failure (ADHF)., Methods: The clinical data of 30 hospitalized patients of ADHF were analyzed. The dying causes included renal, hepatic, respiratory dysfunctions, infection and anemia. All patients received continuous cardiac rhythm monitoring. Their renal, hepatic and respiratory function, infection and anemia were evaluated at admission and during the last 24 hours pre-death respectively. And the results were compared., Results: There were 19 males and 11 females. The average age was (55±22) years old. Among them, 7 cases were of NYHA class III and 23 cases NYHA class IV at admission. The causes of heart failure included valvular heart disease (n=17), dilated cardiomyopathy (n=6), ischemic cardiomyopathy (n=4), valvular heart disease and previous cardiac infarction (n=2) and restrictive cardiomyopathy (n=1). From admission to death, the average hospitalization duration was (8.8±7.4) days. Eleven cases suffered from sudden cardiac death due to lethal arrhythmias including ventricular tachycardia, ventricular fibrillation and sinus arrest. Another 19 cases had no lethal arrhythmias, but they suffered cardiac shock eventually. Among all 30 cases, there were 15 cases with pulmonary infection, 13 cases with hepatic dysfunction, 6 cases with renal dysfunction, 7 cases with respiratory failure, 7 cases with anemia and 15 cases with multiple organ damage at admission. However, the pre-death values increased to 26 (87%, P<0.01), 19 (63%, P<0.05), 24 (80%, P<0.01), 20 (67%, P<0.01), 9 (30%, P>0.05) and 29 (97%, P<0.01) respectively., Conclusion: Multiple organ damage evolves and worsens to result in death in ADHF patients.

Objective: To evaluate the value of NT-proBNP in predicting in-hospital mortality in patients with decompensated systolic heart failure., Methods: Plasma NT-proBNP levels within 24 hours of admission were obtained in 366 patients with decompensated systolic heart failure. The levels were compared between dying patients in hospital and survival patients at discharge. ROC analyses were performed to evaluate if NT-proBNP was a predictor for in-hospital mortality and identify the optimal NT-proBNP cut-off point for predicting in-hospital mortality. A binary logistic regression analysis was used to evaluate if NT-proBNP was an independent predictor for in-hospital mortality., Results: 19 cases of the 366 patients died in hospital. NT-proBNP levels of the dying cases were much higher than those of the survivals 3970 (3452, 6934) pmol/L vs 2340 (1132, 4002) pmol/L respectively, P < 0.01). ROC analysis of NT-proBNP to predict in-hospital mortality had an area under the curve (AUC) of 0.762 (95% CI: 0.657-0.857, P < 0.01), the optimal NT-proBNP cut-off point for predicting in-hospital mortality was 3500 pmol/L with a sensitivity of 73.7%, a specificity of 66.9%, an accuracy of 67.6% and a negative predictive value of 97.9%. Patients whose NT-proBNP levels were equal or more than 3500 pmol/L had an in-hospital mortality of 10.9%, compare with 2.1% in those NT-proBNP levels less than 3500 pmol/L (P < 0.01). Binary logistic regression analysis demonstrated that NT-proBNP was an independent predictor for in-hospital mortality in patients with decompensated systolic heart failure (P < 0.01)., Conclusion: Admission plasma NT-proBNP level is an independent predictor for in-hospital mortality in patients with decompensated systolic heart failure. The optimal NT-proBNP cut-off point for predicting in-hospital mortality is 3500 pmol/L.

Supplemental Digital Content is available in the text. Background: The adult mammalian cardiomyocytes lose their proliferative capacity, which is responsible for cardiac dysfunction and heart failure following injury. The molecular mechanisms underlying the attenuation of adult cardiomyocyte proliferation remain largely unknown. Because long noncoding RNAs (lncRNAs) have a critical role in the development of cardiovascular problems, we investigated whether lncRNAs have any role in the regulation of cardiomyocyte proliferation and cardiac repair. Methods: Using bioinformatics and initial analysis, we identified an lncRNA, named CPR (cardiomyocyte proliferation regulator), that has a potential regulatory role in cardiomyocyte proliferation. For in vivo experiments, we generated CPR knockout and cardiac-specific CPR-overexpressing mice. In isolated cardiomyocytes, we used adenovirus for silencing (CPR–small interfering RNA) or overexpressing CPR. To investigate the mechanisms of CPR function in cardiomyocyte proliferation, we performed various analyses including quantitative reverse transcription–polymerase chain reaction, Western blot, histology, cardiac function (by echocardiography), transcriptome analyses (microarray assay), RNA pull-down assay, and chromatin immunoprecipitation assay. Results: CPR level is comparatively higher in the adult heart than in the fetal stage. The silencing of CPR significantly increased cardiomyocyte proliferation in postnatal and adult hearts. Moreover, CPR deletion restored the heart function after myocardial injury, which was evident from increased cardiomyocyte proliferation, improvement of myocardial function, and reduced scar formation. In contrast, the neonatal cardiomyocyte proliferation and cardiac regeneration were remarkably suppressed in CPR-overexpressing mice or adeno-associated virus serotype 9–CPR—overexpressing heart. These results indicate that CPR acts as a negative regulator of cardiomyocyte proliferation and regeneration. Next, we found that CPR targets minichromosome maintenance 3, an initiator of DNA replication and cell cycle progression, to suppress cardiomyocyte proliferation. CPR silenced minichromosome maintenance 3 expression through directly interacting and recruiting DNMT3A to its promoter cysteine-phosphate-guanine sites, as evident from decreased minichromosome maintenance 3 promoter methylation and increased minichromosome maintenance 3 expression in CPR knocked-down cardiomyocytes and CPR knockout mouse heart. These results were confirmed in CPR-overexpressing cardiomyocytes and CPR-overexpressing mouse heart. Conclusions: Together, our findings identified that CPR is a suppressor of cardiomyocyte proliferation and indicated that lncRNAs take part in the regulation of cardiomyocyte proliferation and cardiac repair. Our study provides an lncRNA-based therapeutic strategy for effective cardiac repair and regeneration. [ABSTRACT FROM AUTHOR]