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Background In patients with heart failure, left atrial remodeling often occurs to varying degrees. Left atrial enlargement has been proved to be an important predictor of cardiovascular‐related adverse events. However, the relationship between left atrial diameter (LAD) with heart failure (HF) with preserved ejection fraction (HFpEF), reduced ejection fraction (HFrEF) and mid‐range ejection fraction (HFmrEF) remains unclear. Hypothesis We want to explore the correlation between left atrial diameter and HFpEF, HFmrEF, and HFrEF. Methods A total of 210 patients with heart failure who underwent hospitalization in Ningbo Medical Center Lihuili Hospital, Zhejiang, China, from January 1, 2020, to June 31, 2021, were reviewed. The basic demographic characteristics, blood test, and the related indexes of echocardiography of the subjects were collected and analyzed. Results There is a significant difference between HFpEF and HFrEF group in LAD (p = .007), and LAD is negatively correlated with left ventricular ejection fraction (LVEF) (p = .002, r = −.209). Conclusion LAD is negatively correlated with LVEF, which may predict the prevalence of HFrEF. We studied the data of 210 individuals with heart failure. There is a significant difference between HFpEF and HFrEF groups in LAD (p = .007). And LAD is negatively correlated with LVEF (p = .002, r = −.209), which may predict the prevalence of HFrEF.

Cardiovascular Diseases (CVDs) are the leading cause of death globally. More than 17 million people die worldwide from CVD per year. There is considerable evidence suggesting that estrogen modulates cardiovascular physiology and function in both health and disease, and that it could potentially serve as a cardioprotective agent. The effects of estrogen on cardiovascular function are mediated by nuclear and membrane estrogen receptors (ERs), including estrogen receptor alpha (ERα), estrogen receptor beta (ERβ), and G-protein-coupled ER (GPR30 or GPER). Receptor binding in turn confers pleiotropic effects through both genomic and non-genomic signaling to maintain cardiovascular homeostasis. Each ER has been implicated in multiple pre-clinical cardiovascular disease models. This review will discuss current reports on the underlying molecular mechanisms of the ERs in regulating vascular pathology, with a special emphasis on hypertension, pulmonary hypertension, and atherosclerosis, as well as in regulating cardiac pathology, with a particular emphasis on ischemia/reperfusion injury, heart failure with reduced ejection fraction, and heart failure with preserved ejection fraction.

Aims Patients with heart failure (HF) have a poor prognosis and are categorized by ejection fraction. We performed a meta‐analysis to compare baseline characteristics and long‐term outcomes of patients with heart failure with reduced (HFrEF), mid‐range (HFmrEF), and preserved ejection fraction (HFpEF). Methods and Results A total of 27 prospective studies were included. Patients with HFpEF were older and had a higher proportion of females, hypertension, diabetes, and insufficient neuroendocrine antagonist treatments, while patients with HFrEF and HFmrEF had a higher prevalence of coronary heart disease and chronic kidney disease. After more than 1‐year of follow‐up, all‐cause mortality was significantly lower in patients with HFmrEF 9388/25 042 (37.49%) than those with HFrEF 39 333/90 023 (43.69%) and HFpEF 24 828/52 492 (47.30%) (p < .001). Cardiovascular mortality was lowest in patients with HFpEF 1130/9904 (11.41%), highest in patients with HFrEF 3419/16 277 (21.07%) mainly coming from HF death and sudden cardiac death, and middle in patients with HFmrEF 699/5171 (13.52%) and the non‐cardiovascular mortality was on the contrary. Subgroup analysis showed that in high‐risk patients with atrial fibrillation, the all‐cause mortality of HFpEF was significantly higher than both HFrEF and HFmrEF (p < .001). HF hospitalization was lowest in patients with HFmrEF 1822/5285 (34.47%), highest in patients with HFrEF 12 607/28 590 (44.10%) and middle in patients with HFpEF 8686/22 763 (38.16%) and the composite of all‐cause mortality and HF hospitalization was also observed similar results. Conclusions In summary, patients with HFmrEF had the lowest incidence of all‐cause mortality and HF hospitalization, while the highest all‐cause mortality and HF hospitalization rates were HFpEF and HFrEF patients, respectively.

ObjectiveTo determine the prognostic value of atrial fibrillation (AF) in patients with heart failure (HF) and preserved, mid-range or reduced ejection fraction (EF).MethodsPatients hospitalised for acute HF were enrolled in the Korean Acute Heart Failure registry, a prospective, observational, multicentre cohort study, between March 2011 and February 2014. HF types were defined as reduced EF (HFrEF, LVEF <40%), mid-range EF (HFmrEF, LVEF 40%–49%) or preserved EF (HFpEF, LVEF ≥50%).ResultsOf 5414 patients enrolled, HFrEF, HFmrEF and HFpEF were seen in 3182 (58.8%), 875 (16.2%) and 1357 (25.1%) patients, respectively. The prevalence of AF significantly increased with increasing EF (HFrEF 28.9%, HFmrEF 39.8%, HFpEF 45.2%; p for trend <0.001). During follow-up (median, 4.03 years; IQR, 1.39–5.58 years), 2806 (51.8%) patients died. The adjusted HR of AF for all-cause death was 1.06 (0.93–1.21) in the HFrEF, 1.10 (0.87–1.39) in the HFmrEF and 1.22 (1.02–1.46) in the HFpEF groups. The HR for the composite of all-cause death or readmission was 0.97 (0.87–1.07), 1.14 (0.93–1.38) and 1.03 (0.88–1.19) in the HFrEF, HFmrEF and HFpEF groups, respectively, and the HR for stroke was 1.53 (1.03–2.29), 1.04 (0.57–1.91) and 1.90 (1.13–3.20), respectively. Similar results were observed after propensity score matching analysis.ConclusionsAF was more common with increasing EF. AF was seen to be associated with increased mortality only in patients with HFpEF and was associated with an increased risk of stroke in patients with HFrEF or HFpEF.Trial registration number NCT01389843

Patients with type 2 diabetes mellitus are at a higher risk of developing heart failure compared with the healthy population. In recent landmark clinical trials, sodium-glucose co-transporter 2 (SGLT2) inhibitor therapies improve blood glucose control and also reduce cardiovascular events and heart failure hospitalisations in patients with type 2 diabetes. Intriguingly, such clinical benefits have also been seen in patients with heart failure in the absence of type 2 diabetes although the underlying mechanisms are not clearly understood. Potential pathways include improved glycaemic control, diuresis, weight reduction and reduction in blood pressure, but none fully explain the observed improvements in clinical outcomes. More recently, novel mechanisms have been proposed to explain these benefits that include improved cardiomyocyte calcium handling, enhanced myocardial energetics, induced autophagy and reduced epicardial fat. We provide an up-to-date review of cardiac-specific SGLT2 inhibitor–mediated mechanisms and highlight studies currently underway investigating some of the proposed mechanisms of action in cardiovascular health and disease.

Heart failure (HF) is the most rapidly growing cardiovascular health burden worldwide. HF can be classified into three groups based on the percentage of the ejection fraction (EF): heart failure with reduced EF (HFrEF), heart failure with mid-range—also called mildly reduced EF— (HFmrEF), and heart failure with preserved ejection fraction (HFpEF). HFmrEF can progress into either HFrEF or HFpEF, but its phenotype is dominated by coronary artery disease, as in HFrEF. HFrEF and HFpEF present with differences in both the development and progression of the disease secondary to changes at the cellular and molecular level. While recent medical advances have resulted in efficient and specific treatments for HFrEF, these treatments lack efficacy for HFpEF management. These differential response rates, coupled to increasing rates of HF, highlight the significant need to understand the unique pathogenesis of HFrEF and HFpEF. In this review, we summarize the differences in pathological development of HFrEF and HFpEF, focussing on disease-specific aspects of inflammation and endothelial function, cardiomyocyte hypertrophy and death, alterations in the giant spring titin, and fibrosis. We highlight the areas of difference between the two diseases with the aim of guiding research efforts for novel therapeutics in HFrEF and HFpEF.

Aims Available evidence is incomplete and inconsistent in the outcomes of heart failure (HF) patients with preserved ejection fraction (HFpEF), mildly reduced ejection fraction (HFmrEF), and reduced ejection fraction (HFrEF). There are also limited data on the proportions and long‐term prognosis among the three HF phenotypes in China. We aimed to characterize the 5 year prognosis in three HF phenotypes according to EF in a cohort of hospitalized HF patients undergoing coronary angiography in southern China. Methods and results Hospitalized patients with HF were enrolled from the Cardiorenal ImprovemeNt registry (CIN; ClinicalTrials.gov NCT04407936) between January 2007 and December 2014. HF phenotypes were defined as HFpEF (EF ≥ 50%), HFmrEF (EF 41–49%), and HFrEF (EF ≤ 40%). Kaplan–Meier and Cox proportional hazards models were constructed to examine differences in 5 year outcomes in HF patients with different phenotypes. A total of 4880 HF patients [mean age: 61.8 ± 10.3, male: 3156 (64.7%)] were included: 2768 (57%) had HFpEF, 1015 (21%) had HFmrEF, and 1097 (22%) had HFrEF. Patients with HFrEF were older than those with HFpEF (62.5 ± 10.6 vs. 61.3 ± 10.1, P < 0.001) and more likely to be male (78.0% vs. 55.9%, P < 0.001). With 5 year follow‐up through the end of December 2019, 1624 (27.6%) patients died. Controlling confounding variables, declined EF category was independently associated with increased 5 year mortality HFrEF 25.2% vs. HFpEF 13.4%, adjusted hazard ratio [aHR]: 1.85 [95% confidence interval (CI): 1.45 to 2.35]; HFmrEF 18.1% vs. HFpEF 13.4%, aHR: 1.40 [95% CI: 1.08 to 1.81]; HFrEF 25.2% vs. HFmrEF 18.1%, aHR: 1.32 [95% CI: 1.02 to 1.71]. Conclusions In this Chinese cohort, patients with HFrEF account for less than a fourth of HF patients. One‐sixth individuals with HF died in 5 years. HFrEF was associated with a nearly two‐fold increased risk of 5 year mortality than HFpEF. Further studies are needed to prospectively evaluate the efficacy of improving treatment on outcomes in all three HF phenotypes.

In order to explore the proteomic signatures of epicardial adipose tissue (EAT) related to the mechanism of heart failure with reduced and mildly reduced ejection fraction (HFrEF/HFmrEF) and heart failure (HF) with preserved ejection fraction (HFpEF), a comprehensive proteomic analysis of EAT was made in HFrEF/HFmrEF (n = 5) and HFpEF (n = 5) patients with liquid chromatography–tandem mass spectrometry experiments. The selected differential proteins were verified between HFrEF/HFmrEF (n = 20) and HFpEF (n = 40) by ELISA (enzyme‐linked immunosorbent assay). A total of 599 EAT proteins were significantly different in expression between HFrEF/HFmrEF and HFpEF. Among the 599 proteins, 58 proteins increased in HFrEF/HFmrEF compared to HFpEF, whereas 541 proteins decreased in HFrEF/HFmrEF. Of these proteins, TGM2 in EAT was down‐regulated in HFrEF/HFmrEF patients and was confirmed to decrease in circulating plasma of the HFrEF/HFmrEF group (p = 0.019). Multivariate logistic regression analysis confirmed plasma TGM2 could be an independent predictor of HFrEF/HFmrEF (p = 0.033). Receiver operating curve analysis indicated that the combination of TGM2 and Gensini score improved the diagnostic value of HFrEF/HFmrEF (p = 0.002). In summary, for the first time, we described the proteome in EAT in both HFpEF and HFrEF/HFmrEF and identified a comprehensive dimension of potential targets for the mechanism behind the EF spectrum. Exploring the role of EAT may offer potential targets for preventive intervention of HF.

Background Cystatin C (CysC)'s predictive utility for long‐term adverse outcomes in heart failure (HF) patients with normal to mild renal insufficiency remains unclear. This study investigates the relationship between CysC and adverse outcomes in HF patients across the whole ejection fraction (EF) spectrum with normal to mild renal insufficiency. Methods In this single‐center cohort study, 637 HF patients with normal to mild renal insufficiency were categorized into reduced EF (HFrEF), mid‐range EF (HFmrEF), and preserved EF (HFpEF) groups. Associations between natural log unit (CysC) and risks of all‐cause mortality and HF rehospitalization were examined using Cox regression models. C‐index, IDI, and NRI assessed the incremental prognostic value. Results Over a follow‐up of 9.4 years, 271 patients died, and 330 were rehospitalized for HF. Multivariate Cox regression analysis indicated significant associations between elevated CysC levels and increased risks of all‐cause mortality (HR = 1.99, 95% CI: 1.57–2.54) and HF rehospitalization (HR = 1.95, 95% CI: 1.57–2.42) across all patients. HR's for all‐cause mortality observed for HFmrEF (HR 4.73, 95% CI: 2.08−10.74) and HFrEF (HR 15.11, 95% CI: 6.24−36.60) were higher compared to those for HFpEF patients (HR = 1.48, 95% CI 0.98−2.23), and CysC showed less prognostic impact on all‐cause mortality in HFpEF patients. Including CysC in the MAGGIC risk score‐based model provided additional prognostic value for all subjects, even with N‐terminal pro‐brain natriuretic peptide (NT‐proBNP) levels added. Conclusions CysC is an independent risk factor for adverse outcomes in HF patients across EF spectrum with normal to mild renal insufficiency. Integrating CysC into the MAGGIC risk score‐based model enhances its prognostic capability for predicting adverse outcomes in the general HF population. Its prognostic effect on all‐cause mortality is limited in HFpEF patients. Methods and cohort: HF patients with normal to mild renal insufficiency (n = 637), divided into HFpEF, HFmrEF, and HFrEF. Statistical Method: Cox regression models, Kaplan‐Meier Curves, C‐index, IDI, and NRI. Findings: Over a follow‐up of 9.4 years, significant associations of elevated CysC levels with increased risks of all‐cause mortality and HF rehospitalization across all patients were found. Including CysC in the MAGGIC risk score‐based model provided additional prognostic value for patients with normal to mild renal insufficiency. In subgroup analysis, comparable results were observed in HFmrEF and HFrEF patients. However, CysC showed less prognostic impact on all‐cause mortality in HFpEF patients (HR = 1.48, 95% CI: 0.98−2.23). Conclusions: CysC is an independent risk factor for adverse outcomes in HF patients across the EF spectrum with normal to moderate renal insufficiency. Integrating CysC into the MAGGIC risk score‐based model enhances its prognostic capability for predicting adverse outcomes in the general HF population, although its prognostic effect on all‐cause mortality is limited in HFpEF patients. Summary Our research is the first to demonstrate a significant correlation between Cystatin C levels and long‐term outcomes across all hospitalized heart failure patient types with normal to mildly impaired renal function, backed by an extensive follow‐up period. It is also the first to reveal the incremental prognostic benefit of adding Cystatin C to the MAGGIC risk score‐based model for all HF patient groups. Cystatin C proves to be a valuable biomarker for predicting the risk of adverse outcomes in heart failure patients with normal to mildly impaired renal function and coronary heart disease, based on a median follow‐up period of 9.4 years. However, in patients with heart failure with preserved ejection fraction, Cystatin C showed a reduced predictive value for all‐cause mortality. Incorporating Cystatin C into the MAGGIC risk score‐based model enhances its prognostic value for predicting adverse outcomes.

BackgroundClinical drug trials in patients with heart failure and preserved ejection fraction have failed to demonstrate improvements in mortality.MethodsWe systematically searched Medline, Embase and the Cochrane Central Register of Controlled Trials for randomised controlled trials (RCT) assessing pharmacological treatments in patients with heart failure with left ventricular (LV) ejection fraction≥40% from January 1996 to May 2016. The primary efficacy outcome was all-cause mortality. Secondary outcomes were cardiovascular mortality, heart failure hospitalisation, exercise capacity (6-min walk distance, exercise duration, VO2 max), quality of life and biomarkers (B-type natriuretic peptide, N-terminal pro-B-type natriuretic peptide). Random-effects models were used to estimate pooled relative risks (RR) for the binary outcomes, and weighted mean differences for continuous outcomes, with 95% CI.ResultsWe included data from 25 RCTs comprising data for 18101 patients. All-cause mortality was reduced with beta-blocker therapy compared with placebo (RR: 0.78, 95%CI 0.65 to 0.94, p=0.008). There was no effect seen with ACE inhibitors, aldosterone receptor blockers, mineralocorticoid receptor antagonists and other drug classes, compared with placebo. Similar results were observed for cardiovascular mortality. No single drug class reduced heart failure hospitalisation compared with placebo.ConclusionThe efficacy of treatments in patients with heart failure and an LV ejection fraction≥40% differ depending on the type of therapy, with beta-blockers demonstrating reductions in all-cause and cardiovascular mortality. Further trials are warranted to confirm treatment effects of beta-blockers in this patient group.