Search

This study aims to develop a new heart failure with preserved ejection fraction (HFpEF) diagnostic algorithm tailored to Asian populations, addressing limitations of current diagnostic models. Existing HFpEF diagnostic algorithms primarily target patients with dyspnea and metabolic comorbidities, such as obesity, which are more prevalent in Western populations. However, in Asian countries, HFpEF cases are less frequently associated with obesity, leading to less prominent dyspnea and more noticeable symptoms such as fatigue. By incorporating exercise stress echocardiography and focusing on early-stage HFpEF, particularly in patients with symptoms beyond dyspnea, we seek to enable early diagnosis and intervention, ultimately extending healthy life expectancy and improving quality of life. The STOP-HFPEF (The Multicenter STudy On a Precise algorithm for diagnosis of Heart Failure with Preserved Ejection Fraction) study is a multicenter prospective observational investigation in Japan. Certified by the Japanese Society of Echocardiography, the study includes participants aged 20 and older who undergo exercise stress echocardiography. The primary goal is to develop a scoring model for diagnosing HFpEF in heart-failure stages A, B, and C. Secondary outcomes will assess the clinical utility of the new diagnostic score by comparing heart-failure incidence, cardiovascular events, and mortality rates. Study registration: Registered at the UMIN registry (UMIN000054565) on 1 July 2024. [ABSTRACT FROM AUTHOR]

Rationale: In chronic obstructive pulmonary disease (COPD), impaired left ventricular (LV) filling might be associated with coexisting heart failure with preserved ejection fraction (HFpEF) or due to reduced pulmonary venous return indicated by small LV size. Objectives: We investigated the all-cause mortality associated with small LV or HFpEF and clinical features discriminating between both patterns of impaired LV filling in patients with COPD. Methods: We performed transthoracic echocardiography (TTE) in patients with stable COPD from the COSYCONET (COPD and Systemic Consequences and Comorbidities Network) cohort to define small LV as LV end-diastolic diameter below the normal range and HFpEF features according to recommendations of the European Society of Cardiology. We assessed the ratio of early to late ventricular filling velocity (E/A), ratio of early mitral inflow velocity to annular early diastolic velocity (E/e′), serum N-terminal pro-brain natriuretic peptide, high-sensitivity troponin I, airflow limitation (FEV1), lung hyperinflation (residual volume), and gas transfer capacity (DlCO) and discriminated patients with small LV from those with HFpEF features or no relevant cardiac dysfunction as per TTE (normalTTE). The primary outcome was all-cause mortality after 4.5 years. Measurements and Main Results: In 1,752 patients with COPD, the frequency of small LV, HFpEF features, and normalTTE was 8%, 16%, and 45%, respectively. Patients with small LV or HFpEF features had higher all-cause mortality rates than patients with normalTTE: hazard ratio, 2.75 (95% confidence interval, 1.54–4.89) and 2.16 (95% confidence interval, 1.30–3.61), respectively. Small LV remained an independent predictor of all-cause mortality after adjusting for confounders including exacerbation frequency and measures of residual lung volume, DlCO, or FEV1. Compared with normalTTE, patients with small LV had reduced LV filling, as indicated by lowered E/A. Yet, in contrast to patients with HFpEF features, patients with small LV had normal LV filling pressure (E/e′) and lower concentrations of N-terminal pro-brain natriuretic peptide and high-sensitivity troponin I. Conclusions: In COPD, both small LV and HFpEF features are associated with increased all-cause mortality and represent two distinct patterns of impaired LV filling. Clinical trial registered with (NCT01245933). [ABSTRACT FROM AUTHOR]

Liraglutide has been shown to alleviate heart failure in patients with type 2 diabetes. High-intensity interval training (HIIT) has also been proven to improve cardiac function in diabetes. The present study explored the effects and underlying mechanisms of liraglutide and HIIT combination therapy in alleviating diabetic cardiomyopathy (DCM). A high-fat diet and low-dose streptozotocin (STZ) were utilized to induce the DCM model. Eight weeks of liraglutide injection and HIIT were used to treat DCM. Subsequently, cardiac function, serum metabolic biomarkers, serum glucagon-like peptide-1 (GLP-1), histology examination, cardiac alpha-myosin heavy chain (α-MHC), and β-MHC messenger RNA (mRNA) expression, forkhead box protein O1 (FOXO1) and muscle-specific RING finger protein 1 (MURF1) mRNA expression and colocalization, and expression of GLP-1 and GLP-1 receptor (GLP-1R) proteins were detected after the intervention. Results showed that DCM rats developed hyperglycemia with eccentric hypertrophy, fibrosis, and reduced systolic and diastolic function. All interventions significantly reversed the development of heart failure by alleviating the disruption of contractile apparatus, reversed the adult α-MHC transformed to fetal β-MHC, and reduced FOXO1 and MURF1 mRNA expression. Combination therapy had a better effect in alleviating cardiac fibrosis, reducing cardiovascular risk biomarkers, controlling eccentric hypertrophy, and improving systolic function. Combination therapy significantly reduced FOXO1 and MURF1 colocalization and improved the GLP-1R sensitivity in diabetic hearts. Overall, these findings demonstrate that combination therapy can reverse cardiac failure in diabetic rats by controlling the degradation of contractile apparatus by downregulating the cardiac atrophy gene expression and interrupting their colocalization, as well as upregulating GLP-1 signaling. [ABSTRACT FROM AUTHOR]

The rising prevalence of obesity and its association with heart failure with preserved ejection fraction (HFpEF) highlight an urgent need for a diagnostic approach tailored to this population. Diagnosing HFpEF is hampered by the lack of a single non-invasive diagnostic criterion. While this makes a firm diagnosis of HFpEF already notoriously difficult in the general population, it is even more challenging in individuals with obesity. The challenges stem from a range of factors, including the use of body mass index as a conceptually suboptimal indicator of health risks associated with increased body mass, symptom overlap between HFpEF and obesity, limitations in physical examination, difficulties in electrocardiographic and echocardiographic evaluation, and reduced diagnostic sensitivity of natriuretic peptides in individuals with obesity. In this review, we examine these diagnostic challenges and propose a diagnostic algorithm specifically tailored to improve the accuracy and reliability of HFpEF diagnosis in this growing patient demographic. Proposed obesity-adjusted HFpEF score. HFpEF, Heart failure with preserved ejection fraction. Created with BioRender.com. [ABSTRACT FROM AUTHOR]

Heart failure with preserved ejection fraction (HFpEF) is a prevalent and complex condition with limited effective treatments. Endothelial dysfunction is a significant component of HFpEF pathophysiology, and glucagon-like peptide-1 receptor (GLP-1R) agonists have shown potential benefits in improving endothelial function. This study aims to explore the relationship between endothelial dysfunction in HFpEF and the mechanisms of action of GLP-1R agonists, highlighting their potential therapeutic benefits. A comprehensive review of the literature was conducted to examine the etiology of HFpEF, the role of endothelial dysfunction, and the effects of GLP-1R agonists on endothelial function and heart failure outcomes. The findings indicate that HFpEF is associated with various comorbidities, such as obesity, diabetes mellitus, and hypertension, which contribute to endothelial dysfunction. GLP-1R agonists, including semaglutide and liraglutide, have demonstrated significant cardioprotective effects, such as improving vascular endothelial function, reducing inflammation, and preventing atherosclerosis. Clinical trials, such as the STEP-HFpEF trial, have shown positive results in reducing symptoms and physical restrictions in HFpEF patients. GLP-1R agonists present a promising therapeutic option for HFpEF by targeting endothelial dysfunction and other pathophysiological mechanisms. Further research is needed to elucidate the precise mechanisms through which GLP-1R agonists exert their benefits and to establish their long-term safety and efficacy in diverse HFpEF populations. [ABSTRACT FROM AUTHOR]

In this report, we present the case of an older adult with severe obesity and multiple comorbidities, including heart failure with preserved ejection fraction (HFpEF), who experienced a prolonged decline complicated by recurrent hospitalizations and skilled nursing facility stays during the two years preceding death. This case highlights challenges in prognostication attributed to severe obesity complicated by HFpEF, which likely delayed goals of care conversations, and access to palliative care and hospice, despite high symptom burden. We discuss prognostic uncertainty among those with severe obesity and outline potential future directions. [ABSTRACT FROM AUTHOR]

Objective To observe the effect of canagliflozin combined with oral sacubitril/valsartan in the treatment of non-diabetic heart failure with preserved ejection fraction (HFpEF). Methods Seventy non-diabetic HFpEF patients were randomly divided into the observation group and control group, with 35 cases in each group. Patients in the observation group were given canagliflozin (100 mg, once a day) and sacubitril/valsartan (25-200 mg, twice a day) orally on the basis of conventional treatment, while patients in the control group were given sacubitril/valsartan (25-200 mg, twice a day) orally on the basis of conventional treatment. Blood pressure, blood glucose, BMI and uric acid of the two groups were detected before and after treatment. Peripheral venous blood of the two groups were collected before and after treatment, and serum N-terminal brain natriuretic peptide precursor (NT-proBNP), high-sensitive C-reactive protein (hs-CRP) and interleukin-6 (IL-6) were detected. Ventricular ejection fraction (LVEF), left atrial diameter (LAD), left ventricular end-diastolic diameter (LVEDD) and E/A values were calculated by echocardiography. The cardiac function was evaluated by New York Heart Association (NYHA) and 6-minute walking test. The therapeutic effect was evaluated according to the improvement of cardiac function. Results Compared with the control group, systolic blood pressure and diastolic blood pressure decreased in the observation group after treatment (both P<0. 05). Compared with those before treatment, the levels of serum NT-proBNP, hs-CRP, and IL-6 decreased in the two groups after treatment, and the decrease was more significant in the observation group (all P<0. 05). Compared with those before treatment, the E/A values of both groups increased after treatment, and the increase was more obvious in the observation group (P<0. 05). The 6-minute walking distance of the observation group and control group increased after treatment in comparison with that before treatment (P<0. 05). Compared with the control group, the observation group had a longer 6-minute walking distance after treatment (P<0. 05). The improvement of cardiac function in the observation group was higher than that in the control group (P<0. 05). Conclusion Canagliflozin combined with oral sacubitril/valsartan is effective in the treatment of non-diabetic HFpEF, and can significantly improve the cardiac function of patients through the mechanisms such as lowering blood pressure, reducing the preload and afterload of the heart, preventing or reversing myocardial remodeling. [ABSTRACT FROM AUTHOR]

Objective To analyze the relationship between ultrasound left atrial volume index (LAVI) and pericardial fat thickness in patients with heart failure with preserved ejection fraction (HFpEF), and to explore the potential predictive value of pericardial fat thickness for HFpEF. Methods Seventy-two patients with HFpEF were selected as the HFpEF group, and 69 healthy individuals without a history of heart failure were selected as the control group. Echocardiography was performed on the subjects using a colour ultrasound diagnostic instrument, and LAVI was detected using the modified Simpson method. The measurements of epicardial adipose tissue (EAT) thickness on the anterior wall right ventricular, paracardial adipose tissue (PAT) thickness on the anterior wall of right ventricular, and EAT thickness in the left atrioventricular groove were obtained at end-diastole. The receiver operating characteristic (ROC) curves were plotted, and the area under the curve (AUC) was calculated to analyse the predictive efficacy of right ventricular anterior wall EAT thickness, right ventricular anterior wall PAT thickness and left atrioventricular groove EAT thickness on LAVI ≥ 34 mL/m² in patients with HFpEF; Spearman correlation analysis was employed to examine correlations between the right ventricular anterior wall EAT thickness, right ventricular anterior wall PAT thickness, left atrioventricular EAT thickness and LAVI in HFpEF patients. Results LAVI, right ventricular anterior wall EAT thickness, right ventricular anterior wall PAT thickness and left atrioventricular groove EAT thickness were higher in the HFpEF group than in the control group (all P< 0. 05). ROC curve analysis showed that the AUC of the right ventricular anterior wall EAT thickness, right ventricular anterior wall PAT thickness and left atrioventricular groove EAT thickness in the prediction of LAVI ≥ 34 mL/m² was 0. 710,0. 508, and 0. 684. Spearman correlation analysis showed that the right ventricular anterior wall EAT thickness, left atrioventricular groove EAT thickness were positively correlated with LAVI (r = 0. 334,0. 275, respectively; both P< 0. 01), and there was no correlation between right ventricular anterior wall PAT thickness and LAVI (r = 0. 060,P= 0. 477). Conclusion Ultrasound LAVI in patients with HFpEF was positively correlated with right ventricular anterior wall EAT thickness and left atrioventricular groove EAT thickness, and the correlation between right ventricular anterior wall EAT thickness and LAVI was even higher, which might be one of the relevant indexes to assess HFpEF. [ABSTRACT FROM AUTHOR]

Background: Insulin resistance (IR) plays a pivotal role in the interplay between metabolic disorders and heart failure with preserved ejection fraction (HFpEF). Various non-insulin-based indices emerge as reliable surrogate markers for assessing IR, including the triglyceride-glucose (TyG) index, the TyG index with body mass index (TyG-BMI), atherogenic index of plasma (AIP), and the metabolic score for insulin resistance (METS-IR). However, the ability of different IR indices to predict outcome in HFpEF patients has not been extensively explored. Methods: Patients having HFpEF were recruited from January 2012 and December 2023. The outcome was defined as major adverse cardiovascular event (MACE), encompassing all-cause mortality and rehospitalization for heart failure. The potential linear relationship was visualized by the restricted cubic spline (RCS) curve. Both univariable and multivariable Cox proportional hazards models were employed to examine the association between the IR indexes and MACE. Furthermore, to assess the incremental prognostic value of the TyG index, we conducted comprehensive analyses using area under the curve (AUC), the continuous net reclassification index (cNRI), and the integrated discrimination index (IDI). Results: A total of 8693 patients met the inclusion criteria and were included in the final analysis. The mean age of the patients was 70.59 ± 10.6 years, with 5045 (58.04%) being male. The Kaplan-Meier survival analysis revealed that higher degree of the four IR indexes was associated with higher risk of MACE (all log-rank P < 0.05). When treated as a continuous variable, the TyG index showed a significant association with MACE (HR 2.1, 95% CI 1.98–2.23, P < 0.001 in model 1; HR 1.81, 95% CI 1.73–1.9, P < 0.001 in model 2; HR 1.68, 95% CI 1.6–1.76, P < 0.001 in model 3). When categorized into quartiles, the highest quartile of the TyG index (Q4) was significantly associated with MACE (HR 2.48, 95% CI 2.24–2.76, P < 0.001 in model 3). Similar significant associations were found between TyG-BMI, AIP, METS-IR, and MACE. The TyG index was found to enhance the risk stratification capability of the MAGGIC score (AUC from 0.601 to 0.666). When compared to other IR indicators, the TyG index exhibited superior discrimination and reclassification abilities in predicting MACE. Additionally, the TyG-BMI index revealed a U-shaped correlation with MACE, indicating that both an elevated and a lower TyG-BMI index were associated with an increased risk. Conclusion: All four IR indices are independently associated with MACE in patients with HFpEF. Notably, these IR indices significantly enhance the predictive accuracy of the MAGGIC score, a widely used risk assessment tool in HFpEF. Among these indices, the TyG index demonstrated the highest discriminatory and reclassification abilities, providing the greatest incremental value in predicting MACE and exhibiting significant superiority compared to the other indices. These findings highlight the importance of assessing IR indices, particularly the TyG index, in the risk assessment and management strategies for HFpEF patients. However, it should be noted that our findings need to be validated in diverse populations to ensure their applicability and generalizability. [ABSTRACT FROM AUTHOR]

Heart failure with preserved ejection fraction (HFpEF) emerges as a singular subclass of heart failure, bereft of specific therapeutic options. Magnesium, an indispensable trace element, is essential to the preservation of cardiac integrity. However, the association between magnesium supplementation and mortality in HFpEF patients remains unclear. This study extracted HFpEF patient data from the MIMIC-IV database between 2008 and 2019. Propensity score matching was conducted to ensure that patients receiving magnesium supplementation (including magnesium sulfate and magnesium oxide) were balanced with those not receiving it in terms of baseline characteristics. The primary analysis focused on the 28-day all-cause mortality rate, with secondary endpoints encompassing ICU and one-year mortality rates, along with the duration of hospitalization. After matching, the study's final cohort balanced at 1970 patients, with 985 patients per group. The results showed that magnesium intake significantly contributed to a decrease in the 28-day all-cause mortality rate (hazard ratio [HR], 0.682; 95% confidence interval [CI], 0.539–0.863), particularly in subgroups such as older patients (HR, 0.65; 95% CI 0.52–0.81), females (HR, 0.55; 95% CI 0.41–0.73), and those with hypertension (HR, 0.62; 95% CI 0.48–0.79) or without diabetes (HR, 0.54; 95% CI 0.41–0.71). Although magnesium treatment improved both ICU and one-year mortality rates, it concurrently resulted in extended ICU and hospital stays. Mediation analysis indicated that blood urea nitrogen partially mediated the association between magnesium intake and mortality, accounting for approximately 22.73% of the observed effect. Magnesium supplementation has illustrated a significant potential for mitigating the mortality rate in the HFpEF patient, particularly among the elderly, female, and individuals with hypertension. Therefore, magnesium supplementation stands as a potentially valuable supplementary treatment modality for patients with HFpEF. Further comprehensive research is warranted to explore its effects more deeply. [ABSTRACT FROM AUTHOR]

Background: Heart failure with preserved ejection fraction (HFpEF) and chronic kidney disease (CKD) have a strong pathophysiological interrelationship, and their combination worsens prognosis. Summary: This article briefly reviews the bidirectional epidemiological burden and the pathophysiological interplay between HFpEF and CKD. It also discusses some of the controversial aspects regarding the diagnosis and screening of HFpEF in CKD patients and focuses on the most effective therapeutic approaches to improve symptoms and prognosis in this high-risk population. Key Messages: Due to its prevalence and prognostic significance, HFpEF screening should be considered in patients with CKD, with careful use of traditional diagnostic tools in this population. Optimal medical therapy has seen major recent advances in patients with both HFpEF and CKD. SGLT2 inhibitors, finerenone, and semaglutide have consistently demonstrated cardio- and renoprotective effects in both conditions. [ABSTRACT FROM AUTHOR]

Heart failure with preserved ejection fraction (HFpEF) is increasingly common but its pathogenesis is poorly understood. The ability to assess genetic and pharmacologic interventions is hampered by the lack of robust preclinical mouse models of HFpEF. We developed a novel "two-hit" model, which combines obesity and insulin resistance with chronic pressure overload to recapitulate clinical features of HFpEF. C57Bl6/NJ mice fed a high-fat diet (HFD) for > 10 weeks were administered an AAV8-driven vector resulting in constitutive overexpression of mouse Renin1d. HFD-Renin (aka "HFpEF") mice demonstrated obesity and insulin resistance, moderate left ventricular hypertrophy, preserved systolic function, and diastolic dysfunction indicated by echocardiographic measurements; increased left atrial mass; elevated natriuretic peptides; and exercise intolerance. Transcriptomic and metabolomic profiling of HFD-Renin myocardium demonstrated upregulation of pro-fibrotic pathways and downregulation of metabolic pathways, in particular branched chain amino acid catabolism, similar to human HFpEF. Treatment with empagliflozin, an effective but incompletely understood HFpEF therapy, improved multiple endpoints. The HFD-Renin mouse model recapitulates key features of human HFpEF and will enable studies dissecting the contribution of individual pathogenic drivers to this complex syndrome. Additional preclinical HFpEF models allow for orthogonal studies to increase validity in assessment of interventions. [ABSTRACT FROM AUTHOR]

AIM: To investigate the effects of the neutrophil elastase (NE) inhibitor sivelestat on the pathological changes of cardiac tissues in mice with heart failure with preserved ejection fraction (HFpEF) . METHODS: Eight-week-old C57BL/6J mice were randomly divided into 3 groups: control group (n=5), model group (n=6), and treatment group (n=18) . The HFpEF mouse model was established using a combined approach of high-fat diet and NG -nitro-L-arginine methyl ester (L-NAME) . The mice in treatment group received intraperitoneal injection of sivelestat at doses of 12. 5, 25 and 50 mg•kg-1 •d-1 (n=6), while those in control and model groups were injected with the same volume of normal saline. After 12 weeks, small animal ultrasound was employed to assess changes in cardiac function, and the lung weight-to-tibia length (LW/TL) ratio was calculated to evaluate pulmonary edema. An exercise fatigue test was conducted to assess exercise intolerance. Histological evaluations were performed using HE, wheat germ agglutinin, dihydroethidium and Sirius red staining to examine overall heart morphology, cross-sectional area of cardiomyocytes, levels of oxidative stress, and the extent of cardiac fibrosis. The expression of fibrosis-related proteins was analyzed using Western blot. RESULTS: Compared with model group, sivelestat at various concentrations significantly improved cardiac diastolic function in HFpEF mice, indicated by an increased E/A ratio and a decreased E/e' ratio (P<0. 05) . The LW/TL ratio decreased, alleviating lung congestion and exercise intolerance (P<0. 05) . The heart weight-to-tibia length (HW/TL) ratio, overall heart cross-sectional area, and cardiomyocyte cross-sectional area all decreased, indicating attenuation in cardiac hypertrophy (P<0. 05) . Additionally, cardiac fibrosis and reactive oxygen species levels were significantly reduced (P<0. 05) . CONCLUSION: Inhibition of NE exerts a protective effect against diastolic dysfunction and cardiac fibrosis induced by HFpEF in mice. [ABSTRACT FROM AUTHOR]

Introduction: The aim of this study was to investigate the expression and predictive value of NOD-like receptor thermal protein domain-related protein 3 (NLRP3) in patients with non-valvular atrial fibrillation (NVAF) with heart failure with preserved ejection fraction (HFpEF). Methods: This was a retrospective analysis of 121 patients diagnosed with NVAF. According to the occurrence of HFpEF, 81 patients were assigned to the NVAF group and 40 patients to the NVAF/HFpEF group. The levels of NLRP3, B natriuretic peptide (BNP), and interleukin-1β (IL-1β) were determined using ELISA. Independent predictors for HFpEF in NVAF were determined using logistic regression. The receiver operating characteristic (ROC) curve was used to evaluate the predictive value of each factor. Results: Expression levels of NLRP3, BNP, and IL-1β in the NVAF/HFpEF group, as well as the H2FPEF score were significantly higher than those in the NVAF group. Pearson analysis showed that NLRP3, BNP, and IL-1β expression levels in NVAF patients and the H2FPEF score was positively correlated (r = 0.409, r = 0.244, r = 0.299, p < 0.001). Multivariate logistic regression analysis showed that the NLRP3, BNP, or H2FPEF score can be used as independent factor for predicting the occurrence of HFpEF in NVAF. ROC curves showed that the areas under the curve of NLRP3, BNP, and H2FPEF scores for predicting the occurrence of HFpEF in NVAF patients were 0.856, 0.831, and 0.811, respectively. Conclusion: The NLRP3 level is elevated in the peripheral blood of NVAF patients with HFpEF and is positively correlated with the H2FPEF score. NLRP3 may serve as a potential predictor of HFpEF in patients with NVAF. [ABSTRACT FROM AUTHOR]

Background: Cardiorenal syndrome (CRS) refers to the bidirectional interactions between the acutely or chronically dysfunctioning heart and kidney that lead to poor outcomes. Due to the evolving literature on renal impairment and heart failure with preserved ejection fraction (HFpEF), this review aimed to highlight the pathophysiological pathways, diagnosis using imaging and biomarkers, and management of CRS in patients with HFpEF. Summary: The mechanism of CRS in HFpEF can be hypothesized due to the interplay of elevated central venous pressure, renin-angiotensin-aldosterone system (RAAS) activation, oxidative stress, endothelial dysfunction, coronary microvascular dysfunction, and chronotropic incompetence. The correlation between HFpEF and worsening renal function seen in both long-term trials and observational data points to the evidence for these mechanisms. Upcoming biomarkers such as cystatin C, NGAL, NAG, KIM-1, ST-2, and galectin-3, along with conventional ones, are promising for early diagnosis, risk stratification, or response to therapy. Despite the lack of specific treatment for CRS in HFpEF, the management can be discussed with similar medications used in goal-directed medical therapy for heart failure with reduced ejection fraction (HFrEF). Additionally, there is increasing evidence for the role of vasodilators, inotropes, assist devices, and renal denervation, although long-term studies are necessary. Key Message: The management of CRS in HFpEF is an evolving field that currently shows promise for using diagnostic and prognostic biomarkers, conventional heart failure medications, and novel therapies such as renal denervation, interatrial shunt, and renal assist devices. Further studies are needed to understand the pathophysiological pathways, validate the use of novel biomarkers, especially for early diagnosis and prognostication, and institute new management strategies for CRS in patients with HFpEF. [ABSTRACT FROM AUTHOR]

Sleep-disordered breathing is common among patients with heart failure with preserved ejection fraction (HFpEF), and might impact their quality of life due to nighttime hypoxemia and awakenings. However, the factors contributing to deterioration in quality of life remain unclear. This study investigated the factors associated with quality of life deterioration in patients with HFpEF and sleep-disordered breathing. This prospective cross-sectional study included inpatients with HFpEF (left ventricular ejection fraction of ≥ 50%). Sleep-disordered breathing and quality of life were evaluated using polysomnography and the Short Form-8 Health Survey, respectively. The patients were grouped based on thei median physical and mental component summary Short Form-8 Health Survey scores. Among the 31 patients with HFpEF (aged 73.7 ± 10.9 years; 67.7% women; left ventricular ejection fraction, 65.3% ± 8.1%), the median apnea–hypopnea index was 11.5 per hour. Although no differences in parameters related to sleep-disordered breathing were found among the physical component summary-stratified groups, the low mental component summary group exhibited significantly lower nadir oxygen saturation than those exhibited by the high mental component summary group (84.3 ± 5.7% vs. 88.5 ± 3.9%; p = 0.02); this difference remained significant even when adjusted for potential confounders (β = 0.43; p = 0.02). Nocturnal hypoxemia may be a contributing factor to the decline in the mental health aspect of quality of life in patients with HFpEF. Thus, clinicians should consider hypoxemia when managing HFpEF and sleep-disordered breathing. [ABSTRACT FROM AUTHOR]