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Aims: To investigate the prognostic value of diagnostic scores for heart failure (HF) with preserved ejection fraction (HFpEF).Methods and Results: Consecutive patients with HFpEF admitted for unequivocal decompensated HF treated with intravenous loop diuretics were evaluated (n = 443; mean age 78 ± 12 years; 60% women). The HFA-PEFF and H2 FPEF scores were calculated for all patients with echocardiography data available within 1 year and the population was stratified according to HFA-PEFF scores 2-4 (n = 79), 5 (n = 93), or 6 (n = 271) and H2 FPEF score probabilities <90% (n = 80), 90-95% (n = 61), and 96-100% (n = 293). HF readmission rates (95% confidence intervals) increased from 28.9 (22.7-35.0) per 100 patient-years in HFA-PEFF 2-4 to 46.0 (38.5-53.5) in HFA-PEFF 5 and 45.0 (40.1-49.8) in HFA-PEFF 6. Similarly, HF readmission rates increased with increasing H2 FPEF probability: <0.90 [31.8 (25.3-38.2) per 100 patient-years], 0.90-0.95 [41.5 (32.9-50.1)], and 0.96-1.00 [45.9 (41.2-50.6]. Median survival was 65 months (36-89 months) in HFA-PEFF score 2-4, 45 months (26-59 months) in HFA-PEFF score 5, and 28 months (22-42 months) in HFA-PEFF score 6 (P < 0.001), while the hazard ratio (95% confidence interval) for all-cause mortality was 1.16 (1.02-1.32) per 0.10 increase in H2 FPEF probability.Conclusions: Among patients hospitalized with HFpEF, higher HFpEF probability according to diagnostic scores is associated with increased risk of subsequent HF readmissions and all-cause mortality. [ABSTRACT FROM AUTHOR]

Background: Right ventricular (RV) apical pacing is associated with systolic dysfunction and heart failure. Paced QRS duration has been suggested as a predictor of heart failure and left ventricular (LV) systolic dysfunction. However, the effect of paced QRS duration on LV diastolic function is not well known.Objective: This study was designed to evaluate the relationship between paced QRS duration and LV diastolic function.Methods: This retrospective study included 88 patients who had chronic RV apical pacing. Myocardial relaxation was assessed with tissue Doppler imaging. Patients with severe valvular dysfunction or significant structural heart disease were excluded. Paced QRS duration was measured with standard 12‑lead ECG at follow-up.Results: Median age of the patients was 65.9 years (interquartile ranges (IQR), 56.5, 72.7) with 64.8% of female patients. Median duration of RV pacing was 8.6 years (IQR, 5.3, 11.1). Major indication of RV pacing was complete atrioventricular block (89.8%), and dual chamber pacemakers were predominantly implanted (89.8%). Mean of paced QRS duration was 160.5 ± 18.2 msec. Median LV ejection fraction (EF) was 63% (IQR, 55.5, 67.5), and negatively correlated with paced QRS duration (R = -0.478, p < 0.001). LV end diastolic dimension was positively correlated with paced QRS duration (R = 0.531, p < 0.001). Mean E' velocity at the septal mitral annulus was 5.2 ± 1.5 and negatively related to paced QRS duration (R = -0.521, p < 0.001). After adjusting covariables, paced QRS duration was independently related to E' velocity (beta = -0.038, p = 0.005). Paced QRS duration was also associated with worsening functional capacity or elevated LV filling pressure in patients with preserved EF (odd ratio = 1.10; 95% confidence interval, 1.02-1.20, p = 0.015).Conclusion: Paced QRS duration was associated with LV relaxation which might be another possible mechanism of worsening heart failure in patients with long paced QRS duration. [ABSTRACT FROM AUTHOR]

Heart failure (HF) with normal ejection fraction - the isolated diastolic heart failure, depicts increasing prevalence and health care burden in recent times. Having less mortality rate compared to systolic heart failure but high morbidity, it is evolving as a major cardiac concern. With increasing clinical use of Left atrial volume (LAV) quantitation in clinical settings, LAV has emerged as an important independent predictor of cardiovascular outcome in HF with normal ejection fraction. This article is intended to review the diastolic and systolic heart failure, their association with left atrial volume, in depth study of Left atrial function dynamics with determinants of various functional and structural changes. [ABSTRACT FROM AUTHOR]

UnlabelledMarked elevations of B-type natriuretic peptide (BNP) are not generally seen in patients with heart failure and preserved ejection fraction (HFpEF). The objective of this study was to examine the clinical and laboratory characteristics of a large cohort of patients with HFpEF and markedly elevated BNP. A retrospective examination of 421 inpatients at a university hospital admitted with a diagnosis of HFpEF was performed. Clinical and echocardiographic data in 4 groups of patients with levels of BNP ≤ 100 pg/mL, 100-400 pg/mL, 400-1,000 pg/mL and > 1,000 pg/mL were compared. Patients with HFpEF and BNP > 1,000 pg/mL (28% of the population) were characterized by impaired renal function and greater use of anti-hypertensive medications. A subset of these patients with BNP > 1,000 pg/mL had normal renal function (21%) and were significantly older, more frequently female, and tended to have lower ejection fractions. Conversely, patients with HFpEF and BNP ≤ 100 pg/mL were younger and had preserved renal function. BNP was inversely related to the likelihood of subsequent admission for heart failure, but not to myocardial infarction or death.In conclusionBNP > 1,000 pg/mL is seen in almost 1/3 of patients hospitalized with HFpEF. This elevation of BNP often reflects impaired renal function, but can also be seen in patients with preserved renal function but relatively impaired systolic function.

BackgroundIn the main Digitalis Investigation Group (DIG) trial, digoxin reduced the risk of 30-day all-cause hospitalization in older systolic heart failure patients. However, this effect has not been studied in older diastolic heart failure patients.MethodsIn the ancillary DIG trial, of the 988 patients with chronic heart failure and preserved (> 45%) ejection fraction, 631 were age ≥ 65 years (mean age 73 years, 45% women, 12% non-whites), of whom 311 received digoxin.ResultsAll-cause hospitalization 30-day post randomization occurred in 4% of patients in the placebo group and 9% each among those in the digoxin group receiving 0.125 mg and ≥ 0.25 mg a day dosage (P = .026). Hazard ratios (HR) and 95% confidence intervals (CI) for digoxin use overall for 30-day, 3-month, and 12-month all-cause hospitalizations were 2.46 (1.25-4.83), 1.45 (0.96-2.20) and 1.14 (0.89-1.46), respectively. There was one 30-day death in the placebo group. Digoxin-associated HRs (95% CIs) for 30-day hospitalizations due to cardiovascular, heart failure, and unstable angina causes were 2.82 (1.18-6.69), 0.51 (0.09-2.79), and 6.21 (0.75-51.62), respectively. Digoxin had no significant association with 30-day all-cause hospitalization among younger patients (6% vs 7% for placebo; HR 0.80; 95% CI, 0.36-1.79).ConclusionsIn older patients with chronic diastolic heart failure, digoxin increased the risk of 30-day all-cause hospital admission, but not during longer follow-up. Although chance finding due to small sample size is possible, these data suggest that unlike in systolic heart failure, digoxin may not reduce 30-day all-cause hospitalization in older diastolic heart failure patients.

The article presents the case report of a rare hereditary form of systemic ATTR-amyloidosis in Russian patient with a discussion of approaches to the diagnosis and treatment of this form, also based on the own experience in the management of such patients. Modern ideas about the pathogenesis of the disease as well as detailed information about the clinical manifestations of amyloid cardiopathy and of other organs are presented. The nature of structural and hemodynamic changes in the heart is discussed on the basis of experience, including own, ultrasound examination of the heart in patients with amyloidosis, especially the article focuses the reader's attention on the true infiltrative nature of transtiretin amyloid cardiopathy in contrast to AL-amyloidosis, in which there is a significant inflammatory component that determines a more unfavorable natural course of AL-amyloidosis of the heart. The article discusses the differential diagnosis of different types of amyloidosis, the diagnostic difficulties associated with weak congophilia of transtiretin amyloidosis and at the same time substantiates the need for morphological verification of the diagnosis. Modern methods of treatment of ATTR-amyloidosis are discussed.

Abstract Background Liraglutide is an antidiabetic agent with cardioprotective effect. The purpose of this study is to test efficacy of liraglutide to improve diabetic cardiomyopathy in patients with diabetes mellitus type 2 (DM2) without cardiovascular disease. Methods Patients with DM2 were randomly assigned to receive liraglutide 1.8 mg/day or placebo in this double-blind trial of 26 weeks. Primary outcome measures were LV diastolic function (early (E) and late (A) transmitral peak flow rate, E/A ratio, early deceleration peak (Edec), early peak mitral annular septal tissue velocity (Ea) and estimated LV filling pressure (E/Ea), and systolic function (stroke volume, ejection fraction, cardiac output, cardiac index and peak ejection rate) assessed with CMR. Intention-to-treat analysis of between-group differences was performed using ANCOVA. Mean estimated treatment differences (95% confidence intervals) are reported. Results 23 patients were randomized to liraglutide and 26 to placebo. As compared with placebo, liraglutide significantly reduced E (− 56 mL/s (− 91 to − 21)), E/A ratio (− 0.17 (− 0.27 to − 0.06)), Edec (− 0.9 mL/s2 * 10−3 (− 1.3 to − 0.2)) and E/Ea (− 1.8 (− 3.0 to − 0.6)), without affecting A (3 mL/s (− 35 to 41)) and Ea (0.4 cm/s (− 0.9 to 1.4)). Liraglutide reduced stroke volume (− 9 mL (− 16 to − 2)) and ejection fraction (− 3% (− 6 to − 0.1)), but did not change cardiac output (− 0.4 L/min (− 0.9 to 0.2)), cardiac index (− 0.1 L/min/m2 (− 0.4 to 0.1)) and peak ejection rate (− 46 mL/s (− 95 to 3)). Conclusions Liraglutide reduced early LV diastolic filling and LV filling pressure, thereby unloading the left ventricle. LV systolic function reduced and remained within normal range. Future studies are needed to investigate if liraglutide-induced left ventricular unloading slows progression of diabetic cardiomyopathy into symptomatic stages. Trial registration ClinicalTrials.gov: NCT01761318.

Background : Femoral neck fracture is common in the elderly population. Acute kidney injury (AKI) is an important risk factor for mortality in patients who have had such fracture. We evaluated the incidence of AKI in patients who had femoral neck fracture and identified risk factors for AKI and mortality. Methods : This was an observational cohort study including 285 patients who were ≥ 65 years of age and who underwent femoral neck fracture surgery between 2013 and 2017. Results : The mean age was 78.63 ± 6.75 years. A total of 67 (23.5%) patients developed AKI during the hospital stay: 57 (85.1%), 5 (7.5%), and 5 (7.5%) patients were classified as having stage 1, 2, and 3 AKI, respectively. Patients with AKI had a lower baseline estimated glomerular filtration rate and higher left atrial dimension, left ventricular mass index, pulmonary artery pressure, and the ratio of early mitral inflow velocity to early diastolic mitral annulus velocity (E/e') and were more likely to have diabetes or hypertension (HTN) (P < 0.05). The presence of HTN (odds ratio [OR], 4.570; 95% confidence interval [CI], 1.632-12.797) higher E/e' (OR, 1.105; 95% CI, 1.019-1.198), and lower hemoglobin (OR, 0.704; 95% CI, 0.528-0.938) were independently associated with a higher risk for developing AKI. Severe AKI (OR, 24.743; 95% CI, 2.822-212.401) was associated with a higher risk of mortality. Conclusion : Elderly patients with femoral neck fracture had a high incidence of AKI. Diastolic dysfunction was associated with AKI. Severe AKI was associated with in-hospital mortality.

Background/Aims Left ventricular diastolic dysfunction (LVDD) is an early manifestation of cardiac dysfunction in patients with liver cirrhosis (LC). However, the effect of LVDD on survival has not been clarified, especially in decompensated LC. Methods We prospectively enrolled 70 patients with decompensated LC, including ascites or variceal bleeding, at Daejeon St. Mary’s Hospital from April 2013 to April 2015. The cardiac function of these patients was evaluated using 2D echocardiography with tissue Doppler imaging. The diagnosis of LVDD was based on the American Society of Echocardiography guidelines. The primary endpoint was overall survival. Results Forty-four patients (62.9%) had LVDD. During follow-up (22.3 months), 18 patients died (16 with LVDD and 2 without LVDD). The survival rate was significantly lower in patients with LVDD than in those without LVDD (31.1 months vs. 42.6 months, P=0.01). In a multivariate analysis, the Child-Pugh score and LVDD were independent predictors of survival. Moreover, patients with a ratio of early filling velocity to early diastolic mitral annular velocity (E/e’) ≥ 10 (LVDD grade 2) had lower survival than patients with E/e’ ratio < 10. Conclusions The presence of LVDD is associated with poor survival in patients with decompensated LC. Therefore, it may be important to monitor and closely follow LVDD patients.

Seipin deficiency can induce hypertrophic cardiomyopathy and heart failure, which often leads to death in humans. To explore the effects and the possible mechanisms of Seipin deficiency in myocardial remodeling, Seipin knockout (SKO) mice underwent transverse aortic constriction (TAC) for 12 weeks. We found a more severe left ventricular hypertrophy and diastolic heart failure and increases in inflammatory cell infiltration, collagen deposition, and apoptotic bodies in the SKO group compared to those in the wild type (WT) group after TAC. Electron microscopy also showed a more extensive sarcoplasmic reticulum expansion, deformation of microtubules, and formation of mitochondrial lesions in the cardiomyocytes of SKO mice than in those of WT mice after TAC. Compared with the WT group, the SKO group showed increases in endoplasmic reticulum (ER) stress-, inflammation-, and fibrosis-related gene expression, while calcium ion-related factors, such as Serca2a and Ryr, were decreased in the SKO group after TAC. Increased levels of the ER stress-related protein GRP78 and decreased SERCA2a and P-RYR protein levels were detected in the SKO group compared with the WT group after TAC. Slowing of transient Ca2+ current decay and an increased SR Ca2+ content in myocytes were detected in the cardiomyocytes of SKO mice. Adipose tissue transplantation could not rescue the cardiac hypertrophy after TAC in SKO mice. In conclusion, we found that Seipin deficiency could promote cardiac hypertrophy and diastolic heart failure after TAC in mice. These changes may be related to the impairment of myocardial calcium handling, ER stress, inflammation, and apoptosis.

Background: Determinants of adverse diastolic remodeling in ST-elevated myocardial infarction (STEMI) after successful revascularization are not well established. Besides, the relationship between Pentraxin-3 (PTX-3) and diastolic function deterioration is unknown. This study hypothesizes that PTX-3 level would be associated with diastolic remodeling. Materials and Methods: Ninety-eight STEMI patients were included in our study. Echocardiography was performed before and 12–18 weeks after discharge. Two groups were generated according to the PTX-3 value, and the follow-up/baseline echocardiographic parameters were compared. Diastolic adverse remodeling was accepted as a persistent restrictive filling pattern or an increase in at least one grade of diastolic dysfunction. The independent predictors of diastolic adverse remodeling were investigated. Results: Adverse diastolic remodeling was detected in 19.3% of patients. High left ventricular mass index (odds ratio [OR]: 1.096, confidence interval [CI] 95%: 1.023–1.174, P = 0.009), high PTX-3 (OR: 1.005, CI 95%: 1.001–1.009, P = 0.024), and failing to achieve thrombolysis in myocardial infarction flow 3 after percutaneous coronary intervention (OR: 6.196, CI 95%: 1.370–28.023, P = 0.005) were determined as independent predictors of adverse diastolic remodeling. The ratio of follow-up/baseline left atrial volume index was higher in the high PTX-3 group (1.15 vs. 1.05, P = 0.029). Moreover, being in the high PTX-3 group predicted adverse diastolic remodeling at 7.4 times. Conclusion: Higher PTX-3 level is associated with adverse diastolic remodeling in STEMI patients. [ABSTRACT FROM AUTHOR]

The impact of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) on diastolic function is less known. We describe a 46‐year‐old man with a history of mild hypertension who presented to the emergency department with fever, cough, and myalgia for 2 days. The patient was tested positive for SARS‐CoV‐2. He was admitted and started on a combination of antiviral and antimicrobial therapy. He developed respiratory distress 2 days later, and O2 saturation declined. Blood tests showed an increased N‐terminal pro‐B type natriuretic peptide (NT‐proBNP) level, and echocardiography showed normal left ventricular ejection fraction and E/e′ ratio of 16. Computed tomography scan showed interstitial pulmonary oedema and prominent peripheral pulmonary vascular markings. Given these findings, heart failure with preserved ejection fraction (HFpEF) was considered. Low‐dose diuretic was started, and fluid administration was restricted, resulting in a decrease in NT‐proBNP level, clinical and haemodynamic stabilization, and improved oxygenation. This case highlights the occurrence of HFpEF in coronavirus disease 2019. [ABSTRACT FROM AUTHOR]

Purpose of review: Patients often present with a mixed phenotype of pulmonary vascular disease and heart failure with preserved ejection fraction (HFpEF). Identifying the exact hemodynamic culprits in such cases has important therapeutic implications. This review discusses the hemodynamic characterization and treatment options in patients with pulmonary vascular disease, HFpEF, and their combination. Recent findings: The threshold for pulmonary hypertension (PH) has been lowered toward a mean pulmonary arterial pressure (mPAP) > 20 mmHg at rest. Exercise-induced PH is defined as mPAP > 30 mmHg during exercise with a mPAP/cardiac output slope > 3 mmHg/L/min. A blunted pulmonary vasodilatory reserve is observed early on in HFpEF, before an elevated pulmonary vascular resistance or right ventricular remodeling is evident. Long-term exposure to elevated left heart filling pressures in HFpEF induces hemangiomatosis-like endothelial cell proliferation and smooth muscular hypertrophy, predominantly at the venous side of the pulmonary circulation. Enhanced ventricular interdependence because of pericardial constraint may play an important role in the pathophysiology of HFpEF, especially when pulmonary vascular disease is present. Summary: Established and emerging treatment strategies for pulmonary vascular disease and HFpEF should target drivers of the underlying disease process and subsequent organ damage. Careful hemodynamic characterization is vital to guide treatment decisions. [ABSTRACT FROM AUTHOR]

BACKGROUND: It has been proposed that left ventricular diastolic dysfunction (LVDD) is a possible physiological link between high body mass index (BMI) and future occurrence of heart failure (HF). The present cross-sectional study was aimed to analyze the association between BMI and LVDD by transthoracic echocardiography (TTE).METHODS: This study was conducted from May 2017 to September 2019 in Khorshid Hospital of Isfahan University of Medical Sciences, Isfahan, Iran. Based on the calculated BMI (kg/m²), patients were divided into three groups: group 1: subjects with BMI < 25, as a normal group (n = 75), group 2: volunteer cases with 40 > BMI ≥ 30, as an obese group (n = 98), and group 3: patients with BMI ≥ 40, as a morbidly obese group (n = 100). TTE was performed by a trained cardiologist and associated variables including left atrium (LA) volume, E, septal e’, lateral e’,andE/e’ were assessed and also subjects were characterized as normal diastolic function, abnormal diastolic function, and inconclusive diagnosis of diastolic dysfunction (DD).RESULTS: Apart from the ejection fraction (EF) and the tricuspid regurgitation velocity (TRV), there was a significant difference between the other echocardiographic variables including LA volume, E, septal e’, lateral e’, and E/e’ (P < 0.05). One patient with morbid obesity in our study revealed LVDD. There was no significant difference between three groups (P = 0.42).CONCLUSION: There is no considerable relationship between obesity and LVDD. It seems that the absence of associated comorbidities such as diabetes, coronary disorders, etc. plays a crucial role in preventing LVDD, but for realistic and definitive decision, more cellular and molecular investigations and studies with larger sample size are necessary.

BACKGROUND: It has been proposed that left ventricular diastolic dysfunction (LVDD) is a possible physiological link between high body mass index (BMI) and future occurrence of heart failure (HF). The present cross-sectional study was aimed to analyze the association between BMI and LVDD by transthoracic echocardiography (TTE). METHODS: This study was conducted from May 2017 to September 2019 in Khorshid Hospital of Isfahan University of Medical Sciences, Isfahan, Iran. Based on the calculated BMI (kg/m²), patients were divided into three groups: group 1: subjects with BMI < 25, as a normal group (n = 75), group 2: volunteer cases with 40 > BMI ≥ 30, as an obese group (n = 98), and group 3: patients with BMI ≥ 40, as a morbidly obese group (n = 100). TTE was performed by a trained cardiologist and associated variables including left atrium (LA) volume, E, septal e’, lateral e’, and E/e’ were assessed and also subjects were characterized as normal diastolic function, abnormal diastolic function, and inconclusive diagnosis of diastolic dysfunction (DD). RESULTS: Apart from the ejection fraction (EF) and the tricuspid regurgitation velocity (TRV), there was a significant difference between the other echocardiographic variables including LA volume, E, septal e’, lateral e’, and E/e’ (P < 0.05). One patient with morbid obesity in our study revealed LVDD. There was no significant difference between three groups (P = 0.42). CONCLUSION: There is no considerable relationship between obesity and LVDD. It seems that the absence of associated comorbidities such as diabetes, coronary disorders, etc. plays a crucial role in preventing LVDD, but for realistic and definitive decision, more cellular and molecular investigations and studies with larger sample size are necessary. [ABSTRACT FROM AUTHOR]

Heart failure (HF) patients frequently present with comorbidities such as atrial fibrillation (AF) or other cardiovascular conditions, elevating their risk of thromboembolic events. Consequently, anticoagulation therapy is often considered for thromboprophylaxis, although its initiation in HF patients is complicated by concomitant bleeding risk factors. This review explores the paradoxical relationship between HF, increased bleeding risk, and the potential benefits of anticoagulation. Through an examination of existing evidence from clinical trials, observational studies, and meta-analyses, we aim to elucidate the role of anticoagulation in HF patients with increased bleeding risk. Despite guidelines recommending anticoagulation for certain HF patients with AF or other thromboembolic risk factors, uncertainty persists regarding the optimal management strategy for those at heightened risk of bleeding. The review discusses the pathophysiological mechanisms linking HF and thrombosis, challenges in bleeding risk assessment, and strategies to minimize bleeding risk while optimizing thromboprophylaxis. Shared decision-making between clinicians and patients is emphasized as essential for individualized treatment plans that balance the potential benefits of anticoagulation against the risk of bleeding complications. Furthermore, it examines emerging anticoagulant agents and their potential role in HF management, highlighting the need for further research to delineate optimal management strategies and inform evidence-based practice. In conclusion, while anticoagulation holds promise for improving outcomes in HF patients, careful consideration of patient-specific factors and ongoing research efforts are essential to optimize therapeutic strategies in this population., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2024, Saeed et al.)

Heart failure (HF) with left ventricular diastolic dysfunction is a growing global concern. This study evaluated myocardial oxidized nicotinamide adenine dinucleotide (NAD + ) levels in human systolic and diastolic HF and in a murine model of HF with preserved ejection fraction, exploring NAD + repletion as therapy. We quantified myocardial NAD + and nicotinamide phosphoribosyltransferase levels, assessing restoration with nicotinamide riboside (NR). Findings show significant NAD + and nicotinamide phosphoribosyltransferase depletion in human diastolic HF myocardium, but NR successfully restored NAD + levels. In murine HF with preserved ejection fraction, NR as preventive and therapeutic intervention improved metabolic and antioxidant profiles. This study underscores NAD + repletion's potential in diastolic HF management., Competing Interests: This work was supported by the Sydney Medical School Foundation (Dr O’Sullivan); Sydney Cardiovascular Fellowship (Dr O’Sullivan), NSW Health Early-Mid Career Fellowship and Clinician-Scientist Awards (Dr O’Sullivan; DOH1003 and DOH1006), National Heart Foundation Future Leader Fellowship (Dr O’Sullivan; NHF104853), National Heart Foundation Future Leader Fellowship (Dr Koay; NHF107180), NSW Cardiovascular Collaborative Grant (Dr Koay), and philanthropic support from The University of Sydney donors (Dr Lal). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (© 2024 The Authors.)

Aims: To study the impact of heart failure with preserved ejection fraction (HFpEF) vs. aortic stenosis (AS) lesion severity on left ventricular (LV) hypertrophy, diastolic dysfunction, left atrial (LA) dysfunction, haemodynamics, and exercise capacity., Methods and Results: Patients (n = 206) with at least moderate AS (aortic valve area ≤0.85 cm/m2) and discordant symptoms underwent cardiopulmonary exercise testing with simultaneous echocardiography. The population was stratified according to the probability of underlying HFpEF by the heavy, hypertension, atrial fibrillation, pulmonary hypertension, elder, filling pressure (H2FPEF) score [0-5 (AS/HFpEF-) vs. 6-9 points (AS/HFpEF+)] and AS severity (Moderate vs. Severe). Mean age was 73 ± 10 years with 40% women. Twenty-eight patients had Severe AS/HFpEF+ (14%), 111 Severe AS/HFpEF- (54%), 13 Moderate AS/HFpEF+ (6%), and 54 Moderate AS/HFpEF- (26%). AS/HFpEF+ vs. AS/HFpEF- patients, irrespective of AS severity, had a lower LV global longitudinal strain, impaired diastolic function, reduced LV compliance, and more pronounced LA dysfunction. The pulmonary arterial pressure-cardiac output slope was significantly higher in AS/HFpEF+ vs. AS/HFpEF- (5.4 ± 3.1 vs. 3.9 ± 2.2 mmHg/L/min, respectively; P = 0.003), mainly driven by impaired cardiac output and chronotropic reserve, with signs of right ventricular pulmonary arterial uncoupling. AS/HFpEF+ vs. AS/HFpEF- was associated with a lower peak aerobic capacity (11.5 ± 3.7 vs. 15.9 ± 5.9 mL/min/kg, respectively; P < 0.0001) but did not differ between Moderate and Severe AS (14.7 ± 5.5 vs. 15.2 ± 5.9 mL/min/kg, respectively; P = 0.6)., Conclusion: A high H2FPEF score is associated with a reduced exercise capacity and adverse haemodynamics in patients with moderate to severe AS. Both exercise performance and haemodynamics correspond better with intrinsic cardiac dysfunction than AS severity., Competing Interests: Conflict of interest: None declared., (© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background Data on the association of systolic and diastolic blood pressure with the structure and function of failing hearts with preserved ejection fraction (EF) are sparse. Methods and Results This analysis included 935 patients with heart failure (49.4% women; mean age, 69.9 years) with preserved EF (≥45%) enrolled in the TOPCAT (Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist) Trial before initiation of randomized therapy. Left ventricular (LV) structure (dimensions, wall thickness, and mass index), diastolic function (left atrial volume index, transmitral blood flow, and mitral annular velocities), and systolic function (EF and longitudinal strain) were assessed echocardiographically. In multivariable‐adjusted analyses, association sizes expressed per 1‐SD (14.8–mm Hg) increment in systolic blood pressure were 0.020 cm (P=0.003) and 0.018 cm (P=0.004) for LV septal and posterior wall thickness, respectively, and 2.42 mg/m2 (P=0.018) for LV mass index. The corresponding associations with diastolic blood pressure were nonsignificant (P≥0.067). In similarly adjusted analyses, the association sizes expressed per 1‐SD (10.7–mm Hg) increment in diastolic blood pressure were −0.15 for E/A (P

Background Heart failure with preserved ejection fraction (HFpEF) is an increasingly prevalent form of heart failure, representing half of the total burden of heart failure. We hypothesised that modulation of the phosphodiesterase type 3/cyclic AMP using a novel oral formulation of milrinone might exert favorable effects HFpEF via pulmonary and systemic vasodilation and enhancement of ventricular relaxation. We assessed the safety and efficacy of oral milrinone on quality of life and functional outcomes in patients with HFpEF. Methods and Results The MilHFPEF (Extended Release Oral Milrinone for the Treatment of Heart Failure With Preserved Ejection Fraction) study was a randomized, double‐blind, placebo‐controlled pilot study in 23 patients with symptomatic HFpEF. Efficacy end points included changes from baseline in Kansas City Cardiomyopathy Questionnaire summary score and 6‐minute walk distance. The primary safety end point was the development of clinically significant arrhythmia. The Kansas City Cardiomyopathy Questionnaire score improved significantly in milrinone‐treated patients compared with placebo (+10±13 versus −3±15; P=0.046). Six‐minute walk distance also tended to improve in the treatment group compared with placebo (+22 [−8 to 49] versus −47 [−97 to 12]; P=0.092). Heart rate (−1±5 versus −2±9 bpm; P=0.9) and systolic blood pressure (−3±18 versus +1±12 mm Hg; P=0.57) were unchanged. Early filling velocity/early mitral annular velocity (−0.3±3.0 versus −1.9±4.8; P=0.38) was unchanged. One patient in the placebo arm was hospitalized for heart failure. Holter monitoring did not demonstrate evidence of a proarrhythmic effect of milrinone. Conclusions In this novel pilot study, extended release oral milrinone was well tolerated and associated with improved quality of life in patients with HFpEF. Further longer‐term studies are warranted to establish the role of this therapeutic approach in HFpEF. Registration URL: https://www.anzctr.org.au/; Unique identifier: ACTRN12616000619448.

Patients with diabetes are prone to develop a distinct primary myocardial condition, diabetic cardiomyopathy, placing them at an increased risk for heart failure [1-3]. This occurs independently of hypertension, coronary artery disease, and other established causes of heart failure. Pertinent findings include increased mass, concentric changes, and diastolic dysfunction of the left ventricle [4,5]. Such adverse remodeling is common among patients with diabetes and appears to be strongly associated with its duration, suggesting a role for persistent metabolic stress [6-8]. However, which exact components of the diabetic syndrome determine these cardiac alterations is not clear. Moreover, most studies have investigated patients with type 2 diabetes, and it is uncertain whether patients with type 1 diabetes experience similar myocardial changes. Continue reading the full text in the PDF version.

Heart failure (HF) is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood. American College of Cardiology Foundation / American Heart Association 2013 guidelines have classified HF into two categories: (i) HF with reduced (≤40%) ejection fraction (HFrEF) or systolic HF, and (ii) HF with preserved (≥50%) ejection fraction (HFpEF) or diastolic HF. Risk factors for HFpEF include age more than 70 years, female gender, hypertension, wide pulse pressure, diabetes mellitus, chronic renal insufficiency, left ventricular hypertrophy, atrial fibrillation, smoking, recent weight gain, and exercise intolerance. Cardiac catheterization and echocardiography are used for the confirmation of diagnosis of HFpEF. Intraoperatively, the hemodynamic goals in patients with HFpEF are avoidance of tachycardia, maintenance of sinus rhythm, and maintenance of higher than usual filling pressure. No specific treatment for HFpEF is established, and therapeutic options include an intravenous diuretic, a beta blocker or calcium channel blocker, a venodilator, and management of co-morbidities.

BACKGROUND: Although the significant burden of heart failure (HF) is well recognized, the relative contributions of systolic HF versus diastolic HF are less defined. OBJECTIVE: To explore the differential burden between patients with systolic and diastolic HF in terms of treatment patterns, healthcare resource utilization (HCRU), costs, and mortality risk. METHODS: This retrospective cohort study used administrative claims data from a large US commercial health insurer integrated with mortality data. Patients newly diagnosed with HF between January 1, 2010, and June 30, 2016, were identified and grouped according to systolic HF or diastolic HF diagnosis and were followed up to 4 years after diagnosis. Treatment patterns, HCRU, costs, and mortality were compared between the 2 groups of patients. RESULTS: Overall, 46,885 patients with systolic HF and 21,854 with diastolic HF were identified and included in the study. Patients with systolic HF had less HCRU than those with diastolic HF during the first year after HF diagnosis, including hospital admissions (70.2% vs 82.4%, respectively; P <.001) and emergency department visits (30.5% vs 39.1%, respectively; P <.001). The average per-patient costs for patients with systolic HF during the 1-year follow-up were higher than for those with diastolic HF ($64,154 vs $59,652, respectively; P <.001), but lower during years 2 through 4 (approximately $23,000-$25,000 annually vs approximately $28,000-$29,000 annually; P <.001). Patients with diastolic HF had a higher adjusted hospitalization risk (odds ratio, 1.62; 95% confidence interval [CI], 1.55-1.69), but comparable adjusted costs (exponentiated estimate, 1.01; 95% CI, 0.99-1.02) and slightly lower mortality risk (hazard ratio, 0.96; 95% CI, 0.93-0.99) versus patients with systolic HF. The number of HF-related medication classes received for other diagnoses during the year preceding an HF diagnosis was associated with lower risks for hospitalization, mortality, and lower costs, with a trend in benefits toward patients with systolic HF. Of note, 21.9% of patients with systolic HF and 25% of patients with diastolic HF filled no HF-related prescriptions in the year after diagnosis. CONCLUSION: This real-world analysis confirms a high disease burden associated with HF and provides insight across the systolic HF and diastolic HF phenotypes. HF-related medication use after diagnosis was suboptimal and underscores a gap in patient care. [ABSTRACT FROM AUTHOR]

• NT-proBNP showed the best diagnostic performance for detecting non-reduced LVEF HF in patients with symptomatic persistent atrial fibrillation. • We might consider higher cut-off points than those presently recommended. • Troponin was the best biomarker in distinguish HFmrEF and HFpEF in patients with symptomatic persistent atrial fibrillation. Atrial fibrillation (AF) and heart failure (HF) with non-reduced left ventricle ejection fraction (LVEF) present a diagnostic overlap. In this paper, we analyze differences in biomarkers between patients with and without HF, in a cohort of patients presenting with symptomatic AF. Differences in biomarkers between patients with medium range ejection fraction HF (HFmrEF) and those with preserved ejection fraction HF (HFpEF) are also analyzed. A total of 115 patients with symptomatic persistent AF were included. Seven biomarkers were measured: NT-proBNP, high sensitivity T troponin (hsTNT), galectin-3, ST2, fibrinogen, urate and C-reactive protein. Patients with non-reduced LVEF HF had significantly higher NT-proBNP levels than those without HF. This biomarker was the only variable independently related with the presence of non-reduced LVEF HF. Troponin was the only factor independently related with the presence of HFmrEF. NT-proBNP showed the best diagnostic accuracy for detecting the presence of non-reduced LVEF HF. We found higher diagnostic NT-proBNP cut-off values than those previously reported. Troponin was the most accurate biomarker differentiating HFmrEF from HFpEF. [ABSTRACT FROM AUTHOR]

Purpose of Review: Heart failure with preserved ejection fraction (HFpEF) or diastolic heart failure (DHF) makes up more than half of all congestive heart failure presentations (CHF). With an ageing population, the case load and the financial burden is projected to increase, even to epidemic proportions. CHF hospitalizations add too much of the financial and infrastructure strain. Unlike systolic heart failure (SHF), much is still either uncertain or unknown. Specifically, in epidemiology, the disease burden is established; however, risk factors and pathophysiological associations are less clear; diagnostic tools are based on rigid parameters without the ability to accurately monitor treatments effects and disease progression; finally, therapeutics are similar to SHF but without prognostic data for efficacy. Recent Findings: The last several years have seen guidelines changing to account for greater epidemiological observations. Most of these remain general observation of shortness of breath symptom matched to static echocardiographic parameters. The introduction of exercise diastolic stress test has been welcome and warrants greater focus. Summary: HFpEF is likely to see new thinking in the coming decades. This review provides some of perspective on this topic. [ABSTRACT FROM AUTHOR]

A number of studies have suggested that autoantibodies against β1-adrenoreceptors (β1R-AAbs) have an important role in pathophysiological processes of heart failure. The aim of the present study was to determine whether β1R-AAbs are implicated in cardiac dysfunction following acute myocardial infarction (AMI) and their association with prognosis. A total of 33 cases with systolic heart failure (SHF), 49 with diastolic heart failure (DHF) and 44 with normal heart function following AMI were recruited. β1R-AAbs were detected by ELISA and major adverse cardiac events (MACEs) were recorded during the 5-year follow-up. The positive rate of β1R-AAbs in the SHF group (45.5%) was significantly higher compared with that in the DHF (22.4%; P<0.05) and normal (15.9%; P<0.05) groups. The area under the receiver operating characteristics curve for the diagnosis of SHF was 0.630 (95% CI: 0.514–0.747, P=0.026). During a median follow-up period of 51.0±15.4 months, the positive rate of β1R-AAbs in the MACEs group was significantly higher compared with that in the non-MACEs group (P<0.05). Multivariate logistic regression analysis indicated that the left ventricular ejection fraction and diabetes were independent predictors of 5-year MACEs following AMI, whereas β1R-AAbs were not. Kaplan-Meier analysis revealed that the cumulative MACEs-free survival rate was the lowest in the SHF group, followed by the DHF and normal groups (P<0.05). Therefore, β1R-AAbs were indicated to be of value for early diagnosis of SHF after AMI but not as independent predictors for the prognosis of patients with AMI. [ABSTRACT FROM AUTHOR]

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