European Journal of Heart Failure最新文献

{"title":"August 2023 at a glance: Focus on epidemiology and medical therapy","authors":"Daniela Tomasoni, Marianna Adamo, Marco Metra","doi":"10.1002/ejhf.3004","DOIUrl":"https://doi.org/10.1002/ejhf.3004","url":null,"abstract":"An early diagnosis, and hence treatment, of heart failure (HF) may have a major impact on health care resources and patients’ longevity and quality of life.1 The Heart Failure Association (HFA) of the European Society of Cardiology (ESC) provided a clinical consensus statement addressed to general practitioners and to non-cardiology physicians to facilitate the early diagnosis of HF with a major role to screening strategies, including the measurement of brain natriuretic peptides (BNP).2","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"25 8","pages":"1177-1180"},"PeriodicalIF":18.2,"publicationDate":"2023-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5875898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"July 2023 at a glance: heart failure with preserved ejection fraction and comorbidities","authors":"Daniela Tomasoni,&nbsp;Marianna Adamo,&nbsp;Marco Metra","doi":"10.1002/ejhf.2976","DOIUrl":"https://doi.org/10.1002/ejhf.2976","url":null,"abstract":"Heart failure (HF) with preserved ejection fraction (HFpEF) is a heterogeneous syndrome.1–3 A scientific statement from the Heart Failure Association (HFA) described most common HFpEF phenotypes, related comorbidities and treatment options for each phenotype.4 Exercise testing has a key role in the diagnosis and prognostic assessment of HFpEF.1,5,6 In a study by Alogna et al.,7 398 patients with HFpEF undergoing comprehensive echocardiography and invasive cardiopulmonary exercise testing were categorized low versus preserved biventricular cardiac power output (BCPO) reserve (< vs≥median of 1.57 W). Lower BCPO was associated with more advanced HFpEF, increased systemic and pulmonary vascular resistance, reduced exercise capacity and increased adverse events. Atrial fibrillation (AF) is common among patients with HFpEF. Filippatos et al.8 performed a secondary analysis of the EMPEROR-Preserved trial to assess efficacy of empagliflozin in patients with and without AF. Empagliflozin successfully reduced the risk of serious HF events and slowed the decline of renal function, irrespective of AF. Quality of life is impaired also in patients with HFpEF.9,10 Pooling data from DAPA-HF and DELIVER trials, Bhatt et al.11 analysed the benefits of dapagliflozin on health status, measured by the Kansas City Cardiomyopathy Questionnaire (KCCQ), across the full spectrum of left ventricular ejection fraction (LVEF). A total of 11 007 participants were included and KCCQ was evaluated at 4 and 8 months. Dapagliflozin improved all key domains of health status irrespective of LVEF. Some studies showed a U-shaped relationship between LVEF and outcome, with patients with supranormal ejection fraction (HFsnEF, LVEF >65%) having a higher risk of events.12–14 Among 11 573 patients hospitalized for HF and enrolled in the nationwide Japanese registry, 16.8% were classified as HFsnEF, 28.3% as HF with normal ejection fraction (HFnEF), 17.5% as HF with mildly reduced ejection fraction (HFmrEF) and 37.4% as HF with reduced ejection fraction (HFrEF). Patients with HFsnEF were older, more likely to be women, had lower natriuretic peptide values, and had smaller left ventricles than those with HFnEF. Patients with HFsnEF, compared to those with HFnEF, had a similar risk of the .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. primary composite endpoint of cardiovascular (CV) death or HF readmission but with a lower adjusted hazard ratio (HR) for HF readmission.15","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"25 7","pages":"925-928"},"PeriodicalIF":18.2,"publicationDate":"2023-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5740456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heart failure after myocardial infarction: Glass emptier than full","authors":"Josephine Harrington,&nbsp;Javed Butler","doi":"10.1002/ejhf.2961","DOIUrl":"https://doi.org/10.1002/ejhf.2961","url":null,"abstract":"Heart failure (HF) is an ominous and common complication following an acute myocardial infarction (MI). In fact, there is no single greater predictor of mortality following an MI than acute symptoms of HF.1 Once the acute period surrounding an MI is past, the risk continues, and an estimated 12–15% of all patients experiencing an MI will develop HF requiring hospitalization within a year. This risk appears to be especially high for patients who are older, female, who have reduced ejection fraction or acute congestion at the time of MI, and/or in those with certain comorbidities such as type 2 diabetes or chronic kidney disease.1 Once patients develop HF following an MI, their risk of death is markedly elevated. The risk of death associated with HF is substantially higher than the risk of death associated with a recurrent MI.2 As a result, a number of drugs with demonstrated risk reduction in death and/or HF hospitalization are routinely used as guideline-directed medical therapy (GDMT) in high-risk patients following an MI, including beta-blockers, angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, and mineralocorticoid receptor antagonists.3 It has been two decades since a post-MI drug trial identified a therapy that could reduce the risk for HF.3 Despite this, there are reasons to be hopeful that medical care for this population has improved, with regional efforts to improve acute coronary syndrome care management and activation of catheterization laboratories, new trials in antiplatelet therapies, and improved implementation of GDMT in this population, all of which may all contribute to improvements in outcomes for these patients.1,4 Given the high morbidity and mortality associated with HF after an MI, it is important to understand the contemporary demographic and clinical profile of these high-risk patients in order to provide best care, and to inform future trials investigating potential therapies for this vulnerable population. We therefore read with great interest the paper by Docherty et al.5 exploring trends in HF hospitalization after a first-time acute","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"25 8","pages":"1225-1227"},"PeriodicalIF":18.2,"publicationDate":"2023-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5745735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Foetal recapitulation of nutrient surplus signalling by O-GlcNAcylation and the failing heart","authors":"Milton Packer","doi":"10.1002/ejhf.2972","DOIUrl":"https://doi.org/10.1002/ejhf.2972","url":null,"abstract":"<p>The development of the foetal heart is driven by increased glucose uptake and activation of mammalian target of rapamycin (mTOR) and hypoxia-inducible factor-1α (HIF-1α), which drives glycolysis. In contrast, the healthy adult heart is governed by sirtuin-1 (SIRT1) and adenosine monophosphate-activated protein kinase (AMPK), which promote fatty-acid oxidation and the substantial mitochondrial ATP production required for survival in a high-workload normoxic environment. During cardiac injury, the heart recapitulates the foetal signalling programme, which (although adaptive in the short term) is highly deleterious if sustained for long periods of time. Prolonged increases in glucose uptake in cardiomyocytes under stress leads to increased flux through the hexosamine biosynthesis pathway; its endproduct – uridine diphosphate <i>N</i>-acetylglucosamine (UDP-GlcNAc) – functions as a critical nutrient surplus sensor. UDP-GlcNAc drives the post-translational protein modification known as O-GlcNAcylation, which rapidly and reversibly modifies thousands of intracellular proteins. Both O-GlcNAcylation and phosphorylation act at serine/threonine residues, but whereas phosphorylation is regulated by hundreds of specific kinases and phosphatases, O-GlcNAcylation is regulated by only two enzymes, O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), which adds or removes GlcNAc (N-acetylglucosamine), respectively, from target proteins. Recapitulation of foetal programming in heart failure (regardless of diabetes) is accompanied by marked increases in O-GlcNAcylation, both experimentally and clinically. Heightened O-GlcNAcylation in the heart leads to impaired calcium kinetics and contractile derangements, arrhythmias related to activation of voltage-gated sodium channels and Ca²⁺/calmodulin-dependent protein kinase II, mitochondrial dysfunction, and maladaptive hypertrophy, microvascular dysfunction, fibrosis and cardiomyopathy. These deleterious effects can be prevented by suppression of O-GlcNAcylation, which can be achieved experimentally by upregulation of AMPK and SIRT1 or by pharmacological inhibition of OGT or stimulation of OGA. The effects of sodium–glucose cotransporter 2 (SGLT2) inhibitors on the heart are accompanied by reduced O-GlcNAcylation, and their cytoprotective effects are reportedly abrogated if their action to suppress O-GlcNAcylation is blocked. Such an action may represent one of the many mechanisms by which enhanced AMPK and SIRT1 signalling following SGLT2 inhibition leads to cardiovascular benefits. These observations, taken collectively, suggest that UDP-GlcNAc functions as a critical nutrient surplus sensor (which acting in concert with mTOR and HIF-1α) can promote the development of cardiomyopathy.</p>","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"25 8","pages":"1199-1212"},"PeriodicalIF":18.2,"publicationDate":"2023-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ejhf.2972","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6178614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"June 2023 at a glance: focus on worsening heart failure, heart failure with preserved ejection fraction and valvular heart disease","authors":"Daniela Tomasoni,&nbsp;Marianna Adamo,&nbsp;Marco Metra","doi":"10.1002/ejhf.2954","DOIUrl":"https://doi.org/10.1002/ejhf.2954","url":null,"abstract":"Episodes of worsening heart failure (HF) are landmark events in the clinical course, followed by an increased risk of hospitalizations and death.1–5 The Heart Failure Association (HFA) of the European Society of Cardiology (ESC) provided a new definition of worsening chronic HF: worsening symptoms and signs of HF in patients with pre-existing HF, requiring intensification of treatment, most often diuretic therapy. Of note, intensification of treatment also includes escalation of oral diuretics and/or admission to ambulatory or emergency department.6 A secondary analysis of the REPORT-HF (prospective international REgistry to assess medical Practice with lOngitudinal obseRvation for Treatment of Heart Failure) registry sought to examine the utilization of healthcare resources for hospitalized patients with HF across the spectrum of left ventricular ejection fraction (LVEF). HF with reduced ejection fraction (HFrEF) was the most prevalent. The length of hospitalization was similar irrespective of LVEF. Prescription of neurohormonal antagonists was suboptimal in HFrEF at discharge, similar to what shown in other registries.7 The risk of 12-month all-cause and cardiovascular mortality were lower for HF with mildly reduced ejection fraction and HF with preserved ejection fraction (HFpEF), compared to HFrEF.8,9 Changes in plasma concentrations of biomarkers may predict the development of HF or worsening HF events.10–12 Oyama et al.13 investigated the role of three biomarkers – high-sensitivity troponin T (hsTnT), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and growth differentiation factor-15 (GDF-15) – measured at baseline and at 12 months in predicting HF outcome among patients with atrial fibrillation enrolled in the ENGAGE AF-TIMI 48 trial. Serial measurement of hsTnT, NT-proBNP, and GDF-15 revealed that higher baseline values, and increasing or persistently elevated values over 1 year are associated with higher risk of HF outcomes in patients with atrial fibrillation regardless of HF history or HF phenotype based on LVEF. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. . Heart failure with preserved ejection fraction","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"25 6","pages":"773-775"},"PeriodicalIF":18.2,"publicationDate":"2023-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6162524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Supplement Article","authors":"","doi":"10.1002/ejhf.2927","DOIUrl":"https://doi.org/10.1002/ejhf.2927","url":null,"abstract":"","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"25 S2","pages":"3-457"},"PeriodicalIF":18.2,"publicationDate":"2023-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ejhf.2927","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5726089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sodium–glucose cotransporter 2 inhibitors in heart failure with preserved ejection fraction: Treat the heart, cherish the kidney","authors":"Geert Voordes,&nbsp;Kevin Damman","doi":"10.1002/ejhf.2963","DOIUrl":"https://doi.org/10.1002/ejhf.2963","url":null,"abstract":"","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"25 8","pages":"1349-1351"},"PeriodicalIF":18.2,"publicationDate":"2023-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6089820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exercise left atrial compliance: One more tool in the heart failure with preserved ejection fraction assistance toolbox?","authors":"Cho-Kai Wu,&nbsp;Li-Tan Yang,&nbsp;Chung-Lieh Hung","doi":"10.1002/ejhf.2966","DOIUrl":"https://doi.org/10.1002/ejhf.2966","url":null,"abstract":"This article refers to ‘Diagnostic value of reduced left atrial compliance during ergometry exercise in heart failure with preserved ejection fraction’ by T. Harada et al. , published in this issue on pages 1 293– 1 303. Heart failure with preserved ejection fraction (HFpEF) accounts for approximately half of all heart failure cases; however, the exact clinical diagnosis of HFpEF remains challenging. According to the 202 1 European Society of Cardiology guidelines, exercise invasive haemodynamic cardiac catheterization remains the gold standard to unequivocally confirm the diagnosis of HFpEF for those with inconclusive results from diagnostic criteria. 1 Typical haemodynamic presentations in HFpEF patients may include elevations in left ventricular end-diastolic pressure (LVEDP), pulmonary capillary wedge pressure (PCWP), and pulmonary artery pressure, which occur in parallel to each other. Provoked haemodynamics during exercise is crucial for patients with HFpEF, as some patients with HFpEF may show normal PCWP at rest under scenarios of decon-gestive or euvolaemic status (masked) and manifest a steep rise of PCWP during exercise from increased venous return into a more stiff left ventricle. 2 In this case, abnormal haemodynamic responses during exercise, yet maintained within normal range at rest, reflects impaired diastolic functional reserve in HFpEF, and may lead to limited exercise capacity presenting with exertional dyspnoea and effort intolerance ( Figure 1 A ). 3 This emphasizes the role of","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"25 8","pages":"1307-1309"},"PeriodicalIF":18.2,"publicationDate":"2023-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6089826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reply to ‘Vericiguat in heart failure with reduced ejection fraction: the right choice above all else? The answer\u0000may lie in time’","authors":"Burkert Pieske,&nbsp;Paul W. Armstrong,&nbsp;for the VICTORIA Study Group","doi":"10.1002/ejhf.2964","DOIUrl":"https://doi.org/10.1002/ejhf.2964","url":null,"abstract":"","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"25 8","pages":"1470-1471"},"PeriodicalIF":18.2,"publicationDate":"2023-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6089827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Changes in mid-regional pro-adrenomedullin during treatment with sacubitril/valsartan","authors":"Peder L. Myhre,&nbsp;Yuxi Liu,&nbsp;Ian J. Kulac,&nbsp;Brian L. Claggett,&nbsp;Margaret F. Prescott,&nbsp;G. Michael Felker,&nbsp;Javed Butler,&nbsp;Ileana L. Pi?a,&nbsp;Jean L. Rouleau,&nbsp;Michael R. Zile,&nbsp;John J.V. McMurray,&nbsp;Jonathan H. Ward,&nbsp;Scott D. Solomon,&nbsp;James L. Januzzi","doi":"10.1002/ejhf.2957","DOIUrl":"https://doi.org/10.1002/ejhf.2957","url":null,"abstract":"Adrenomedullin is a vasodilatory peptide with a role in microcirculatory and endothelial homeostasis. Adrenomedullin is a substrate for neprilysin and may therefore play a role in beneficial effects of sacubitril/valsartan (Sac/Val) treatment.","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"25 8","pages":"1396-1405"},"PeriodicalIF":18.2,"publicationDate":"2023-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ejhf.2957","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5968440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}