ESC Heart Failure最新文献

{"title":"Phenotyping patients with chronic obstructive pulmonary disease and heart failure.","authors":"Peter Moritz Becher, Felix Lindberg, Lina Benson, Camilla Hage, Ulf Dahlström, Stephan Rosenkranz, Francesco Cosentino, Giuseppe M C Rosano, Stefan Blankenberg, Paulus Kirchhof, Frieder Braunschweig, Lars H Lund, Gianluigi Savarese","doi":"10.1002/ehf2.15127","DOIUrl":"https://doi.org/10.1002/ehf2.15127","url":null,"abstract":"<p><strong>Aims: </strong>Chronic obstructive pulmonary disease (COPD) and heart failure (HF) are prevalent comorbidities associated with significant morbidity/mortality. We assessed prevalence of, patient profiles and outcomes associated with COPD across the ejection fraction (EF) spectrum.</p><p><strong>Methods: </strong>HF patients enrolled in the Swedish HF registry between 2005 and 2021 were considered. Multivariable logistic regression models were fitted to assess patient characteristics independently associated with COPD and Cox regression models for investigating the associations between COPD and outcomes, that is, morbidity/mortality.</p><p><strong>Results: </strong>Among 97 904 HF patients, COPD prevalence was 13%, highest in HF with preserved EF [HFpEF: 16%, HF with mildly reduced EF (HFmrEF): 12%, HF with reduced EF (HFrEF): 11%]. Key patient characteristics independently associated with a diagnosis of COPD included higher EF, female sex, smoking, obstructive sleep disorder, peripheral artery disease, a lower educational level, more severe HF, more likely mineralocorticoid receptor antagonist and diuretic use but less likely use of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers/angiotensin-receptor-neprilysin inhibitors (not in HFrEF), beta-blockers, HF device therapies, and follow-up in HF nurse-led clinics. COPD was independently associated with a 15% higher risk of cardiovascular (CV) death/HF hospitalization [hazard ratio: 1.15 (95% confidence interval: 1.11-1.18)], CV death, non-CV death, all-cause death and HF hospitalizations, regardless of EF.</p><p><strong>Conclusions: </strong>COPD was present in every eight patient with HF, and more common with preserved EF. Patients with COPD had more severe HF, heavier comorbidity burden and worse morbidity/mortality regardless of EF. Our results call for improved diagnostic and management strategies in patients with HF and COPD.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevalence of transthyretin cardiac amyloidosis in undifferentiated heart failure with preserved ejection fraction.","authors":"L Healy, G Giblin, A Gray, N Starr, L Murphy, D O'Sullivan, E Kavanagh, C Howley, C Tracey, E Morrin, A McDaid, A Clarke, J O O'Neill, E Joyce, M O'Connell, N G Mahon","doi":"10.1002/ehf2.15112","DOIUrl":"https://doi.org/10.1002/ehf2.15112","url":null,"abstract":"<p><strong>Aims: </strong>Transthyretin amyloid cardiomyopathy (ATTR-CM) is an increasinglyrecognized cause of heart failure with preserved ejection fraction (HFpEF), which may be diagnosed non-invasively using ⁹⁹ ^mTc 3,3-diphosphono-1,2-propanodicarboxylic acid (DPD) scintigraphy-based diagnostic criteria. Our aim was to determine the prevalence of ATTR-CM in an undifferentiated HFpEF cohort with a DPD scintigraphy-based screening protocol.</p><p><strong>Methods: </strong>Patients with HFpEF [ejection fraction (EF) ≥50%] aged ≥60 years and no prior evaluation for cardiac amyloidosis or known monoclonal gammopathy attending a regional cardiology network were screened with DPD scintigraphy. Patients with positive myocardial uptake (Perugini grade 2 or 3) were tested for a monoclonal protein and transthyretin gene variant.</p><p><strong>Results: </strong>Eighty-six subjects were prospectively enrolled: 56% female, mean age 77 ± 8 years, 63% New York Heart Association (NYHA) Class III and median N-terminal pro-brain natriuretic peptide (NT-proBNP) 1766 ng/L [inter-quartile range (IQR) 731-3703]. DPD scintigraphy was positive in seven patients (8%). Monoclonal gammopathy of undetermined significance was present in one out of seven patients, and no pathogenic TTR gene variant was identified. The prevalence of wild-type ATTR-CM was 8% of this cohort. Compared with the HFpEF DPD scintigraphy-negative cohort, DPD scintigraphy-positive patients were older (86 ± 3 vs. 76 ± 8 years), more frequently male (16% vs. 2%, P = 0.02), and had significantly greater left ventricular (LV) wall thickness (16 vs. 12 mm; P = 0.002) and higher high-sensitivity troponin levels at diagnosis [78 ng/L (IQR 21-116) vs. 11 ng/L (IQR 9-17); P < 0.001].</p><p><strong>Conclusions: </strong>In an undifferentiated HFpEF cohort, 8% were found to have wild-type ATTR-CM using a DPD scintigraphy-based screening protocol. Screening undifferentiated HFpEF patients is associated with a significant diagnostic yield, which can be further increased by targeting older males with increased LV wall thickness and elevated high-sensitivity troponin levels.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Real-world characteristics and treatment of cardiac transthyretin amyloidosis: A multicentre, observational study.","authors":"Richard J Nies, Svenja Ney, Ingrid Kindermann, Yvonne Bewarder, Angela Zimmer, Fabian Knebel, Katrin Hahn, Sebastian Spethmann, Peter Luedike, Lars Michel, Tienush Rassaf, Maria Papathanasiou, Stefan Störk, Vladimir Cejka, Amin Polzin, Fabian Voss, Malte Kelm, Bernhard Unsöld, Christine Meindl, Michael Paulus, Ali Yilmaz, Bishwas Chamling, Caroline Morbach, Roman Pfister","doi":"10.1002/ehf2.15126","DOIUrl":"https://doi.org/10.1002/ehf2.15126","url":null,"abstract":"<p><strong>Aims: </strong>Data on the clinical profiles of patients with transthyretin amyloidosis cardiomyopathy (ATTR-CM) in the post-approval era of tafamidis 61 mg are lacking. Study aims were characterization of contemporary ATTR-CM patients, analysis of potential eligibility for the 'Transthyretin Amyloidosis Cardiomyopathy Clinical Trial' (ATTR-ACT) and identification of factors associated with the decision on tafamidis 61 mg treatment.</p><p><strong>Methods and results: </strong>This retrospective study analysed ATTR-CM patients seen at eight University Hospitals in the first year after approval of tafamidis 61 mg for ATTR-CM in Germany (April 2020 to March 2021). The cohort comprised 366 patients (median age 79 [74; 82] years, 84% male), with 47% and 45% of the cohort being in National Amyloidosis Centre ATTR stage ≥ II and NYHA class ≥ III, respectively. Sixty-four per cent of patients met key eligibility criteria of the pivotal ATTR-ACT. In recently diagnosed patients (58% with diagnosis ≤6 months), the rate of variant ATTR was significantly lower than in patients diagnosed more than 6 months ago (9.3% vs. 19.7%). Of the 293 patients without prior ATTR specific treatment, tafamidis 61 mg was newly initiated in 77%. Patients with tafamidis 61 mg treatment were significantly younger, were more often eligible for ATTR-ACT, had lower NYHA class and higher serum albumin levels. These variables explained 16% of the variance of treatment decision. Unadjusted survival was higher in patients with than those without treatment (1-year survival 98.6% vs. 87.3%, P < 0.001).</p><p><strong>Conclusions: </strong>Wild-type ATTR was the primary aetiology amongst contemporary ATTR-CM patients and almost two-thirds of patients were in an advanced disease stage. Clinical profiles of 64% of patients in routine care matched those of the ATTR-ACT. Further effort is needed to detect patients at an earlier disease stage and to validate criteria justifying treatment initiation.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prognostic impact of iron deficiency in new-onset chronic heart failure: Danish Heart Failure Registry insights.","authors":"Abdullahi Ahmed Mohamed, Daniel Mølager Christensen, Milan Mohammad, Christian Torp-Pedersen, Lars Køber, Emil Loldrup Fosbøl, Tor Biering-Sørensen, Morten Lock Hansen, Mariam Elmegaard Malik, Nina Nouhravesh, Charlotte Anderrson, Morten Schou, Gunnar Gislason","doi":"10.1002/ehf2.15149","DOIUrl":"https://doi.org/10.1002/ehf2.15149","url":null,"abstract":"<p><strong>Aims: </strong>Iron deficiency (ID) is prevalent in chronic heart failure (HF) but lacks a consensus definition. This study evaluates the prevalence and the prognostic impact of ID using different criteria on all-cause and cardiovascular mortality, as well as first hospitalization for HF in patients with new-onset chronic HF.</p><p><strong>Methods: </strong>In this nationwide registry-based cohort, we explored four definitions of ID: the current European Society of Cardiology (ESC) guidelines [ferritin <100 ng/mL or ferritin 100-299 ng/mL and transferrin saturation (TSAT) <20%], ferritin level <100 ng/mL, TSAT < 20% and serum iron ≤13 μmol/L. Patients were identified through the Danish Heart Failure Registry.</p><p><strong>Results: </strong>Of 9477 new-onset chronic HF patients registered in the Danish Heart Failure Registry from April 2003 to December 2019, we observed ID prevalence rates ranging from 35.8% to 64.3% depending on the ID definition used. Among patients with ID defined by iron ≤13 μmol/L or TSAT < 20%, 26% and 15.5%, respectively, did not meet the ESC guidelines definition for ID. Conversely, 11% of patients meeting the ESC criteria exhibited serum iron >13 μmol/L and TSAT > 20%. Regardless of anaemia status, ID defined by TSAT < 20% or serum iron ≤13 μmol/L was associated with all-cause mortality [non-anaemic, hazard ratio (HR): 1.57, 95% confidence interval (CI): 1.30-1.89 and HR: 1.47, 95% CI: 1.24-1.73; anaemic, HR: 1.22, 95% CI: 1.07-1.38 and HR: 1.25, 95% CI: 1.09-1.44, respectively] and cardiovascular mortality (non-anaemic, HR: 2.21, 95% CI: 1.59-3.06 and HR: 1.47, 95% CI: 1.12-1.95; anaemic, HR: 1.37, 95% CI: 1.11-1.69 and HR: 1.28, 95% CI: 1.02-1.61, respectively), as well as increased risk of first hospitalization for HF (non-anaemic, HR: 1.28, 95% CI: 1.09-1.1.50 and HR: 1.27, 95% CI: 1.10-1.46; anaemic, HR: 1.25, 95% CI: 1.08-1.44 and HR: 1.22, 95% CI: 1.05-1.42, respectively). ID defined by ESC guidelines was associated with all-cause and cardiovascular mortality only in non-anaemic patients (HR: 1.41, 95% CI: 1.18-1.1.70 and HR: 1.58, 95% CI: 1.18-2.12.). Furthermore, the ESC guideline definition was associated with increased risk of first hospitalization for HF, regardless of anaemia status (non-anaemic, HR: 1.26, 95% CI: 1.08-1.1.47; anaemic, HR: 1.34, 95% CI: 1.17-1.53).</p><p><strong>Conclusions: </strong>ID, when defined by TSAT < 20% or serum iron ≤13 μmol/L, is associated with increased risk of all-cause and cardiovascular mortality, as well as first hospitalization for HF in patients with new-onset chronic HF, regardless of anaemia status. Conversely, ID defined as ESC guidelines is associated with all-cause and cardiovascular mortality only in non-anaemic patients.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causal correlations between inflammatory proteins and heart failure: A two-sample Mendelian randomization analysis.","authors":"Xian-Guan Zhu, Gui-Qin Liu, Ya-Ping Peng, Li-Ling Zhang, Xian-Jin Wang, Liang-Chuan Chen, Yuan-Xi Zheng, Xue-Jun Xiang, Rui Qiao, Xian-He Lin","doi":"10.1002/ehf2.15151","DOIUrl":"https://doi.org/10.1002/ehf2.15151","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Aims: &lt;/strong&gt;Inflammation plays a critical role in both the development and progression of heart failure (HF), which is a leading cause of morbidity and mortality worldwide. However, the causality between specific inflammation-related proteins and HF risk remains unclear. This study aims to investigate the genetically supported causality between inflammatory proteins and HF using a two-sample Mendelian randomization (MR) analysis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods and results: &lt;/strong&gt;We utilized genome-wide association study (GWAS) data of 91 inflammation-related proteins as exposures from the SCALLOP Consortium (14,824 participants), alongside outcome GWAS summary statistics from FinnGen (29,218 cases/381,838 controls) and HERMES (47,309 cases/930,014 controls) for HF, to conduct a two-sample MR analysis. For each inflammatory protein, instrumental variables (IVs) were chosen following the three foundational assumptions of the MR analysis, requiring a minimum of three qualifying single nucleotide polymorphisms (SNPs) each with a P &lt; 5e-8. Associations between inflammatory proteins and HF were assessed through inverse-variance weighted (IVW), MR-Egger regression, weighted median and weighted mode analysis. The reliability and validity of the results were evaluated by examining heterogeneity, horizontal pleiotropy, leave-one-out analysis, meta-analysis and reverse MR analysis. Heterogeneity refers to the variation in results across different genetic variants. Horizontal pleiotropy occurs when a genetic variant influences multiple traits through different biological pathways. Addressing both heterogeneity and horizontal pleiotropy is crucial for ensuring the reliability and interpretability of MR results. Our analysis identified associations between three inflammatory proteins and HF risk. Matrix metalloproteinase-1 (MMP-1) (OR, 1.09; 95% CI, 1.00-1.18; P = 0.04) and TNF-beta (OR, 1.05; 95% CI, 1.01-1.09; P = 0.01) were positively associated with HF risk in FinnGen. In contrast, urokinase-type plasminogen activator (uPA) was inversely associated with HF risk in both FinnGen (OR, 0.85; 95% CI, 0.78-0.92; P = 3.27e-5) and HERMES (OR, 0.93; 95% CI, 0.87-0.99; P = 0.03). No evidence of heterogeneity and horizontal pleiotropy was observed in the MR analysis, indicating the robustness of our findings. A meta-analysis further supported this association, indicating a reduced risk (OR, 0.89; 95% CI, 0.81-0.98; P = 0.02). No reverse causality was found between HF and these three inflammatory proteins (P &gt; 0.05 for all).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;This study provides genetically supported evidence of the causal association of specific inflammatory proteins with HF risk. The positive association of MMP-1 and TNF-beta with HF suggests their roles in disease pathogenesis, whereas the inverse association of the uPA indicates its potential protective effect. Our findings highlight the potential of targeting specific inflammatory pathways as a therapeut","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic abnormalities and reprogramming in cats with naturally occurring hypertrophic cardiomyopathy.","authors":"Qinghong Li, Max Homilius, Erin Achilles, Laura K Massey, Victoria Convey, Åsa Ohlsson, Ingrid Ljungvall, Jens Häggström, Brittany Vester Boler, Pascal Steiner, Sharlene Day, Calum A MacRae, Mark A Oyama","doi":"10.1002/ehf2.15135","DOIUrl":"https://doi.org/10.1002/ehf2.15135","url":null,"abstract":"<p><strong>Background and aims: </strong>The heart is a metabolic organ rich in mitochondria. The failing heart reprograms to utilize different energy substrates, which increase its oxygen consumption. These adaptive changes contribute to increased oxidative stress. Hypertrophic cardiomyopathy (HCM) is a common heart condition, affecting approximately 15% of the general cat population. Feline HCM shares phenotypical and genotypical similarities with human HCM, but the disease mechanisms for both species are incompletely understood. Our goal was to characterize global changes in metabolome between healthy control cats and cats with different stages of HCM.</p><p><strong>Methods: </strong>Serum samples from 83 cats, the majority (70/83) of which were domestic shorthair and included 23 healthy control cats, 31 and 12 preclinical cats with American College of Veterinary Internal Medicine (ACVIM) stages B1 and B2, respectively, and 17 cats with history of clinical heart failure or arterial thromboembolism (ACVIM stage C), were collected for untargeted metabolomic analysis. Multiple linear regression adjusted for age, sex and body weight was applied to compare between control and across HCM groups.</p><p><strong>Results: </strong>Our study identified 1253 metabolites, of which 983 metabolites had known identities. Statistical analysis identified 167 metabolites that were significantly different among groups (adjusted P < 0.1). About half of the differentially identified metabolites were lipids, including glycerophospholipids, sphingolipids and cholesterol. Serum concentrations of free fatty acids, 3-hydroxy fatty acids and acylcarnitines were increased in HCM groups compared with control group. The levels of creatine phosphate and multiple Krebs cycle intermediates, including succinate, aconitate and α-ketoglutarate, also accumulated in the circulation of HCM cats. In addition, serum levels of nicotinamide and tryptophan, precursors for de novo NAD+ biosynthesis, were reduced in HCM groups versus control group. Glutathione metabolism was altered. Serum levels of cystine, the oxidized form of cysteine and cysteine-glutathione disulfide, were elevated in the HCM groups, indicative of heightened oxidative stress. Further, the level of ophthalmate, an endogenous glutathione analog and competitive inhibitor, was increased by more than twofold in HCM groups versus control group. Finally, several uremic toxins, including guanidino compounds and protein bound putrescine, accumulated in the circulation of HCM cats.</p><p><strong>Conclusions: </strong>Our study provided evidence of deranged energy metabolism, altered glutathione homeostasis and impaired renal uremic toxin excretion. Altered lipid metabolism suggested perturbed structure and function of cardiac sarcolemma membrane and lipid signalling.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Left ventricular diastolic dysfunction worsens prognosis in patients with heart failure due to dilated cardiomyopathy.","authors":"Mateusz Winiarczyk, Ewa Dziewięcka, Sylwia Wiśniowska-Śmiałek, Agnieszka Stępień, Katarzyna Graczyk, Agata Leśniak-Sobelga, Marta Hlawaty, Jakub Woźniak, Maryia Savitskaya, Katarzyna Holcman, Magdalena Kostkiewicz, Piotr Podolec, Paweł Rubiś","doi":"10.1002/ehf2.15119","DOIUrl":"https://doi.org/10.1002/ehf2.15119","url":null,"abstract":"<p><strong>Aims: </strong>The prognostic significance of left ventricular (LV) diastolic dysfunction (LVDD) severity in patients with dilated cardiomyopathy (DCM) remains uncertain. This study aimed to evaluate the association of LVDD severity and elevated left atrial pressure (eLAP) with patient outcomes in stable, non-acutely decompensated patients with DCM.</p><p><strong>Methods: </strong>This single-centre, retrospective, observational study involved 740 DCM patients (either inpatients or outpatients) managed at our tertiary cardiac centre between 2010 and 2021. Due to incomplete data, 96 patients were excluded. LVDD and eLAP were assessed using echocardiography according to the 2016 guidelines of the European Association of Cardiovascular Imaging (EACVI). The primary outcomes were all-cause mortality and heart failure (HF)-related mortality.</p><p><strong>Results: </strong>The final cohort comprised of 644 DCM patients [mean age: 52 ± 12 years, LV ejection fraction (LVEF): 26 ± 10%]. Over a median follow-up period of 41 (18.5-66.7) months, 105 (16.3%) patients died: 8 (5.3%) patients in the normal left atrial pressure (nLAP) group and 97 (19.6%) patients in the eLAP group. eLAP was identified as an independent prognostic factor for both all-cause mortality [hazard ratio (HR) 2.0; 95% confidence interval (CI) 1.1-3.7; P = 0.01] and HF-related mortality (HR 2.5; 95% CI 1.01-6.5; P = 0.04), even after adjusting for LVEF and atrial fibrillation (AF) presence. Additionally, HF-related mortality rates were significantly higher in patients with moderate to severe LVDD compared with those with mild LVDD [5 (3.3%) vs. 67 (13.6%), P < 0.05].</p><p><strong>Conclusions: </strong>This study's findings highlight the importance of assessing the severity of LVDD in patients with DCM, which provides incremental prognostic information over LVEF.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142574912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Delphi consensus project to capture experts' opinion on hyperkalaemia management across the cardiorenal spectrum.","authors":"Christina Chrysohoou, Maria Marketou, Maria Aktsiali, Ioannis Griveas","doi":"10.1002/ehf2.15153","DOIUrl":"https://doi.org/10.1002/ehf2.15153","url":null,"abstract":"<p><p>The main purpose of this project was to capture experts' opinion on hyperkalaemia management and form best practice recommendations for cardiorenal patients in Greece. A steering committee of nephrologists and cardiologists developed 37 statements. An online questionnaire completed by 32 experts in cardiorenal management in Greece. Median score used to determine the level of agreement and disagreement index (DI) used to determine the level of consensus for each statement. Statements divided in four sectors: hyperkalaemia risk management, preventative measures, treatment and collaboration between specialties. The rate of the first round of the consensus was 94.6%. Median score was >7 for 36 of 37 statements and DI ≤ 1 for 35 of 37. Among other statements, consensus reached for recognizing levels K+ > 5.0 mEq/L as associated with elevated mortality risk; retaining renin-angiotensin-aldosterone system inhibitors (RAASi) on maximum recommended dose for cardiorenal patients; and using novel K+ binders to help enabling guideline-recommended doses of RAASi therapy. Cardiologists compared to nephrologists showed higher reluctance to discontinue down-titrate RAASi and MRA in patients with K+ levels above 5 mEq/L. Additionally, 88.9% of nephrologists and 71.4% of cardiologists agreed that cross-specialty alignment on a serum K+ concentration level (K > 5.5 mEq/L) is needed to initiate hyperkalaemia treatment. Both cardiologists and nephrologists showed disagreement with the statement on keeping titration in cardiorenal patients with K+ > 5.5 mEq/L or preserving fruit and vegetable consumption when moderate or severe hyperkalaemia exhibits. This Delphi project pointed out nephrologists' and cardiologists' agreement on hyperkalaemia management in cardiorenal patients; thus, it can help a cross-specialty optimal management of cardiorenal patients, with hyperkalaemia not being an obstacle for disease-optimizing therapy. Novel potassium binding agents can enable guideline-recommended doses of potassium-sparing medication.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A phenomap of TTR amyloidosis to aid diagnostic screening.","authors":"Alexios S Antonopoulos, Theodoros Tsampras, George Lazaros, Konstantinos Tsioufis, Charalambos Vlachopoulos","doi":"10.1002/ehf2.15143","DOIUrl":"https://doi.org/10.1002/ehf2.15143","url":null,"abstract":"<p><p>Cardiac amyloidosis due to transthyretin (ATTR) remains an underdiagnosed cause of cardiomyopathy. As awareness of the disease grows and referrals for ATTR increase, clinicians are likely to encounter more atypical forms of the condition in clinical practice. Therefore, physicians and treating cardiologists should be aware of the full phenotypic spectrum of ATTR. The phenotypic manifestation of ATTR varies depending on the stage of the disease, the presence and type of TTR mutation and the patient's comorbidities. ATTR findings can be grouped into four major categories: clinical profile and cardiac phenotype, extra-cardiac findings, electrocardiogram and imaging findings, which cumulatively form the full phenomap of ATTR. Results from any diagnostic test for ATTR should be interpreted in light of the pre-test probability for the disease. Findings that suggest negative markers for ATTR can point towards other forms of amyloidosis (such as AL amyloidosis) or alternate causes of left ventricular hypertrophy, including hypertrophic cardiomyopathy or Fabry disease. The rising number of referrals for ATTR cardiomyopathy presents a challenge in daily clinical practice. To prevent an increase in false-positive diagnostic test results, an ATTR phenomap can serve as a valuable tool for guiding diagnostic assessments, interpreting test outcomes and prioritizing appropriate referrals for ATTR screening.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Semaglutide normalizes increased cardiomyocyte calcium transients in a rat model of high fat diet-induced obesity.","authors":"Vasco Sequeira, Julia Theisen, Katharina J Ermer, Marie Oertel, Anton Xu, David Weissman, Katharina Ecker, Jan Dudek, Martin Fassnacht, Alexander Nickel, Michael Kohlhaas, Christoph Maack, Ulrich Dischinger","doi":"10.1002/ehf2.15152","DOIUrl":"https://doi.org/10.1002/ehf2.15152","url":null,"abstract":"<p><strong>Aims: </strong>Obesity increases the risk of heart failure with preserved (HFpEF), but not reduced ejection fraction (HFrEF). The glucagon-like peptide-1 receptor agonist (GLP-1-RA) semaglutide improves outcome of patients with obesity with or without HFpEF, while GLP-1-RAs were associated with adverse outcome in patients with HFrEF. Here, we investigate the effect of in vivo treatment with semaglutide on excitation-contraction coupling in a rat model of obesity.</p><p><strong>Methods and results: </strong>Rats received high-fat/high-fructose diet for 8 weeks and were then randomized to semaglutide (HFD/Sema) or vehicle (HFD/Veh) for another 8 weeks, during which they could choose between HFD and a low-fat/high-fructose diet (LFD). Control rats received either standard chow (CON), HFD or LFD only, without treatment. After 16 weeks, sarcomere shortening and cytosolic Ca²⁺ concentrations ([Ca²⁺]_c) were determined in isolated cardiomyocytes. Compared with CON, HFD/Veh increased the amplitude of [Ca²⁺]_c transients and systolic sarcomere shortening in absence or presence of β-adrenergic stimulation, which was reversed by HFD/Sema. Caffeine-induced sarcoplasmic reticulum (SR) Ca²⁺ release and L-type Ca²⁺ channel (LTCC) currents were reduced by HFD/Sema versus HFD/Veh, while SR Ca²⁺ ATPase activity remained unaffected. Compared with HFD, LFD increased [Ca²⁺]_c transients and sarcomere shortening further despite similar effects on body weight.</p><p><strong>Conclusions: </strong>While HFD increased cardiomyocyte [Ca²⁺]_c transients and systolic sarcomere shortening, semaglutide normalized these alterations, mediated by reduced SR Ca²⁺ load and LTCC currents. Because increased LTCC currents were previously traced to cardiac hypertrophy, these effects may explain why GLP-1-RAs provide benefits for patients with obesity with or without HFpEF, but rather adverse outcome in HFrEF.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}