Rachel K Hopper, Georg Hansmann, Seth A Hollander, Anne I Dipchand, Oscar van der Have, Colleen Iler, Cynthia Herrington, Erika B Rosenzweig, Juan C Alejos, Karin Tran-Lundmark
{"title":"Clinical Management and Transplant Considerations in Pediatric Pulmonary Hypertension Due to Left Heart Disease: A Scientific Statement From the American Heart Association.","authors":"Rachel K Hopper, Georg Hansmann, Seth A Hollander, Anne I Dipchand, Oscar van der Have, Colleen Iler, Cynthia Herrington, Erika B Rosenzweig, Juan C Alejos, Karin Tran-Lundmark","doi":"10.1161/HHF.0000000000000086","DOIUrl":"10.1161/HHF.0000000000000086","url":null,"abstract":"<p><p>Children with left heart disease are at risk for developing pulmonary hypertension, initially secondary to pulmonary venous hypertension that can progress to include elevated pulmonary vascular resistance, known as combined pre- and postcapillary pulmonary hypertension. Elevated pulmonary vascular resistance may pose a risk to the right ventricle of a newly transplanted heart because of increased afterload and is an important consideration for heart transplant eligibility. However, the epidemiology, pathophysiology, optimal diagnostic and treatment approaches, and thresholds for pulmonary vascular resistance in pulmonary hypertension associated with left heart disease remain unclear because of lack of evidence, particularly in pediatrics. The result is heterogeneity with respect to hemodynamic assessment, use of pulmonary vasodilator therapies, and heart transplant listing. This scientific statement aims to synthesize the available data and highlight areas of general consensus as well as important knowledge gaps.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e000086"},"PeriodicalIF":7.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794253","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}
Circulation: Heart FailurePub Date : 2025-01-01Epub Date: 2024-11-29DOI: 10.1161/CIRCHEARTFAILURE.124.011724
María Villalba-Orero, Marina López-Olañeta, Belén Campos-Olmo, Daniel Jimenez-Carretero, Lucía Sánchez, Fátima Sánchez-Cabo, Antonella Ausiello, Rodrigo Cañas-Álvaro, Emilio Camafeita, Jesús Vázquez, Pablo García-Pavía, Domingo Pascual-Figal, Enrique Lara-Pezzi
{"title":"Unraveling Comorbidities Contribution to Cardiac Diastolic Dysfunction and Heart Failure.","authors":"María Villalba-Orero, Marina López-Olañeta, Belén Campos-Olmo, Daniel Jimenez-Carretero, Lucía Sánchez, Fátima Sánchez-Cabo, Antonella Ausiello, Rodrigo Cañas-Álvaro, Emilio Camafeita, Jesús Vázquez, Pablo García-Pavía, Domingo Pascual-Figal, Enrique Lara-Pezzi","doi":"10.1161/CIRCHEARTFAILURE.124.011724","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.011724","url":null,"abstract":"<p><strong>Background: </strong>Heart failure with preserved ejection fraction (HFpEF) is a major public health problem characterized by multiple simultaneous comorbidities whose specific contribution is challenging to disentangle in humans, leading to a generalized therapeutic approach that may not account for the underlying pathology.</p><p><strong>Methods: </strong>We followed distinct mouse models of major HFpEF comorbidities for 2.5 years to unveil their specific contribution to the syndrome.</p><p><strong>Results: </strong>All comorbidities contributed to HFpEF through partially distinct routes. Aging alone resulted in HFpEF in old age, with delayed left ventricular relaxation and kidney fibrosis. Obesity induced a faster deterioration of relaxation associated with enlarged left ventricle and liver fibrosis. Hypertension caused delayed ventricular relaxation independent from structural changes that preceded left atrial dilatation linked to aortic stiffness and increased fibrosis in myocardium and kidney. Chronic intermittent hypoxia led to HFpEF and relaxation impairment associated with pulmonary hypertension. Hyperglycemia accelerated diastolic dysfunction and HFpEF onset associated with reduced arterial flow and left ventricular remodeling. Therefore, the pathological substrates contributing to HFpEF included cardiac and noncardiac alterations with differential features for each comorbidity. Critically, the characteristics linked to diastolic dysfunction and HFpEF across the various comorbidities agreed with phenogroups observed in human patients.</p><p><strong>Conclusions: </strong>The identification of time-dependent pathological features provides a comprehensive picture of HFpEF progression associated with each comorbidity.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e011724"},"PeriodicalIF":7.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750117","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}
Circulation: Heart FailurePub Date : 2025-01-01Epub Date: 2024-11-16DOI: 10.1161/CIRCHEARTFAILURE.124.012514
Pablo M Marti-Castellote, Christopher Reeder, Brian Claggett, Pulkit Singh, Emily S Lau, Shaan Khurshid, Puneet Batra, Steven A Lubitz, Mahnaz Maddah, Orly Vardeny, Eldrin F Lewis, Marc Pfeffer, Pardeep Jhund, Akshay S Desai, John J V McMurray, Patrick T Ellinor, Jennifer E Ho, Scott D Solomon, Jonathan W Cunningham
{"title":"Natural Language Processing to Adjudicate Heart Failure Hospitalizations in Global Clinical Trials.","authors":"Pablo M Marti-Castellote, Christopher Reeder, Brian Claggett, Pulkit Singh, Emily S Lau, Shaan Khurshid, Puneet Batra, Steven A Lubitz, Mahnaz Maddah, Orly Vardeny, Eldrin F Lewis, Marc Pfeffer, Pardeep Jhund, Akshay S Desai, John J V McMurray, Patrick T Ellinor, Jennifer E Ho, Scott D Solomon, Jonathan W Cunningham","doi":"10.1161/CIRCHEARTFAILURE.124.012514","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012514","url":null,"abstract":"<p><strong>Background: </strong>Medical record review by a physician clinical events committee is the gold standard for identifying cardiovascular outcomes in clinical trials, but is labor-intensive and poorly reproducible. Automated outcome adjudication by artificial intelligence (AI) could enable larger and less expensive clinical trials but has not been validated in global studies.</p><p><strong>Methods: </strong>We developed a novel model for automated AI-based heart failure adjudication (Heart Failure Natural Language Processing) using hospitalizations from 3 international clinical outcomes trials. This model was tested on potential heart failure hospitalizations from the DELIVER trial (Dapagliflozin Evaluation to Improve the Lives of Patients With Preserved Ejection Fraction Heart Failure), a cardiovascular outcomes trial comparing dapagliflozin with placebo in 6063 patients with heart failure with mildly reduced or preserved ejection fraction. AI-based adjudications were compared with adjudications from a clinical events committee that followed Food and Drug Administration-based criteria.</p><p><strong>Results: </strong>AI-based adjudication agreed with the clinical events committee in 83% of events. A strategy of human review for events that the AI model deemed uncertain (16%) would have achieved 91% agreement with the clinical events committee while reducing the adjudication workload by 84%. The estimated effect of dapagliflozin on heart failure hospitalization was nearly identical with AI-based adjudication (hazard ratio, 0.76 [95% CI, 0.66-0.88]) compared with clinical events committee adjudication (hazard ratio, 0.77 [95% CI, 0.67-0.89]). The AI model extracted symptoms, signs, and treatments of heart failure from each medical record in tabular format and quoted sentences documenting them.</p><p><strong>Conclusions: </strong>AI-based adjudication of clinical outcomes has the potential to improve the efficiency of global clinical trials while preserving accuracy and interpretability.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012514"},"PeriodicalIF":7.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11910182/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643876","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}
Circulation: Heart FailurePub Date : 2025-01-01Epub Date: 2024-11-11DOI: 10.1161/CIRCHEARTFAILURE.124.012545
Ahmad Masri, Neal K Lakdawala
{"title":"Stop Dreaming: Mavacamten REMS Data Are Here.","authors":"Ahmad Masri, Neal K Lakdawala","doi":"10.1161/CIRCHEARTFAILURE.124.012545","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012545","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012545"},"PeriodicalIF":7.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615726","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}
Circulation: Heart FailurePub Date : 2025-01-01Epub Date: 2024-11-29DOI: 10.1161/CIRCHEARTFAILURE.124.012530
Neal M Dixit, Saul Schaefer
{"title":"Is It Primetime for Finerenone in Heart Failure?","authors":"Neal M Dixit, Saul Schaefer","doi":"10.1161/CIRCHEARTFAILURE.124.012530","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012530","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012530"},"PeriodicalIF":7.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750103","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}
Circulation: Heart FailurePub Date : 2024-12-01Epub Date: 2024-11-07DOI: 10.1161/CIRCHEARTFAILURE.124.012075
Peter Miller, Pierre Elias, Andrew J Einstein, Mathew S Maurer, Gasmelseed Y Ahmed, Timothy J Poterucha
{"title":"Socioeconomic Disparities Are Associated With Delayed Access to Tafamidis in Transthyretin Cardiac Amyloidosis.","authors":"Peter Miller, Pierre Elias, Andrew J Einstein, Mathew S Maurer, Gasmelseed Y Ahmed, Timothy J Poterucha","doi":"10.1161/CIRCHEARTFAILURE.124.012075","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012075","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012075"},"PeriodicalIF":7.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11652229/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590189","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}
Circulation: Heart FailurePub Date : 2024-12-01Epub Date: 2024-11-08DOI: 10.1161/CIRCHEARTFAILURE.124.012244
Stefano Toldo, Guglielmo Gallone, Antonio Abbate
{"title":"Inhibitors of the Interleukin-1 Receptor Accessory Protein Signaling: Another Asset in the Cardio-Immunology Toolbox.","authors":"Stefano Toldo, Guglielmo Gallone, Antonio Abbate","doi":"10.1161/CIRCHEARTFAILURE.124.012244","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012244","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012244"},"PeriodicalIF":7.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11652230/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603409","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":"Acute Heart Failure Caused by Rupture of Sinus of Valsalva Into Right Atrium in a Patient With Possible Infective Endocarditis After Tricuspid Annuloplasty: A Misdirected Clinical Decision-Making.","authors":"Daiki Toyoshima, Yasuhide Mochizuki, Sunao Handa, Daisuke Yokokawa, Saori Chino, Rumi Hachiya, Hiroto Fukuoka, Toshiro Shinke","doi":"10.1161/CIRCHEARTFAILURE.124.011600","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.011600","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e011600"},"PeriodicalIF":7.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142575386","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}
Circulation: Heart FailurePub Date : 2024-12-01Epub Date: 2024-11-08DOI: 10.1161/CIRCHEARTFAILURE.124.011761
Scott A Hubers, Sherry L Benike, Bradley K Johnson, Paul M McKie, Christopher Scott, Horng H Chen
{"title":"Renal Effects of Combination Phosphodiesterase V Inhibition and Low-Dose B-Type Natriuretic Peptide in Acute Heart Failure: A Randomized Clinical Trial.","authors":"Scott A Hubers, Sherry L Benike, Bradley K Johnson, Paul M McKie, Christopher Scott, Horng H Chen","doi":"10.1161/CIRCHEARTFAILURE.124.011761","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.011761","url":null,"abstract":"<p><strong>Background: </strong>Cardiorenal dysfunction with impaired cyclic GMP (cGMP) response is common in patients presenting with acute heart failure (HF). Type V phosphodiesterase (PDEV) is known to be upregulated in HF and may explain the dysfunction of renal response. The aim of this study was to determine whether B-type natriuretic peptide (BNP) alone or in combination with PDEV inhibition improves renal function and increases urinary sodium and cGMP excretion in acute HF.</p><p><strong>Methods: </strong>This open-label study included 67 patients hospitalized with acute HF and renal dysfunction. Patients were randomized to standard care, low-dose intravenous BNP (0.005 µg/kg per minute), or combination BNP/PDEV inhibition with sildenafil (25 mg q12 hours) for 48 hours. The coprimary end points were the percent change in estimated glomerular filtration rate and blood urea nitrogen from baseline to 48 hours.</p><p><strong>Results: </strong>Treatment with BNP and BNP/PDEV inhibitor significantly increased plasma cGMP at 24 hours (+25.6% [+9.8%, +84.7%] and +60.8% [+32.3%, +103.8%] for BNP and BNP/PDEV versus -13.5% [-29.1%, +14.2%] with standard care; <i>P</i>=0.001). However, there was no significant change in estimated glomerular filtration rate 0 (-10.8%, +12.7%) for standard care versus 0 (-15.3%, +11.8%) for the BNP group versus -8.8% (-14.3%, +8.3%) for the BNP/PDEV group (<i>P</i>=0.60) or blood urea nitrogen -1.4% (-10.7%, +12.0%) for standard care versus -5.9% (-14.6%, +9.4%) for the BNP group versus +6.9% (-5.3%, +18.8%) for the BNP/PDEV group (<i>P</i>=0.38) between groups. Hypotension was more common in the BNP/PDEV inhibitor group.</p><p><strong>Conclusions: </strong>BNP and combination BNP/PDEV inhibition increased plasma cGMP in patients with acute HF but did not improve renal function or urinary sodium/cGMP excretion. Our study does not support the use of intravenous low-dose BNP with or without PDEV inhibition to enhance renal function in patients admitted with acute HF.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT00972569.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e011761"},"PeriodicalIF":7.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11653223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603338","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}