Circulation: Heart Failure最新文献

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Cardiogenic Shock Teams: Past, Present, and Future Directions. 心源性休克团队:过去、现在和未来的方向。
IF 7.8 1区 医学
Circulation: Heart Failure Pub Date : 2025-03-28 DOI: 10.1161/CIRCHEARTFAILURE.124.011630
Vanessa Blumer, Thomas C Hanff, Ann Gage, Benedikt Schrage, Manreet K Kanwar
{"title":"Cardiogenic Shock Teams: Past, Present, and Future Directions.","authors":"Vanessa Blumer, Thomas C Hanff, Ann Gage, Benedikt Schrage, Manreet K Kanwar","doi":"10.1161/CIRCHEARTFAILURE.124.011630","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.124.011630","url":null,"abstract":"<p><p>Cardiogenic shock (CS) remains a significant challenge in cardiovascular medicine, characterized by substantial morbidity and mortality. Historically, patient outcomes in CS have been varied, highly dependent on the timeliness of interventions and the expertise available at treating centers. Emerging evidence indicates that structured, team-based approaches significantly improve survival rates and diminish complications linked to CS. However, several challenges for implementing a team-based approach persist, including optimizing team composition and resource distribution. This article delves into the evolution, current implementations, and future directions of CS teams, emphasizing their crucial role in enhancing patient outcomes. We advocate for the adoption of standardized protocols to ensure uniformity of care across institutions, highlighting the critical need for prompt recognition and management strategies that integrate invasive hemodynamic monitoring and early mechanical circulatory support. Looking ahead, we propose the extension of CS team models into regional networks, broadening their impact through education, telemedicine and collaborative protocols. We also emphasize the importance of continuous research and data sharing via national registries to refine CS team strategies and substantiate their effects on patient outcomes. Ultimately, this review highlights the imperative for ongoing innovation and standardization in CS team operations to improve care delivery and enhance survival rates in CS scenarios.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e011630"},"PeriodicalIF":7.8,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143728989","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}
引用次数: 0
Blood Transfusion in Patients With Acute Myocardial Infarction, Anemia, and Heart Failure: Lessons From MINT.
IF 7.8 1区 医学
Circulation: Heart Failure Pub Date : 2025-03-26 DOI: 10.1161/CIRCHEARTFAILURE.124.012495
Andrew M Goldsweig, William J Kostis, Brandon M Herbert, Claire Bouleti, Brian J Potter, Jordan B Strom, Jocelyne Benatar, Thao Huynh, Srikanth Vallurupalli, Estêvão Lanna Figueiredo, J Dawn Abbott, Howard A Cooper, Andrew P DeFilippis, Dean A Fergusson, Shaun G Goodman, Paul C Hébert, Renato D Lopes, Sunil V Rao, Tabassome Simon, Jeffrey L Carson, Maria Mori Brooks, John H Alexander
{"title":"Blood Transfusion in Patients With Acute Myocardial Infarction, Anemia, and Heart Failure: Lessons From MINT.","authors":"Andrew M Goldsweig, William J Kostis, Brandon M Herbert, Claire Bouleti, Brian J Potter, Jordan B Strom, Jocelyne Benatar, Thao Huynh, Srikanth Vallurupalli, Estêvão Lanna Figueiredo, J Dawn Abbott, Howard A Cooper, Andrew P DeFilippis, Dean A Fergusson, Shaun G Goodman, Paul C Hébert, Renato D Lopes, Sunil V Rao, Tabassome Simon, Jeffrey L Carson, Maria Mori Brooks, John H Alexander","doi":"10.1161/CIRCHEARTFAILURE.124.012495","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.124.012495","url":null,"abstract":"<p><strong>Background: </strong>Blood transfusion may precipitate adverse outcomes, including heart failure (HF), among patients with acute myocardial infarction (MI). This study characterizes the effects of a restrictive or liberal transfusion strategy on outcomes in patients with MI and anemia with and without baseline HF.</p><p><strong>Methods: </strong>In the MINT trial (Myocardial Ischemia and Transfusion), 3504 patients with MI and anemia (hemoglobin <10 g/dL) were randomized to a restrictive (hemoglobin <8 g/dL) or liberal (hemoglobin <10 g/dL) transfusion strategy. We compared the effects of transfusion strategy on outcomes among patients with and without baseline HF. The primary outcome was death or HF at 30 days.</p><p><strong>Results: </strong>Compared with patients without baseline HF (n=1633), those with baseline HF (n=1871) had higher rates of death or HF (18.0% versus 10.0%) at 30 days. Restrictive transfusion resulted in numerically higher rates of death or HF (rate ratio, 1.20 [95% CI, 0.99-1.45] versus 0.94 [95% CI, 0.70-1.26]; <i>P</i><sub>interaction</sub>=0.18) in patients with than in those without baseline HF. Among secondary outcomes, death or recurrent MI and death were more frequent among those with baseline HF. Restrictive transfusion resulted in numerically higher rates of death or MI and death in patients with than in those without baseline HF. Rates of HF were similar between restrictive and liberal transfusion in patients with baseline HF but lower with restrictive transfusion (rate ratio, 0.51 [95% CI, 0.29-0.92]; <i>P</i><sub>interaction</sub>=0.02) in patients without baseline HF.</p><p><strong>Conclusions: </strong>A liberal transfusion strategy is safe for patients with MI and anemia, including those with baseline HF. Restrictive transfusion tended to result in worse outcomes, particularly in patients with baseline HF.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT02981407.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012495"},"PeriodicalIF":7.8,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708862","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}
引用次数: 0
Transfusions in Heart Failure and Acute Myocardial Infarction: Novel Data Begets New Questions.
IF 7.8 1区 医学
Circulation: Heart Failure Pub Date : 2025-03-26 DOI: 10.1161/CIRCHEARTFAILURE.125.012877
Claudio Montalto, Stefano Savonitto
{"title":"Transfusions in Heart Failure and Acute Myocardial Infarction: Novel Data Begets New Questions.","authors":"Claudio Montalto, Stefano Savonitto","doi":"10.1161/CIRCHEARTFAILURE.125.012877","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.125.012877","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012877"},"PeriodicalIF":7.8,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708864","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}
引用次数: 0
Reviving the Swan: Presenting the Chicago Hemodynamic Forum.
IF 7.8 1区 医学
Circulation: Heart Failure Pub Date : 2025-03-21 DOI: 10.1161/CIRCHEARTFAILURE.124.012725
Mark N Belkin, Jennifer A Cowger, Marat Fudim, Ryan J Tedford, Jonathan Grinstein
{"title":"Reviving the Swan: Presenting the Chicago Hemodynamic Forum.","authors":"Mark N Belkin, Jennifer A Cowger, Marat Fudim, Ryan J Tedford, Jonathan Grinstein","doi":"10.1161/CIRCHEARTFAILURE.124.012725","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.124.012725","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012725"},"PeriodicalIF":7.8,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669340","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}
引用次数: 0
Multiregional Implementation Initiative's Impact on Guideline-Based Performance Measures for Patients Hospitalized With Heart Failure: IMPLEMENT-HF.
IF 7.8 1区 医学
Circulation: Heart Failure Pub Date : 2025-03-21 DOI: 10.1161/CIRCHEARTFAILURE.124.012547
Andrew J Sauer, Chandler Beon, Sruthi Cherkur, Lynn Mallas-Serdynski, Kathie Thomas, John Spertus, Georges Chahoud, Kanika P Mody, Mitchell T Saltzberg, Lee R Goldberg, JoAnn Lindenfeld, Nancy Sweitzer, Javed Butler, Michelle M Kittleson, Ileana Pina, Sara Paul, Eldrin F Lewis, Joyce Wald, Larry A Allen, Mariell Jessup, Michelle Congdon, Robin Kiser, Clyde Yancy, Gregg C Fonarow
{"title":"Multiregional Implementation Initiative's Impact on Guideline-Based Performance Measures for Patients Hospitalized With Heart Failure: IMPLEMENT-HF.","authors":"Andrew J Sauer, Chandler Beon, Sruthi Cherkur, Lynn Mallas-Serdynski, Kathie Thomas, John Spertus, Georges Chahoud, Kanika P Mody, Mitchell T Saltzberg, Lee R Goldberg, JoAnn Lindenfeld, Nancy Sweitzer, Javed Butler, Michelle M Kittleson, Ileana Pina, Sara Paul, Eldrin F Lewis, Joyce Wald, Larry A Allen, Mariell Jessup, Michelle Congdon, Robin Kiser, Clyde Yancy, Gregg C Fonarow","doi":"10.1161/CIRCHEARTFAILURE.124.012547","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.124.012547","url":null,"abstract":"<p><strong>Background: </strong>Despite randomized data for survival benefit (with class 1 recommendations) for treating heart failure (HF) with reduced ejection fraction using quadruple medical therapy (QMT)-defined as evidence-based β-blockers, sodium-glucose cotransporter 2 inhibitor, preferably angiotensin receptor/neprilysin inhibitor, and mineralocorticoid receptor antagonist-it is underutilized. IMPLEMENT-HF is a multiregional HF quality improvement initiative to improve care and outcomes for patients with HF by enhancing the use of QMT in routine practice.</p><p><strong>Methods: </strong>This analysis of HF with reduced ejection fraction treatment in patients from hospitals participating in the American Heart Association's Get With The Guidelines-HF who volunteered to participate in IMPLEMENT-HF in 7 US regions. IMPLEMENT-HF included multidisciplinary learning to share strategies for formulary changes, electronic health record tools, and patient resources with site-level feedback reports. Participants gathered QMT data at discharge and 30 days after discharge. We evaluated QMT utilization and variation, in addition to other prespecified performance measures, from Q1 2021 to Q2 2023.</p><p><strong>Results: </strong>The median (interquartile range) age of 43 558 admitted patients at 61 hospitals was 74 (63-83) years; 16 530 (38%) belonged to racial and ethnic minorities, and 22 228 (51%) were women. Between Q1 2021 and Q2 2023, defect-free QMT improved from 4.7% to 44.6% at discharge and from 0% to 44.8% at 30 days (both <i>P</i><0.0001). There was also substantially improved incorporation of health-related social needs assessments. The magnitude of improvements was similar when stratified by sex or race and ethnicity, yet there was significant regional variation.</p><p><strong>Conclusions: </strong>Among healthcare systems participating in IMPLEMENT-HF, there was a marked increase in QMT use among eligible patients over the course of the initiative. This quality improvement initiative supports a learning collaborative model to promote improvements in QMT use.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012547"},"PeriodicalIF":7.8,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669325","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}
引用次数: 0
National Organ Procurement and Transplant Network Heart Allocation Policy: 6 Years Later.
IF 7.8 1区 医学
Circulation: Heart Failure Pub Date : 2025-03-21 DOI: 10.1161/CIRCHEARTFAILURE.124.011631
Lauren K Truby, Liviu Klein, Jane E Wilcox, Maryjane Farr
{"title":"National Organ Procurement and Transplant Network Heart Allocation Policy: 6 Years Later.","authors":"Lauren K Truby, Liviu Klein, Jane E Wilcox, Maryjane Farr","doi":"10.1161/CIRCHEARTFAILURE.124.011631","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.124.011631","url":null,"abstract":"<p><p>In 2014, the Organ Procurement and Transplant Network began reappraisal of the United States heart transplant allocation policy. Driven by ongoing discordance between organ supply and demand, high waitlist mortality, and increasing exception requests, the Thoracic Committee radically redesigned the priority scheme and drafted a 6-tiered algorithm, included durable device complications into policy, expanded broader sharing, and increased the number of mandatory listing variables to develop a future heart allocation score. This became the 2018 New Heart Allocation Policy. Changes in allocation priority have resulted in a significant increase in the use of temporary mechanical circulatory support in waitlisted candidates with a concomitant decrease in the number of patients bridged to transplanted with durable left ventricular assist device support. The number of exception requests continues to increase, particularly for patients listed status 2 and for multiorgan transplants. Importantly, fewer patients are being delisted for clinical improvement, suggesting missed opportunities for recovery. The current review will critically evaluate the 2018 heart allocation policy 6 years later, briefly focusing on the history of heart allocation in the United States, the current and evolving algorithms for candidate prioritization including continuous distribution, the impact of technology and innovation on transplant rates and future policy development, and the ongoing regulatory oversight and governance changes in the Organ Procurement and Transplant Network.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e011631"},"PeriodicalIF":7.8,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669333","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}
引用次数: 0
Hepatopulmonary Syndrome or Portopulmonary Hypertension? Two Contrasting Cases of Exertional Hypoxemia From Liver Disease.
IF 7.8 1区 医学
Circulation: Heart Failure Pub Date : 2025-03-14 DOI: 10.1161/CIRCHEARTFAILURE.124.012506
Fadi Adel, Adel Kabbara Allababidi, Yogesh N V Reddy
{"title":"Hepatopulmonary Syndrome or Portopulmonary Hypertension? Two Contrasting Cases of Exertional Hypoxemia From Liver Disease.","authors":"Fadi Adel, Adel Kabbara Allababidi, Yogesh N V Reddy","doi":"10.1161/CIRCHEARTFAILURE.124.012506","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.124.012506","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012506"},"PeriodicalIF":7.8,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623686","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}
引用次数: 0
Hereditary Transthyretin Cardiac Amyloidosis With the p.V142I Variant: Mechanistic Insights and Diagnostic Challenges.
IF 7.8 1区 医学
Circulation: Heart Failure Pub Date : 2025-03-14 DOI: 10.1161/CIRCHEARTFAILURE.124.012469
Simon Vanhentenrijk, Justin L Grodin, Silvio Nunes Augusto, W H Wilson Tang
{"title":"Hereditary Transthyretin Cardiac Amyloidosis With the p.V142I Variant: Mechanistic Insights and Diagnostic Challenges.","authors":"Simon Vanhentenrijk, Justin L Grodin, Silvio Nunes Augusto, W H Wilson Tang","doi":"10.1161/CIRCHEARTFAILURE.124.012469","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.124.012469","url":null,"abstract":"<p><p>The most common form of hereditary transthyretin cardiac amyloidosis (hATTR-CA) in the United States and the United Kingdom is the p.V142I variant. About 3% to 4% of patients with African ancestry carry this genetic predisposition to develop signs and symptoms of hATTR-CA. Nevertheless, clinical manifestations of hATTR-CA appear only late in the fifth and sixth decades of life, despite its clear genetic background. Imbalances in native protein-stabilizing and elementary breakdown cellular mechanisms are postulated as potential causes for affecting transthyretin structural integrity and myocardial fibril deposition. Noncoding variants, epigenetic and environmental factors, as well as gut microbiome derangements may serve as disease-modifying factors that feature detrimental amyloidogenic organ involvement and impact disease severity. Organ amyloid deposition varies widely among different carriers of a genetic transthyretin variant. The genotype-phenotype interdependence causes unpredictable phenotypic penetrance that results in a variety of signs and symptoms and patient outcomes. Cardiovascular biomarkers and multimodality imaging may identify initial amyloidogenic organ involvement. These early clinical clues through the course of hATTR-CA offer a window of opportunity for early treatment onset to cease disease progression and alter prognosis. Identifying at-risk patients requires information on the genetic background of probands and their relatives. Initiatives to reveal asymptomatic gene carriers early in the disease should be encouraged, as it necessitates stringent patient follow-up and immediate treatment onset to reduce the burden of heart failure hospitalization and mortality in hATTR-CA.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012469"},"PeriodicalIF":7.8,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623687","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}
引用次数: 0
Combined Loss of Obsc and Obsl1 in Murine Hearts Results in Diastolic Dysfunction, Altered Metabolism, and Deregulated Mitophagy.
IF 7.8 1区 医学
Circulation: Heart Failure Pub Date : 2025-03-11 DOI: 10.1161/CIRCHEARTFAILURE.124.011867
Kyohei Fujita, Patrick Desmond, Jordan Blondelle, Matúš Soták, Meenu Rohini Rajan, Madison Clark, Éric Estève, Yunghang Chan, Yusu Gu, Virginia Actis Dato, Valeria Marrocco, Nancy D Dalton, Majid Ghassemian, Aryanne Do, Matthew Klos, Kirk L Peterson, Farah Sheikh, Yoshitake Cho, Emma Börgeson, Stephan Lange
{"title":"Combined Loss of Obsc and Obsl1 in Murine Hearts Results in Diastolic Dysfunction, Altered Metabolism, and Deregulated Mitophagy.","authors":"Kyohei Fujita, Patrick Desmond, Jordan Blondelle, Matúš Soták, Meenu Rohini Rajan, Madison Clark, Éric Estève, Yunghang Chan, Yusu Gu, Virginia Actis Dato, Valeria Marrocco, Nancy D Dalton, Majid Ghassemian, Aryanne Do, Matthew Klos, Kirk L Peterson, Farah Sheikh, Yoshitake Cho, Emma Börgeson, Stephan Lange","doi":"10.1161/CIRCHEARTFAILURE.124.011867","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.011867","url":null,"abstract":"<p><strong>Background: </strong>Muscle proteins of the obscurin protein family play important roles in sarcomere organization and sarcoplasmic reticulum and T-tubule architecture and function. However, their precise molecular functions and redundancies between protein family members as well as their involvement in cardiac diseases remain to be fully understood.</p><p><strong>Methods: </strong>To investigate the functional roles of Obsc (obscurin) and its close homolog Obsl1 (obscurin-like 1) in the heart, we generated and analyzed knockout mice for <i>Obsc</i>, <i>Obsl1</i>, as well as <i>Obsc/Obsl1</i> double knockouts.</p><p><strong>Results: </strong>We show that double-knockout mice are viable but show postnatal deficits in cardiac muscle sarcoplasmic reticulum and mitochondrial architecture and function at the microscopic, biochemical, and cellular levels. Altered sarcoplasmic reticulum structure resulted in perturbed calcium cycling, whereas mitochondrial ultrastructure deficits were linked to decreased levels of Chchd3 (coiled-coil-helix-coiled-coil-helix domain containing 3), a Micos (mitochondrial contact site and cristae organizing system) complex protein. Hearts of double-knockout mice also show altered levels of Atg4 proteins, novel Obsl1 interactors, resulting in abnormal mitophagy, and increased unfolded protein response. At the physiological level, loss of obscurin and Obsl1 resulted in a profound delay of cardiac relaxation, associated with metabolic signs of heart failure.</p><p><strong>Conclusions: </strong>Taken together, our data suggest that Obsc and Obsl1 play crucial roles in cardiac sarcoplasmic reticulum structure, calcium cycling, mitochondrial function, turnover, and metabolism.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e011867"},"PeriodicalIF":7.8,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596354","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}
引用次数: 0
Heart Rate Reduction Is Associated With Reverse Left Ventricular Remodeling and Mechanism-Specific Molecular Phenotypes in Dilated Cardiomyopathy.
IF 7.8 1区 医学
Circulation: Heart Failure Pub Date : 2025-03-07 DOI: 10.1161/CIRCHEARTFAILURE.124.012484
Natasha L Altman, Edward A Gill, Rami Kahwash, Leslie K Meyer, Jessica A Wagner, Anis Karimpour-Fard, Amber A Berning, Wayne A Minobe, Ian A Carroll, Eric R Jonas, Dobromir Slavov, Sitaramesh Emani, William T Abraham, Alexa R Gollah, Samuel L Ellis, Matthew R G Taylor, Sharon L Graw, Luisa Mestroni, Timothy A McKinsey, Peter M Buttrick, David P Kao, Michael R Bristow
{"title":"Heart Rate Reduction Is Associated With Reverse Left Ventricular Remodeling and Mechanism-Specific Molecular Phenotypes in Dilated Cardiomyopathy.","authors":"Natasha L Altman, Edward A Gill, Rami Kahwash, Leslie K Meyer, Jessica A Wagner, Anis Karimpour-Fard, Amber A Berning, Wayne A Minobe, Ian A Carroll, Eric R Jonas, Dobromir Slavov, Sitaramesh Emani, William T Abraham, Alexa R Gollah, Samuel L Ellis, Matthew R G Taylor, Sharon L Graw, Luisa Mestroni, Timothy A McKinsey, Peter M Buttrick, David P Kao, Michael R Bristow","doi":"10.1161/CIRCHEARTFAILURE.124.012484","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.124.012484","url":null,"abstract":"<p><strong>Background: </strong>Heart rate (HR) affects heart failure outcomes, via uncertain mechanisms that may include left ventricular remodeling. However, in human ventricular myocardium, HR change has not been associated with a particular remodeling molecular phenotype.</p><p><strong>Methods: </strong>Patients with nonischemic dilated cardiomyopathy (N=22) in sinus rhythm and refractory to β-blockade for both HR lowering and reverse remodeling were randomized 2:1 double-blind to the HCN4 (hyperpolarization-activated cyclic nucleotide-gated potassium channel 4) channel inhibitor ivabradine or placebo for 24 weeks treatment while maintaining target doses of β-blockers. Reverse remodeling was measured by left ventricular ejection fraction (LVEF), and myocardial gene expression by sequencing RNA extracted from endomyocardial biopsies. The primary statistical analysis was between HR change categories divided at the median, which resulted in Decreased HR (N=90) and Unchanged HR (N=8) groups.</p><p><strong>Results: </strong>Respective HRs at baseline and 24 weeks were as follows: Decreased HR, 82.9±6.8 and 69.7±8.0 beats per minute (<i>P</i>=0.0005) and Unchanged HR, 80.8±5.7 and 79.2±11.6 beats per minute (<i>P</i>=0.58). All completing Decreased HR subjects were treated with ivabradine, whereas in the Unchanged HR group, 3 received ivabradine and 5 placebo. In Decreased HR, LVEF increased from 29.4±8.8% at baseline to 44.2±9.4% at 24 weeks (<i>P</i>=0.0003), compared with respective values of 26.6±11.4% and 29.2±12.0% (<i>P</i>=0.28) in Unchanged HR. HR and LVEF changes were not different from a previously conducted β-blocker nonischemic dilated cardiomyopathy study subdivided into LVEF responders and nonresponders. However, differentially expressed genes (N=151) in the Decreased versus Unchanged HR groups were >99% nonconcordant and therefore individually unique compared with β-blocker HR/LVEF responders versus nonresponders (2 shared differentially expressed genes). Multiple unique differentially expressed genes in Decreased HR including <i>NRG1</i> upregulation are considered cardioprotective or involved in cardiac development.</p><p><strong>Conclusions: </strong>In patients with nonischemic dilated cardiomyopathy in sinus rhythm, HR lowering per se (1) is associated with substantial left ventricular reverse remodeling; (2) its absence can cause β-blocker reverse remodeling nonresponse; and (3) when from HCN4 channel inhibition, results in a unique molecular phenotype.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT02973594.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012484"},"PeriodicalIF":7.8,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572332","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}
引用次数: 0
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