Pub Date : 2026-02-01DOI: 10.1016/j.jchf.2025.102704
Isabel R. Wees MD , Colby Ayers MS , Frederick L. Ruberg MD , Mathew S. Maurer MD , Yevgeniy Brailovsky DO, MSc , Lily K. Stern MD , Jan M. Griffin MD , Michel G. Khouri MD , Lori R. Roth PA-C , Justin L. Grodin MD, MPH
{"title":"Clinical Implications of the P.V142I TTR Variant","authors":"Isabel R. Wees MD , Colby Ayers MS , Frederick L. Ruberg MD , Mathew S. Maurer MD , Yevgeniy Brailovsky DO, MSc , Lily K. Stern MD , Jan M. Griffin MD , Michel G. Khouri MD , Lori R. Roth PA-C , Justin L. Grodin MD, MPH","doi":"10.1016/j.jchf.2025.102704","DOIUrl":"10.1016/j.jchf.2025.102704","url":null,"abstract":"","PeriodicalId":14687,"journal":{"name":"JACC. Heart failure","volume":"14 2","pages":"Article 102704"},"PeriodicalIF":11.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145261212","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}
Pub Date : 2026-02-01DOI: 10.1016/j.jchf.2025.102822
Milton Packer MD
For the past decade, the prevailing paradigm to explain heart failure with preserved ejection fraction (HFpEF) has assumed that multiple comorbidities act in concert to trigger a systemic inflammatory state that causes coronary microvascular dysfunction, nitric oxide/cyclic guanosine monophosphate (cGMP) deficiency–dependent titin abnormalities, and load-dependent cellular inflammation and fibrosis of the myocardium. By contrast, the recently proposed adipokine hypothesis elevates one comorbidity—visceral adiposity—to explain the coexistence of systemic inflammation, multiple comorbidities, and HFpEF and identifies a specific proximal causal mechanism (ie, the secretion of a proinflammatory suite of signaling molecules from dysfunctional fat). Excess visceral adiposity and adipokine imbalances have been shown not only to produce HFpEF experimentally but also to directly cause hypertension, insulin resistance and type 2 diabetes, and chronic kidney disease. Visceral adiposity and proinflammatory adipokines can also explain features of HFpEF that are not addressed by the coronary microvascular inflammation hypothesis (eg, atrial fibrillation, skeletal muscle and pulmonary abnormalities, and renal sodium retention and plasma volume expansion). Adipokine imbalances can also cause microvascular dysfunction and defects in cGMP signaling and in titin phosphorylation, and they can directly cause cardiac hypertrophy and fibrosis independently of an effect on the microvasculature. The comorbidity-driven microvascular inflammation hypothesis did not identify a blood-borne molecular mediator that selectively targets the heart, and phenomapping based on the clustering of comorbidities has not yielded reproducible groupings. By contrast, selective silencing of specific proinflammatory adipokines only in adipose tissue causes distant effects on the heart to modulate cardiac structure and the evolution of HFpEF. Clinical trials of drugs that enhance nitric oxide/cGMP signaling or have nonspecific anti-inflammatory effects have not produced favorable effects in clinical HFpEF whereas drugs that produce benefits in HFpEF (eg, glucagon-like peptide 1 receptor agonists, sodium-glucose cotransporter 2 inhibitors) act to normalize the adipokine secretory profile. Finally, whereas coronary microvascular dysfunction is present in 60% to 70% of patients with HFpEF (with endothelium-dependent dysfunction being seen in only 30%), central obesity (assessed by an increased waist-to-height ratio) or visceral adiposity (as by mesenteric or epicardial fat) is present in >85% to 95% of patients with the disorder. Therefore, when compared with the comorbidity-driven coronary microvascular endothelial inflammation hypothesis, the adipokine hypothesis provides an explanatory framework with a stronger evidentiary support and applicable to a broader range of patients with HFpEF. Further work is needed to support these observations.
{"title":"Evolutionary History of the Comorbidity-Driven Coronary Microvascular Endothelial Inflammation Hypothesis and Its Metamorphosis to the Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction","authors":"Milton Packer MD","doi":"10.1016/j.jchf.2025.102822","DOIUrl":"10.1016/j.jchf.2025.102822","url":null,"abstract":"<div><div>For the past decade, the prevailing paradigm to explain heart failure with preserved ejection fraction (HFpEF) has assumed that multiple comorbidities act in concert to trigger a systemic inflammatory state that causes coronary microvascular dysfunction, nitric oxide/cyclic guanosine monophosphate (cGMP) deficiency–dependent titin abnormalities, and load-dependent cellular inflammation and fibrosis of the myocardium. By contrast, the recently proposed adipokine hypothesis elevates one comorbidity—visceral adiposity—to explain the coexistence of systemic inflammation, multiple comorbidities, and HFpEF and identifies a specific proximal causal mechanism (ie, the secretion of a proinflammatory suite of signaling molecules from dysfunctional fat). Excess visceral adiposity and adipokine imbalances have been shown not only to produce HFpEF experimentally but also to directly cause hypertension, insulin resistance and type 2 diabetes, and chronic kidney disease. Visceral adiposity and proinflammatory adipokines can also explain features of HFpEF that are not addressed by the coronary microvascular inflammation hypothesis (eg, atrial fibrillation, skeletal muscle and pulmonary abnormalities, and renal sodium retention and plasma volume expansion). Adipokine imbalances can also cause microvascular dysfunction and defects in cGMP signaling and in titin phosphorylation, and they can directly cause cardiac hypertrophy and fibrosis independently of an effect on the microvasculature. The comorbidity-driven microvascular inflammation hypothesis did not identify a blood-borne molecular mediator that selectively targets the heart, and phenomapping based on the clustering of comorbidities has not yielded reproducible groupings. By contrast, selective silencing of specific proinflammatory adipokines only in adipose tissue causes distant effects on the heart to modulate cardiac structure and the evolution of HFpEF. Clinical trials of drugs that enhance nitric oxide/cGMP signaling or have nonspecific anti-inflammatory effects have not produced favorable effects in clinical HFpEF whereas drugs that produce benefits in HFpEF (eg, glucagon-like peptide 1 receptor agonists, sodium-glucose cotransporter 2 inhibitors) act to normalize the adipokine secretory profile. Finally, whereas coronary microvascular dysfunction is present in 60% to 70% of patients with HFpEF (with endothelium-dependent dysfunction being seen in only 30%), central obesity (assessed by an increased waist-to-height ratio) or visceral adiposity (as by mesenteric or epicardial fat) is present in >85% to 95% of patients with the disorder. Therefore, when compared with the comorbidity-driven coronary microvascular endothelial inflammation hypothesis, the adipokine hypothesis provides an explanatory framework with a stronger evidentiary support and applicable to a broader range of patients with HFpEF. Further work is needed to support these observations.</div></div>","PeriodicalId":14687,"journal":{"name":"JACC. Heart failure","volume":"14 2","pages":"Article 102822"},"PeriodicalIF":11.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145563975","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}
Pub Date : 2026-02-01DOI: 10.1016/j.jchf.2025.102718
Attila Feher MD, PhD , Maria Alwan MD , Catherine X. Wright MD , Kevin J. Clerkin MD, MSc , Andrew J. Einstein MD, PhD , Edward J. Miller MD, PhD , Mouaz H. Al-Mallah MD, MSc
{"title":"Surveillance Patterns for Allograft Vasculopathy in Heart Transplant Recipients in PET Myocardial Perfusion Imaging Performing Centers in the United States","authors":"Attila Feher MD, PhD , Maria Alwan MD , Catherine X. Wright MD , Kevin J. Clerkin MD, MSc , Andrew J. Einstein MD, PhD , Edward J. Miller MD, PhD , Mouaz H. Al-Mallah MD, MSc","doi":"10.1016/j.jchf.2025.102718","DOIUrl":"10.1016/j.jchf.2025.102718","url":null,"abstract":"","PeriodicalId":14687,"journal":{"name":"JACC. Heart failure","volume":"14 2","pages":"Article 102718"},"PeriodicalIF":11.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145300907","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}
Pub Date : 2026-02-01DOI: 10.1016/j.jchf.2025.02.016
Shoichiro Yatsu MD, PhD , Anna Woo MD , Christian M. Horvath MD , Tomoyuki Tobushi MD , Alexander G. Logan MD , John S. Floras MD, DPhil , George Tomlinson PhD , T. Douglas Bradley MD
Background
Sleep-disordered breathing (SDB), comprising obstructive sleep apnea (OSA) and central sleep apnea (CSA), could promote left ventricular (LV) remodeling and systolic dysfunction.
Objectives
The authors tested the hypothesis, in the ADVENT-HF (Adaptive Servo-ventilation for Sleep-disordered Breathing in Patients with Heart Failure with Reduced Ejection Fraction) trial, that SDB is associated with reversible impairment of LV structure and function.
Methods
Participants underwent echocardiography (ejection fraction ≤45%) and polysomnography. They were classified as no-SDB (apnea-hypopnea index [AHI] <15/h); OSA (AHI ≥15/h with ≥50% of events obstructive), or CSA (AHI ≥15 with >50% of events central). Those with SDB were randomized to a control group or to peak-flow-triggered adaptive servo-ventilation (ASVPF) to treat SDB and, in them, echocardiography was repeated 6 months later.
Results
Subjects with OSA (n = 543) had similar LV structure and function to those without SDB (n = 56). Subjects with CSA (n = 201) had greater LV mass index and lower LV ejection fraction than the other groups. LV volumes were higher in the CSA than in the OSA group (P < 0.05 for all). ASVPF abolished SDB, but had no significant effect, whether evaluated by allocation or adherence, 6 months post-randomization on LV structure or function for the entire cohort (n = 549), or either subgroup.
Conclusions
Among patients with heart failure with reduced ejection fraction, those with OSA had similar LV structure and function to those without SDB. Patients with CSA had greater LV remodeling and systolic dysfunction than those with OSA or without SDB. Six months of SDB suppression of OSA and CSA by ASVPF had no impact on LV structure or function. (Adaptive Servo-ventilation for Sleep-disordered Breathing in Patients with Heart Failure with Reduced Ejection Fraction [ADVENT-HF])
{"title":"LV Structure and Function in HFrEF With and Without Peak-Flow-Triggered Adaptive Servo-Ventilation-Treated Sleep-Disordered Breathing","authors":"Shoichiro Yatsu MD, PhD , Anna Woo MD , Christian M. Horvath MD , Tomoyuki Tobushi MD , Alexander G. Logan MD , John S. Floras MD, DPhil , George Tomlinson PhD , T. Douglas Bradley MD","doi":"10.1016/j.jchf.2025.02.016","DOIUrl":"10.1016/j.jchf.2025.02.016","url":null,"abstract":"<div><h3>Background</h3><div>Sleep-disordered breathing (SDB), comprising obstructive sleep apnea (OSA) and central sleep apnea<span> (CSA), could promote left ventricular (LV) remodeling and systolic dysfunction.</span></div></div><div><h3>Objectives</h3><div>The authors tested the hypothesis, in the ADVENT-HF (Adaptive Servo-ventilation for Sleep-disordered Breathing in Patients with Heart Failure with Reduced Ejection Fraction) trial, that SDB is associated with reversible impairment of LV structure and function.</div></div><div><h3>Methods</h3><div><span><span>Participants underwent echocardiography (ejection fraction ≤45%) and </span>polysomnography. They were classified as no-SDB (apnea-hypopnea index [AHI] <15/h); OSA (AHI ≥15/h with ≥50% of events obstructive), or CSA (AHI ≥15 with >50% of events central). Those with SDB were randomized to a control group or to peak-flow-triggered adaptive servo-ventilation (ASV</span><sub>PF</sub>) to treat SDB and, in them, echocardiography was repeated 6 months later.</div></div><div><h3>Results</h3><div><span>Subjects with OSA (n = 543) had similar LV structure and function to those without SDB (n = 56). Subjects with CSA (n = 201) had greater LV mass index and lower LV ejection fraction than the other groups. LV volumes were higher in the CSA than in the OSA group (</span><em>P <</em> 0.05 for all). ASV<sub>PF</sub> abolished SDB, but had no significant effect, whether evaluated by allocation or adherence, 6 months post-randomization on LV structure or function for the entire cohort (n = 549), or either subgroup.</div></div><div><h3>Conclusions</h3><div><span>Among patients with heart failure with reduced ejection fraction, those with OSA had similar LV structure and function to those without SDB. Patients with CSA had greater LV remodeling and systolic dysfunction than those with OSA or without SDB. Six months of SDB suppression of OSA and CSA by ASV</span><sub>PF</sub><span> had no impact on LV structure or function. (Adaptive Servo-ventilation for Sleep-disordered Breathing in Patients with Heart Failure with Reduced Ejection Fraction [ADVENT-HF])</span></div></div>","PeriodicalId":14687,"journal":{"name":"JACC. Heart failure","volume":"14 2","pages":"Article 102434"},"PeriodicalIF":11.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143996640","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}
Pub Date : 2026-02-01DOI: 10.1016/j.jchf.2025.102703
Henri Lu MD , Brian L. Claggett PhD , G. Michael Felker MD, MHS , John J.V. McMurray MD , John R. Teerlink MD , Riccardo M. Inciardi MD, PhD , Marco Metra MD , Stephen B. Heitner MD , Rafael Diaz MD , Fady Malik MD, PhD , Muthiah Vaduganathan MD, MPH , Scott D. Solomon MD
<div><h3>Background</h3><div>Older age is associated with a high prevalence of comorbidities and worse cardiovascular (CV) outcomes in patients with heart failure (HF) with reduced ejection fraction. Omecamtiv mecarbil, a selective cardiac myosin activator, exerts minimal effects on blood pressure and heart rate and has limited extracardiac activity, and thus it may be well-tolerated in older individuals. The safety profile and clinical benefits of omecamtiv mecarbil across the age spectrum remain uncertain.</div></div><div><h3>Objectives</h3><div>This study aims to assess CV outcomes, treatment response, and tolerability to omecamtiv mecarbil according to age in patients enrolled in the GALACTIC-HF (Global Approach to Lowering Adverse Cardiac Outcomes Through Improving Contractility in Heart Failure) trial.</div></div><div><h3>Methods</h3><div>GALACTIC-HF was a randomized, global, double-blind clinical trial testing omecamtiv mecarbil vs placebo in patients with symptomatic HF with reduced ejection fraction. Key eligibility criteria included an age between 18-85 years, elevated natriuretic peptides, and a left ventricular ejection fraction (LVEF) ≤35%. We examined the treatment effect of omecamtiv mecarbil vs placebo for the primary endpoint of CV death or first HF event (hospitalization or urgent visit for HF) in both the overall population and the severe HF subgroup (LVEF ≤30%, NYHA functional class III/IV, HF hospitalization within 6 months), as well as safety outcomes according to prespecified age groups (<65 or ≥65 years).</div></div><div><h3>Results</h3><div>A total of 8,232 patients (age 64.5 ± 11.4 years, 54.5% ≥65 years, 21% female) were included. The rate of the primary outcome was 21.4 per 100 patient years (py) in those <65 years of age and 28.8 per 100 py in those ≥65 years of age. The treatment effect of omecamtiv mecarbil for the primary outcome (HR: 0.92 [95% CI: 0.86-0.99]; <em>P =</em> 0.03) was consistent in age groups (<em>P</em><sub>interaction</sub> = 0.76) and irrespective of age as a continuous variable (<em>P</em><sub>interaction</sub> = 0.19, after adjusting for treatment interactions with known modifiers of the effects of omecamtiv mecarbil: LVEF and baseline atrial fibrillation status). In patients with severe HF, omecamtiv mecarbil significantly reduced the risk of the primary outcome in both patients <65 years of age (HR: 0.77 [95% CI: 0.64-0.92]) and those ≥65 years of age (HR: 0.83 [95% CI: 0.71-0.97]; <em>P</em><sub>interaction</sub> = 0.47). The safety profile of omecamtiv mecarbil was consistent irrespective of age (<em>P</em><sub>interaction</sub> > 0.05 for all).</div></div><div><h3>Conclusions</h3><div>In GALACTIC-HF, older individuals were well-represented and faced higher risks of CV events. Treatment with omecamtiv mecarbil was safe irrespective of age and reduced the risk of CV death or first HF event across the age spectrum, especially in those with severe HF. (Global Approach to Lowering Ad
{"title":"Efficacy and Safety of Omecamtiv Mecarbil in Heart Failure With Reduced Ejection Fraction According to Age","authors":"Henri Lu MD , Brian L. Claggett PhD , G. Michael Felker MD, MHS , John J.V. McMurray MD , John R. Teerlink MD , Riccardo M. Inciardi MD, PhD , Marco Metra MD , Stephen B. Heitner MD , Rafael Diaz MD , Fady Malik MD, PhD , Muthiah Vaduganathan MD, MPH , Scott D. Solomon MD","doi":"10.1016/j.jchf.2025.102703","DOIUrl":"10.1016/j.jchf.2025.102703","url":null,"abstract":"<div><h3>Background</h3><div>Older age is associated with a high prevalence of comorbidities and worse cardiovascular (CV) outcomes in patients with heart failure (HF) with reduced ejection fraction. Omecamtiv mecarbil, a selective cardiac myosin activator, exerts minimal effects on blood pressure and heart rate and has limited extracardiac activity, and thus it may be well-tolerated in older individuals. The safety profile and clinical benefits of omecamtiv mecarbil across the age spectrum remain uncertain.</div></div><div><h3>Objectives</h3><div>This study aims to assess CV outcomes, treatment response, and tolerability to omecamtiv mecarbil according to age in patients enrolled in the GALACTIC-HF (Global Approach to Lowering Adverse Cardiac Outcomes Through Improving Contractility in Heart Failure) trial.</div></div><div><h3>Methods</h3><div>GALACTIC-HF was a randomized, global, double-blind clinical trial testing omecamtiv mecarbil vs placebo in patients with symptomatic HF with reduced ejection fraction. Key eligibility criteria included an age between 18-85 years, elevated natriuretic peptides, and a left ventricular ejection fraction (LVEF) ≤35%. We examined the treatment effect of omecamtiv mecarbil vs placebo for the primary endpoint of CV death or first HF event (hospitalization or urgent visit for HF) in both the overall population and the severe HF subgroup (LVEF ≤30%, NYHA functional class III/IV, HF hospitalization within 6 months), as well as safety outcomes according to prespecified age groups (<65 or ≥65 years).</div></div><div><h3>Results</h3><div>A total of 8,232 patients (age 64.5 ± 11.4 years, 54.5% ≥65 years, 21% female) were included. The rate of the primary outcome was 21.4 per 100 patient years (py) in those <65 years of age and 28.8 per 100 py in those ≥65 years of age. The treatment effect of omecamtiv mecarbil for the primary outcome (HR: 0.92 [95% CI: 0.86-0.99]; <em>P =</em> 0.03) was consistent in age groups (<em>P</em><sub>interaction</sub> = 0.76) and irrespective of age as a continuous variable (<em>P</em><sub>interaction</sub> = 0.19, after adjusting for treatment interactions with known modifiers of the effects of omecamtiv mecarbil: LVEF and baseline atrial fibrillation status). In patients with severe HF, omecamtiv mecarbil significantly reduced the risk of the primary outcome in both patients <65 years of age (HR: 0.77 [95% CI: 0.64-0.92]) and those ≥65 years of age (HR: 0.83 [95% CI: 0.71-0.97]; <em>P</em><sub>interaction</sub> = 0.47). The safety profile of omecamtiv mecarbil was consistent irrespective of age (<em>P</em><sub>interaction</sub> > 0.05 for all).</div></div><div><h3>Conclusions</h3><div>In GALACTIC-HF, older individuals were well-represented and faced higher risks of CV events. Treatment with omecamtiv mecarbil was safe irrespective of age and reduced the risk of CV death or first HF event across the age spectrum, especially in those with severe HF. (Global Approach to Lowering Ad","PeriodicalId":14687,"journal":{"name":"JACC. Heart failure","volume":"14 2","pages":"Article 102703"},"PeriodicalIF":11.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145338757","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}
Pub Date : 2026-02-01DOI: 10.1016/j.jchf.2026.102936
Douglas L. Mann MD , Arthur M. Feldman MD, PhD , Mona Fiuzat PharmD , Chrisopher M. O’Connor MD , J. David Port PhD
{"title":"Michael R. Bristow, MD, PhD","authors":"Douglas L. Mann MD , Arthur M. Feldman MD, PhD , Mona Fiuzat PharmD , Chrisopher M. O’Connor MD , J. David Port PhD","doi":"10.1016/j.jchf.2026.102936","DOIUrl":"10.1016/j.jchf.2026.102936","url":null,"abstract":"","PeriodicalId":14687,"journal":{"name":"JACC. Heart failure","volume":"14 2","pages":"Article 102936"},"PeriodicalIF":11.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146098684","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}
Pub Date : 2026-02-01DOI: 10.1016/j.jchf.2025.102680
Eiran Z. Gorodeski MD, MPH , Shashank Shekhar MD , Chantal ElAmm MD , Michelle M. Kittleson MD , Robert A. Montgomery MD
{"title":"The AHFTC Fellowship Match in an Era of Declining Interest","authors":"Eiran Z. Gorodeski MD, MPH , Shashank Shekhar MD , Chantal ElAmm MD , Michelle M. Kittleson MD , Robert A. Montgomery MD","doi":"10.1016/j.jchf.2025.102680","DOIUrl":"10.1016/j.jchf.2025.102680","url":null,"abstract":"","PeriodicalId":14687,"journal":{"name":"JACC. Heart failure","volume":"14 2","pages":"Article 102680"},"PeriodicalIF":11.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145140319","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":"Effects of GLP-1 RA Initiation in Patients With HFrEF and Implantable Cardiac Devices Divided for BMI Values","authors":"Celestino Sardu MD, MSc, PhD , Ferdinando Carlo Sasso MD , Raffaele Marfella MD, PhD","doi":"10.1016/j.jchf.2025.102839","DOIUrl":"10.1016/j.jchf.2025.102839","url":null,"abstract":"","PeriodicalId":14687,"journal":{"name":"JACC. Heart failure","volume":"14 2","pages":"Article 102839"},"PeriodicalIF":11.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146098444","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}
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