Journal of the American Heart Association最新文献

{"title":"Pediatric and Congenital Cardiac Services: An Innovative and Empowering Approach to Global Training and Equitable Care.","authors":"Wyman W Lai, Dominique Vervoort, David Bradley, Antonio G Cabrera, Casey Culbertson, Alejandro Floh, Saurabh K Gupta, Babar S Hasan, Adrian Holloway, Jeffrey P Jacobs, Kathy J Jenkins, R K Kumar, L A Larrazabal, Colin J McMahon, Daniel J Penny, Alistair Phillips, Emilio Quezada, Craig A Sable, Shubhika Srivastava, Sandra L Staveski, Patcharapong Suntharos, David F Teitel, Betsy Tirado, Brian C Tran, Bistra Zheleva, Liesl Zuhkle, Anthony C Chang","doi":"10.1161/JAHA.124.040003","DOIUrl":"https://doi.org/10.1161/JAHA.124.040003","url":null,"abstract":"<p><p>Congenital heart disease is a leading cause of preventable death in children, with a disproportionate impact on low- and middle-income countries. Despite progress in treating congenital heart disease globally, significant challenges remain in accessing specialized cardiovascular care, particularly cardiac surgery, in low- and middle-income countries. This review examines current models of assistance and proposes a novel global training program to address these inequities. Key challenges identified include building program infrastructure, training health care providers, ensuring financial sustainability, and promoting local engagement. The proposed program, structured under a new international organization, will leverage emerging technologies to deliver accessible and rigorously assessed training in pediatric and congenital cardiac care. By collaborating with local experts and global partners, the program will promote access to education for various health care personnel involved in congenital heart disease care, establish credentialing standards, and foster global collaboration. This unified, scalable approach aims to bridge the health equity gap and accelerate progress toward comprehensive and sustainable cardiac care programs worldwide.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e040003"},"PeriodicalIF":5.0,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143804688","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":"Contribution of the TRPM4 Channel to Osteogenic Differentiation of Human Aortic Valve Interstitial Cells.","authors":"Margaux Aize, Arthur Boilève, Benoit D Roussel, Laura Brard, Harlyne Mpweme Bangando, Corentin Kerevel, Alexandre Lebrun, Hind Messaoudi, Vladimir Saplacan, Alain Manrique, Romain Guinamard, Christophe Simard","doi":"10.1161/JAHA.124.038542","DOIUrl":"https://doi.org/10.1161/JAHA.124.038542","url":null,"abstract":"<p><strong>Background: </strong>Aortic stenosis due to deleterious remodeling of the aortic valve is a health concern since it can be corrected only by valve replacement due to the poor knowledge of cellular mechanisms involved. Fibroblastic valvular interstitial cells (VICs) play a central role in valve leaflet stiffness by trans-differentiation into osteoblast-like cells leading to calcification. The TRPM4 (transient receptor potential melastatin 4) cation channel was shown to participate in cardiac fibroblast remodeling. It is also involved in radiation-induced aortic valve remodeling in vivo in mice. We hypothesized that TRPM4 might participate in human VIC transition to osteoblastic phenotype.</p><p><strong>Methods: </strong>Human aortic valves were collected from patients undergoing surgical valve replacement. Isolated VICs were maintained 14 days in culture in standard or pro-calcifying media and submitted to the TRPM4 inhibitor 9-phenanthrol, or small hairpin RNA-TRPM4. Osteogenic differentiation was evaluated by measuring hydroxyapatite crystals by Alizarin red staining and protein expression of osteogenic markers.</p><p><strong>Results: </strong>Western blot on VICs revealed TRPM4 protein expression and channel functionality was confirmed by patch-clamp recordings exhibiting a cationic current sensitive to voltage and internal Ca²⁺. VICs maintained in pro-calcifying media exhibited a higher mineralization than in standard media, with an increase in osteogenic markers. Mineralization and osteogenic markers (bone morphogenetic protein 2, runt-related transcription factor 2) were decreased when pro-calcifying media contained 9-phenanthrol or small hairpin RNA-TRPM4. Similarly, SMAD1/5 and nuclear factor of activated T-cell pathways were stimulated in pro-calcifying media conditions compared with standard media but reduced by 9-phenanthrol or small hairpin RNA-TRPM4.</p><p><strong>Conclusions: </strong>TRPM4 participates in osteogenic differentiation of human VICs and thus appears as a target to prevent aortic valve remodeling.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e038542"},"PeriodicalIF":5.0,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143804740","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":"Sex Differences and 2-Year Mortality in Patients With Atrial Fibrillation Diagnosed After Stroke and Known Atrial Fibrillation: A Register-Based Study in Sweden.","authors":"Ilham Al Khatib, Adam Viktorisson, Tamar Abzhandadze, Katharina S Sunnerhagen","doi":"10.1161/JAHA.124.037608","DOIUrl":"https://doi.org/10.1161/JAHA.124.037608","url":null,"abstract":"<p><strong>Background: </strong>The objective of this study was to determine associations between atrial fibrillation diagnosed after stroke (AFDAS) and known atrial fibrillation with 2-year mortality among men and women.</p><p><strong>Methods and results: </strong>This longitudinal, register-based study included patients with ischemic stroke admitted to 3 hospitals in Gothenburg, Sweden, between November 1, 2014 and June 30, 2019. The exposures were known atrial fibrillation and AFDAS detected at the stroke units. The outcome was all-cause mortality 2 years after stroke. Cox-regression analyses were conducted to assess sex differences in relation to the adjusted mortality risk. Of 5468 patients with ischemic stroke, 2583 (47%) were women, and the mean age was 74 years (SD 14). Overall, 19% had known atrial fibrillation, and 10% had AFDAS. Women were older and had more severe strokes compared with men. Within the first month, women with AFDAS did not have an increased risk of mortality compared with women with no atrial fibrillation (hazard ratio, 0.93 [95% CI, 0.46-1.88]), in contrast to men with AFDAS who had an increased risk (hazard ratio, 2.14 [95% CI, 1.07-4.26]). Men and women with AFDAS had an increased risk of long-term mortality (31 days to 2 years) compared with those with no atrial fibrillation. Known atrial fibrillation was associated with the highest poststroke mortality irrespective of sex and time interval.</p><p><strong>Conclusions: </strong>Our findings suggest that underlying sex differences exist in the association between the occurrence of AFDAS and poststroke mortality. Sex differences related to the timing of atrial fibrillation diagnosis should be considered when developing preventive measures and medical care after stroke.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e037608"},"PeriodicalIF":5.0,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143804657","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":"Investigation of Myocardial Substrate for Sudden Arrhythmic Death in Coronary Artery Disease Without Acute Coronary Thrombosis or Myocardial Infarction.","authors":"Duncan J Campbell, Victoria C M Francis, Gregory R Young, Noel W F Woodford","doi":"10.1161/JAHA.124.039624","DOIUrl":"https://doi.org/10.1161/JAHA.124.039624","url":null,"abstract":"<p><strong>Background: </strong>This cohort study aimed to evaluate the potential myocardial arrhythmic substrate in people with coronary artery disease who died from sudden arrhythmic death (SAD) without acute coronary thrombosis or myocardial infarction.</p><p><strong>Methods and results: </strong>We performed histological analysis of the left ventricular free wall obtained at autopsy from decedents with ≥1 coronary artery and ≥75% area stenosis who died suddenly from either noncardiac causes (25 men, 23 women) or SAD (25 men, 25 women), matched for age and sex. Decedents with acute coronary thrombosis, myocardial infarction, or other myocardial abnormality were excluded. Decedents with either noncardiac death or SAD had similar height, weight, and heart weight. Decedents with SAD had higher cumulative area stenosis of coronary arteries (mean, 162% versus 134%; mean difference, 29% [95% CI, 1%-56%], <i>P</i>=0.042) and a higher proportion of decedents with SAD had diabetes (mean, 10% versus 0%; mean difference, 10% [95% CI, 2%-18%], <i>P</i>=0.025) and chronic, nonocclusive, organized coronary artery thrombus (mean, 16% versus 0%; mean difference, 16% [95% CI, 6%-26%], <i>P</i>=0.0040). Moreover, decedents with SAD had lower cardiomyocyte width (mean, 18.6 μm versus 19.6 μm; mean difference, 1.0 μm [95% CI, 0.2-1.8], <i>P</i>=0.014) and higher capillary length density (mean, 3618 mm/mm³ versus 3164 mm/mm³; mean difference, 453 mm/mm³ [95% CI, 210-697], <i>P</i>=0.0003) than decedents with noncardiac death.</p><p><strong>Conclusions: </strong>SAD in people with coronary artery disease without acute coronary thrombosis or myocardial infarction was associated with greater coronary artery plaque burden and cardiomyocyte atrophy that may have contributed to myocardial substrate for arrhythmia.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e039624"},"PeriodicalIF":5.0,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143804684","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":"Left Atrial Myocardial Mechanics: Association With Cognitive Dysfunction, Cerebrovascular Disease, and Circulating Biomarkers.","authors":"Eugene S J Tan, Saima Hilal, Siew Pang Chan, Ming Ann Sim, Mitchell K P Lai, Joyce Chong, Caroline Robert, Hazliza Hazli, Lingli Gong, Josephine Lunaria Berboso, Narayanaswamy Venketasubramanian, Boon-Yeow Tan, A Mark Richards, Christopher Chen, Lieng-Hsi Ling","doi":"10.1161/JAHA.123.036931","DOIUrl":"https://doi.org/10.1161/JAHA.123.036931","url":null,"abstract":"<p><strong>Background: </strong>The relationship of left atrial (LA) strain with cognition in the absence of atrial fibrillation is poorly understood. We investigated the association of LA strain with cognitive impairment and its pathogenetic subtype (vascular [VCI] or neurodegenerative) and underlying mechanisms via associations with circulating and neuroimaging markers of cerebrovascular disease.</p><p><strong>Methods and results: </strong>LA strain (reservoir, conduit [LAScd], contractile) was determined using speckle-tracking echocardiography in a prospective memory clinic cohort with brain magnetic resonance imaging, neuropsychological assessments, and circulating biomarker measurements. Cognitive impairment was classified as VCI or neurodegenerative in the presence or absence of significant cerebrovascular disease, respectively. Among 251 subjects (age 75±8 years, 59% women) without atrial fibrillation, 178 (71%) had cognitive impairment (20% mild, 14% moderate, 37% dementia); of these impairments, 58% were VCI and 42% neurodegenerative. Only LAScd was associated with more severe cognitive impairment (moderate/dementia versus none/mild, adjusted odds ratio [aOR] for lowest versus highest tertile >2) and specifically, with worse Mini-Mental State Examination score and memory on neuropsychological testing. LAScd was independently associated with VCI (versus neurodegenerative; aOR for lowest versus highest tertile, 4.22 [95% CI, 1.59-11.2]) and not with neurodegenerative markers (circulating pTau-181 [phosphorylated tau-181], isolated lobar cerebral microbleeds). Both LAScd and LA reservoir strain were associated with increased burden of cerebral small vessel disease on magnetic resonance imaging, but only LAScd correlated with circulating biomarkers, reflecting inflammation, neurotrophic processes, and neuronal damage.</p><p><strong>Conclusions: </strong>Reduced LA strain was associated with cognitive impairment, primarily of vascular origin, and a higher burden of cerebral small vessel disease. LAScd may be a biomarker of VCI in at-risk subjects without atrial fibrillation.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e036931"},"PeriodicalIF":5.0,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143804685","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":"Discordances in Kinetic Energy Between the Superior Cavopulmonary Connection and Single Ventricle Are Associated With Suboptimal Fontan Outcomes: A Pre-Fontan 4-Dimensional Flow Study.","authors":"Jacqueline Contento, Mithra Agamy, Maren Brinken, Ryan O'Hara, Nicholas Mouzakis, Janet Kruetzer, Rittal Mehta, Roland Axt-Fliedner, Elias Balaras, Francesco Capuano, Ravi Vegulla, Yves d'Udekem, Yue-Hin Loke","doi":"10.1161/JAHA.124.037949","DOIUrl":"https://doi.org/10.1161/JAHA.124.037949","url":null,"abstract":"<p><strong>Background: </strong>Patients with functional single ventricle (SV) are at risk for adverse outcomes after staged palliation from the superior cavopulmonary connection (SCPC) to the Fontan. Current pre-Fontan assessment by cardiac magnetic resonance and cardiac catheterization includes measuring atrioventricular valve regurgitation, aortopulmonary collateral burden, and pressures. Four-dimensional flow can quantify complex flows representing hemodynamic inefficiency. This study determined the clinical significance of kinetic energy (KE) and viscous energy loss in patients before the Fontan procedure using 4-dimensional flow.</p><p><strong>Methods and results: </strong>This was a retrospective analysis of patients before the Fontan procedure who underwent ferumoxytol-enhanced cardiac magnetic resonance and same-day catheterization. Four-dimensional flow data sets were analyzed using ITFlow (CardioFlowDesign) to measure KE/viscous energy loss in the atrium, SV, and SCPC. A composite outcome was defined by rejected Fontan candidacy, prolonged hospitalization, lymphatic dysfunction, or heart failure. The relationship between these outcomes and KE/viscous energy loss was assessed by bivariable and multivariable logistic regression analyses as appropriate. Sixty-five patients (3.9±1.5 years, 0.64±0.1 m²) were included. Fifty (77%) proceeded to Fontan operation with median hospitalization time of 8.5 (interquartile range, 7-12.7) days. Twenty-six (40%) experienced a composite outcome, including 9 with rejected candidacy. Lower SCPC flow was associated with an outcome (<i>P</i>=0.042). Meanwhile, higher SV KE and lower SCPC KE were independently associated with composite outcome (odds ratio, 3.63 [95% CI, 1.32-13.2]; <i>P</i>=0.0263; odds ratio, 0.906 [95% CI, 0.814-0.980]; <i>P</i>=0.0377). Higher SV KE and lower SCPC KE corresponded to significant atrioventricular valve regurgitation, higher aortopulmonary collateral burden, and higher cathetherization pressures.</p><p><strong>Conclusions: </strong>Four-dimensional flow analysis provides insight into SV hemodynamics and is associated with short-term outcomes. Future work will analyze the longitudinal implications for patients undergoing the Fontan procedure.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e037949"},"PeriodicalIF":5.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773575","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":"Sodium Alginate Hydrogel Infusion of Bone Marrow Mesenchymal Stem Cell-Derived Extracellular Vesicles and p38α Antagonistic Peptides in Myocardial Infarction Fibrosis Mitigation.","authors":"Siyao Chen, Xiaodong Zeng, Meifeng Wu, Jiade Zhu, Yijin Wu","doi":"10.1161/JAHA.124.036887","DOIUrl":"https://doi.org/10.1161/JAHA.124.036887","url":null,"abstract":"<p><strong>Background: </strong>Myocardial fibrosis is a pathological hallmark of heart failure post infarction, emphasizing the need for innovative treatment strategies. This research assesses the antifibrotic potential of a sodium alginate (SA) hydrogel loaded with extracellular vesicles (EVs) from bone marrow mesenchymal stem cells and PAP (p38α antagonistic peptides), aiming to interfere with fibrosis-inducing pathways in myocardial tissue after infarction.</p><p><strong>Methods: </strong>We induced fibrosis in mouse cardiac fibroblasts through hypoxia and disrupted the <i>Mapk14</i> gene to study its contribution to fibrosis. Mesenchymal stem cell-derived EVs, loaded with PAP, were encapsulated in the SA hydrogel (EVs-PAP@SA). The formulation was tested in vitro for its effect on fibrotic marker expression and cell behavior, and in vivo in a murine model of myocardial infarction for its therapeutic efficacy.</p><p><strong>Results: </strong>Map k14 silencing showed a decrease in the fibrotic response of cardiac fibroblasts. Treatment with the EVs-PAP@SA hydrogel notably reduced profibrotic signaling, increased cell proliferation and migration, and lowered apoptosis rates. The in vivo treatment with the hydrogel post myocardial infarction significantly diminished myocardial fibrosis and improved cardiac performance.</p><p><strong>Conclusions: </strong>The study endorses the SA hydrogel as an effective vehicle for delivering mesenchymal stem cell-derived EVs and PAP to the heart post myocardial infarction, providing a novel approach for modulating myocardial fibrosis and promoting cardiac healing.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e036887"},"PeriodicalIF":5.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143774723","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":"Interactive Effect of Air Temperature and Fine Particulate Matter on the Hospital Admissions for Stroke in Shenzhen, China.","authors":"Xiuling Zhao, Jie Cao, Weiqi Zhou, Andreas M Neophytou","doi":"10.1161/JAHA.124.037329","DOIUrl":"https://doi.org/10.1161/JAHA.124.037329","url":null,"abstract":"<p><strong>Background: </strong>Stroke is a major health challenge in China. Numerous studies have linked stroke with temperature and fine particulate matter (PM_2.5), but findings varied by stroke subtypes and regions, and few explored the interactive effects of air temperature and PM_2.5. This study examines the association between air temperature, PM_2.5, and stroke hospital admissions in Shenzhen, a subtropical monsoon city in southern China.</p><p><strong>Methods and results: </strong>We applied time-series generalized additive models to estimate the individual and interactive effects of air temperature and PM_2.5 on stroke hospital admissions using daily records from 2015 to 2016. Subgroup analysis by sex, age, and education level was conducted, assessing admissions for hemorrhagic (n=8752) and ischemic (n=33 233) stroke separately. For hemorrhagic stroke, a 1 °C increase in temperature was significantly associated with a 2.3% (95% CI, -3.2% to -1.3%) decrease in hospital admissions, whereas higher levels of PM_2.5 indicated an increased risk, though not significant. Conversely, for ischemic stroke, a 1 °C rise was significantly associated with a 1.0% (95% CI, 0.4%-1.6%) increase in admissions. The impact PM_2.5 on stroke was more pronounced at higher concentrations, while showing no evident effects at lower levels. Interaction effects between temperature and PM_2.5 were statistically significant for both stroke types, with stronger effects observed at 10 to 20 °C and PM_2.5 concentration around 80 to 100 μg/m³.</p><p><strong>Conclusions: </strong>This study suggests lower air temperature may increase hemorrhagic stroke risk, whereas higher temperature and higher PM_2.5 exposure may increase ischemic stroke risk. Interactive effects between temperature and PM_2.5 were observed for both stroke types in Shenzhen.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e037329"},"PeriodicalIF":5.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773974","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":"Amyloid β1-40 Predicts Long-Term Mortality Rate in Patients With Acute Myocardial Infarction.","authors":"Aneta Aleksova, Alessandra Lucia Fluca, Alessandro Pierri, Giulia Barbati, Antonio Paolo Beltrami, Laura Padoan, Enzo Merro, Maria Marketou, Donna Zwas, Stefano D'Errico, Gianfranco Sinagra, Milijana Janjusevic","doi":"10.1161/JAHA.124.035620","DOIUrl":"https://doi.org/10.1161/JAHA.124.035620","url":null,"abstract":"<p><strong>Background: </strong>Amyloid β1-40 (Aβ1-40) contributes to atherosclerosis, being involved in plaque formation and destabilization. The prognostic role of Aβ1-40 in patients with acute myocardial infarction is currently limited to non-ST-segment-elevation myocardial infarction (NSTEMI). We examined the prognostic value of Aβ1-40 in a real-world cohort of patients with acute myocardial infarction (both ST-segment-elevation myocardial infarction [STEMI] and NSTEMI) and identified predictors for its elevated levels.</p><p><strong>Methods and results: </strong>Our population included 1119 consecutive patients (mean age, 67 years; 72% men; and STEMI, 68%). The median Aβ1-40 concentration on admission was 86.9 (interquartile range, 54.5-128.9) pg/mL, and there was no difference in Aβ1-40 levels between NSTEMI and STEMI (<i>P</i>=0.1). Higher Aβ1-40 levels were predicted by older age, lower left ventricular ejection fraction, glycated hemoglobin >39 mmol/mol and glomerular filtration rate <60 mL/min per m². From the final multivariable model, a nomogram was computed to determine probability of high Aβ1-40. During the median follow-up of 57 months, 193 patients (17.2%) died. Kaplan-Meier analysis revealed higher mortality risk in patients with Aβ1-40 levels above the median (<i>P</i><0.01), consistent across STEMI (<i>P</i><0.01) and NSTEMI (<i>P</i>=0.01) subgroups. At Cox multivariable analysis including the entire cohort, Aβ1-40 levels were predictive of death (hazard ratio, 1.03; <i>P</i>=0.01), together with older age, higher high-sensitivity C-reactive protein levels, smoking, glomerular filtration rate <60 mL/min per m², worse left ventricular ejection fraction, and previous ischemic events. In the STEMI subcohort, Aβ1-40 remained a significant predictor, along with advanced age, worse left ventricular ejection fraction, smoking, and elevated high-sensitivity C-reactive protein. No such association was found in patients with NSTEMI (<i>P</i>=0.17), likely due to the smaller cohort size and low event rate.</p><p><strong>Conclusions: </strong>Aβ1-40 is an independent predictor of death and improves risk stratification in patients with acute myocardial infarction.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e035620"},"PeriodicalIF":5.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143775013","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":"Outcomes and Left Ventricular Ejection Fraction in Cardiac Magnetic Resonance: Challenging the \"Higher Is Better\".","authors":"Rungroj Krittayaphong, Thammarak Songsangjinda, Kanchalaporn Jirataiporn, Ahthit Yindeengam","doi":"10.1161/JAHA.124.039889","DOIUrl":"https://doi.org/10.1161/JAHA.124.039889","url":null,"abstract":"<p><strong>Background: </strong>Contradictory evidence exists regarding the correlation between supranormal left ventricular ejection fraction (LVEF) and adverse outcomes. This study aimed to elucidate the prognostic value of supranormal LVEF.</p><p><strong>Methods: </strong>This retrospective cohort study analyzed patients referred for cardiac magnetic resonance imaging to assess myocardial ischemia or viability. Subjects were stratified into eig8ht LVEF groups: <20%, 20% to 30%, 30% to 40%, 40% to 50%, 50% to 60%, 60% to 70%, 70% to 80%, and ≥80%. Primary outcomes included cardiovascular death, heart failure, myocardial infarction, and stroke. The extracellular volume fraction was measured.</p><p><strong>Results: </strong>The study cohort comprised 3279 patients (mean age 68.0±12.7 years; 64.0% female). The group with 60% to 70% LVEF had the lowest risk and was used as the reference group. The median follow-up was 41.4 months (interquartile range, 33.9-49.7 months). The group with LVEF <20% exhibited the highest composite outcome risk (unadjusted hazard ratio [HR], 6.77 [95% CI, 3.81-12.03]; <i>P</i><0.001; adjusted HR, 2.68 [95% CI, 1.28-5.62]; <i>P</i><0.001). The groups with LVEF 70% to 80% and ≥80% showed increased risk (adjusted HR, 1.96 [95% CI, 1.23-3.08]; <i>P</i>=0.004; 2.16 [95% CI, 1.33-3.52]; <i>P</i>=0.002, respectively). A greater extracellular volume fraction was associated with an LVEF of 70% to 80% and ≥80% (adjusted odds ratios, 1.34 [95% CI, 1.03-1.74]; <i>P</i>=0.027; and 1.74 [95% CI, 1.30-2.34]; <i>P</i><0.001, respectively).</p><p><strong>Conclusions: </strong>LVEF >70% demonstrated increased event rates compared with an LVEF of 60% to 70%. The supranormal LVEF warrants further investigation into its pathogenesis and management.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e039889"},"PeriodicalIF":5.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143774734","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}