Journal of the American College of Cardiology最新文献

{"title":"Guidance for Incorporating FDA Processes into the ACC/AHA Clinical Practice Guideline Methodology: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.","authors":"Hani Jneid, Abdul R Abdullah, Victor A Ferrari, Richard J Kovacs, Debabrata Mukherjee, Daichi Shimbo","doi":"10.1016/j.jacc.2025.05.006","DOIUrl":"https://doi.org/10.1016/j.jacc.2025.05.006","url":null,"abstract":"","PeriodicalId":17187,"journal":{"name":"Journal of the American College of Cardiology","volume":" ","pages":""},"PeriodicalIF":22.3,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149583","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":"2025 ACC/AHA Clinical Practice Guidelines Core Principles and Development Process: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.","authors":"Catherine M Otto, Abdul R Abdullah, Leslie L Davis, Victor A Ferrari, Stephen Fremes, Debabrata Mukherjee, Lauren Prestera, Boback Ziaeian","doi":"10.1016/j.jacc.2025.06.013","DOIUrl":"10.1016/j.jacc.2025.06.013","url":null,"abstract":"","PeriodicalId":17187,"journal":{"name":"Journal of the American College of Cardiology","volume":" ","pages":""},"PeriodicalIF":22.3,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149546","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":"Global, Regional, and National Burden of Cardiovascular Diseases and Risk Factors in 204 Countries and Territories, 1990-2023.","authors":"","doi":"10.1016/j.jacc.2025.08.015","DOIUrl":"https://doi.org/10.1016/j.jacc.2025.08.015","url":null,"abstract":"<p><strong>Background: </strong>Cardiovascular diseases (CVDs) are the leading cause of mortality and are among the foremost causes of disability globally. CVD burden has continued to increase in most countries since 1990, with trends driven by changing exposures to harmful risk factors, population growth, and population aging.</p><p><strong>Objectives: </strong>We report estimates of global, national, and subnational CVD burden, including 18 subdiseases and 12 associated modifiable risk factors. We analyzed change in CVD burden from 1990 to 2023 and identified drivers of change including population growth, population aging, and risk factor exposure.</p><p><strong>Methods: </strong>The Global Burden of Disease (GBD) 2023 study, a multinational collaborative research study, quantified burden due to 375 diseases including CVD burden and identified drivers of change from 1990 to 2023 using all available data and statistical models. GBD 2023 estimated the population-level burden of diseases in 204 countries and territories from 1990 to 2023.</p><p><strong>Results: </strong>CVDs were the leading cause of disability-adjusted life years (DALYs) and deaths estimated in the GBD. As of 2023, there were 437 million (95% UI: 401 to 465 million) CVD DALYs globally, a 1.4-fold increase from the number in 1990 of 320 million (292 to 344 million). Ischemic heart disease, intracerebral hemorrhage, ischemic stroke, and hypertensive heart disease were the leading cardiovascular causes of DALYs in 2023 globally. As of 2023, age-standardized CVD DALY rates were highest in low and low-middle Socio-demographic Index (SDI) settings and lowest in high SDI settings. The number of CVD deaths increased globally from 13.1 million (95% UI: 12.2 to 14.0 million) in 1990 to 19.2 million (95% UI: 17.4 to 20.4 million) in 2023. The number of prevalent cases of CVD more than doubled since 1990, with 311 million (95% UI: 294 to 333 million) prevalent cases of CVD in 1990 and 626 million (95% UI: 591 to 672 million) prevalent cases in 2023 globally. A total of 79.6% (95% UI: 75.7% to 82.5%) of CVD burden is attributable to modifiable risk factors 347 million [95% UI: 318 to 373 million] DALYs in 2023). Globally, high systolic blood pressure, dietary risks, high low-density lipoprotein cholesterol, and air pollution were the modifiable risks responsible for most attributable CVD burden in 2023. Since 1990, changes in exposure to modifiable risk factors have had mixed effects on CVD burden, with increases in high body mass index, high fasting plasma glucose, and low physical activity leading to higher burden, while reductions in tobacco usage have mitigated some of these increases. Population growth and population aging were the main drivers of the increasing burden since 1990, adding 128 million (95% UI: 115 to 139 million) and 139 million (95% UI: 126 to 151 million) CVD DALYs to the increase in CVD burden since 1990.</p><p><strong>Conclusions: </strong>CVD remains the leading cause","PeriodicalId":17187,"journal":{"name":"Journal of the American College of Cardiology","volume":" ","pages":""},"PeriodicalIF":22.3,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145131144","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":"Long-Term Antithrombotic Therapy in Patients With Atrial Fibrillation and Prior PCI: Insights From EPIC-CAD Trial.","authors":"Seong-Bong Wee, Do-Yoon Kang, Min Soo Cho, Min-Ju Kim, Jung-Min Ahn, Han Su Park, Soo Yeon An, Kyeong-Won Seo, Seung Han Lee, Yong-Seog Oh, Chang Hoon Lee, Eue-Keun Choi, Ji Hyun Lee, Chang Hee Kwon, Gyung-Min Park, Hyung Oh Choi, Kyoung-Ha Park, Kyoung-Min Park, Jongmin Hwang, Ki-Dong Yoo, Young-Rak Cho, Ji Hyun Kim, Ki Won Hwang, Eun-Sun Jin, Osung Kwon, Ki-Hun Kim, Seung-Jung Park, Gi-Byoung Nam, Duk-Woo Park","doi":"10.1016/j.jacc.2025.07.035","DOIUrl":"10.1016/j.jacc.2025.07.035","url":null,"abstract":"","PeriodicalId":17187,"journal":{"name":"Journal of the American College of Cardiology","volume":" ","pages":"940-943"},"PeriodicalIF":22.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144958514","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":"A Polygenic Risk Score to Predict Incident Heart Failure Across the Spectrum of Cardiovascular Risk.","authors":"Paul M Haller, Giorgio E M Melloni, David D Berg, Frederick K Kamanu, Yi-Pin Lai, Elliott M Antman, Deepak L Bhatt, Marc P Bonaca, Christopher P Cannon, Robert P Giugliano, Michelle L O'Donoghue, Benjamin M Scirica, Stephen D Wiviott, Daniel Chasman, Brendan M Everett, Eugene Braunwald, David A Morrow, Paul M Ridker, Patrick T Ellinor, Marc S Sabatine, Christian T Ruff, Nicholas A Marston","doi":"10.1016/j.jacc.2025.06.050","DOIUrl":"10.1016/j.jacc.2025.06.050","url":null,"abstract":"<p><strong>Background: </strong>The clinical utility of a heart failure (HF) polygenic risk score (PRS) is uncertain.</p><p><strong>Objectives: </strong>The purpose of this study was to investigate the ability of an HF PRS to predict new-onset HF in individuals across the spectrum of cardiovascular risk.</p><p><strong>Methods: </strong>An HF PRS (>1 million single nucleotide variations) was used to stratify individuals from 7 clinical studies to low (quintile [Q] 1), intermediate (Q2-Q4), or high (Q5) genetic risk. In 6 trials of patients at elevated cardiovascular risk, HRs adjusted for clinical factors were derived for the risk of hospitalization for HF using Cox-PH models, and discrimination and calibration was explored. Analyses were conducted in a separate data set of individuals at low cardiovascular risk.</p><p><strong>Results: </strong>We studied 74,897 patients without HF, of which 51,627 were at elevated cardiovascular risk (median age 65 years; 71% men; median follow-up 2.5 years). After adjusting for clinical factors, individuals with intermediate and high HF PRS carried a 2- and 5-fold increased rate of new-onset HF, respectively (intermediate risk: HR_adj: 2.01 [95% CI: 1.62-2.49]; P < 0.001; high-risk: HRadj: 5.00 [95% CI: 3.99-6.27]; P < 0.001). Addition of the HF PRS to a clinical model improved the AUC (0.787 [95% CI: 0.775-0.798] to 0.822 [95% CI: 0.811-0.832]). Results were consistent in 23,270 individuals at low cardiovascular risk over 20-year follow-up.</p><p><strong>Conclusions: </strong>An HF PRS is a strong and independent predictor for new-onset HF in individuals across the spectrum of cardiovascular risk. The polygenic contribution to HF is complementary to established clinical risk assessment.</p>","PeriodicalId":17187,"journal":{"name":"Journal of the American College of Cardiology","volume":" ","pages":"860-873"},"PeriodicalIF":22.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144958690","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":"Causes of Myocardial Infarction in Younger Patients: Troponin-Elevation in Persons ≤65 Years Old in Olmsted County.","authors":"Claire E Raphael, Yader Sandoval, Joel D Beachey, Veronique Roger, Mandeep Singh, Matthew P Johnson, Marysia S Tweet, Malcolm R Bell, Amir Lerman, Sharonne N Hayes, David R Holmes, Bernard J Gersh, Allan S Jaffe, Rajiv Gulati","doi":"10.1016/j.jacc.2025.07.012","DOIUrl":"10.1016/j.jacc.2025.07.012","url":null,"abstract":"<p><strong>Background: </strong>The burden and pathophysiologic mechanisms of myocardial infarction (MI) in younger patients remain understudied. Prior studies have been limited by selected cohorts and lack of awareness of nonatherothrombotic causes.</p><p><strong>Objectives: </strong>We sought to determine the incidence and outcomes of MI according to a unique pathophysiologic mechanism in a large community cohort aged ≤65 years, and to evaluate sex-differences in etiology METHODS: We identified all residents of Olmsted County, Minnesota, USA, age ≤65 years who experienced an event associated with a cardiac troponin T >99th percentile of upper reference range (≥0.01 ng/mL) from January 2003 to March 2018. Records and imaging were individually scrutinized. Patients classified as MI were assigned to 1 of 6 adjudicated pathophysiologic mechanisms: atherothrombosis, spontaneous coronary artery dissection (SCAD), embolism, vasospasm, myocardial infarction with nonobstructed coronary arteries not meeting another category (MINOCA-U), and supply/demand mismatch secondary myocardial infarction. We determined incidence and long-term all-cause and cardiovascular mortality for each group.</p><p><strong>Results: </strong>There were 4,116 myocardial injury events in 2,780 patients (36% women) over 15 years. Excluding periprocedural MI, 1,474 events were classified as index MI, of which 68% were caused by atherothrombosis. The population incidence of MI was much lower in women, particularly in MI caused by atherothrombosis (48 vs 137 per 100,000 person years and 23 vs 105 per 100,000 person-years). Incidence of SCAD was much higher in women (3.2 vs 0.9 per 100,000 person-years) with 55% of cases misclassified as MINOCA or atherothrombosis at index presentation. Women with atherothrombosis were similar in age to men (55 ± 8 years vs 54 ± 8 years), with similar disease extent at angiography but greater burden of risk factors. Proportionately, nonatherothrombotic causes comprised the majority of MI in women (atherothrombosis 47% vs 75%, secondary myocardial infarction [SSDM] 34% vs 19%, SCAD 11% vs 0.7%, embolism 2% vs 2%, vasospasm 3% vs 1%, MINOCA-U 3% vs 2%). The 5-year all-cause mortality was highest after SSDM (SSDM 33%, atherothrombosis 8%, embolism 8%, SCAD 0%) with low cardiovascular mortality in all groups.</p><p><strong>Conclusions: </strong>This community-based study demonstrates nonatherothrombotic causes comprise an important burden of acute MI in persons age ≤65 years, particularly women. These cause-specific findings have implications for individualized management and risk stratification and provide epidemiologic benchmarking for future studies.</p>","PeriodicalId":17187,"journal":{"name":"Journal of the American College of Cardiology","volume":" ","pages":"877-888"},"PeriodicalIF":22.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12445014/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144958772","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":"Outcomes of Percutaneous Mechanical Aspiration in Right-Sided Infective Endocarditis: A Multicenter Registry.","authors":"Abdallah El Sabbagh, Benjamin Hibbert, Sripal Bangalore, Pete Fong, David Zlotnick, Bassim El-Sabawi, Robert Zhang, Brittany Zwischenberger, Ahmad Mourad, Leonard Palatnic, Sameh Sayfo, Shenise Gilyard, Stephanie Younes, Ahmad Younes, Joseph Ingrassia, Mohiuddin Cheema, Muhammad Hammadah, Anand Prasad, Nadira Hamid, Konstantinos Voudris, Pedro Villablanca, Amir Kaki, Mohammed Qintar, Zulfiqar Baloch, Marquand Patton, Alejandro Dominguez, Yasir Akhtar, Sidakpal Panaich, Nahyr Lugo-Fagundo, Evin Yucel, David O Hodge, Kenneth Rosenfield, Larry Baddour, Paul Sorajja, John Moriarty, Sahil A Parikh, Sanjum S Sethi","doi":"10.1016/j.jacc.2025.06.054","DOIUrl":"10.1016/j.jacc.2025.06.054","url":null,"abstract":"<p><strong>Background: </strong>Catheter-based percutaneous mechanical aspiration (PMA) is an emerging acute intervention for debulking infective vegetations in right-sided infective endocarditis (RSIE); however, its outcomes and safety remain undefined.</p><p><strong>Objectives: </strong>The authors sought to assess early clinical outcomes and safety of PMA in patients with RSIE.</p><p><strong>Methods: </strong>The CLEAR-IE (Cardiac Lesion Extraction and Aspiration Registry for Infective Endocarditis) is a large multicenter retrospective registry of consecutive patients with RSIE who have undergone PMA. Procedural success was defined as a ≥70% reduction in site-reported vegetation size or a residual size ≤1 cm on intraprocedural echocardiography, which included transesophageal echocardiography (TEE), intracardiac echocardiography (ICE), and transthoracic echocardiography (TTE), selected at the operator's discretion to guide the intervention. The primary endpoint was a composite of in-hospital mortality, new pulmonary embolism (PE), or emergency surgery. Secondary endpoints included each component of the primary endpoint and in-hospital worsening tricuspid regurgitation (TR).</p><p><strong>Results: </strong>Between January 2014 and January 2024, 256 patients from 19 institutions were included. Median age was 43 years; 43% were women, and 51% had history of injection drug use. Acute PE (50.8%) and shock (27%) were frequent at presentation. Tricuspid valve involvement was present in 70%, with a median site-reported vegetation size of 2.4 cm (Q1-Q3: 0.6-9 cm). Severe TR was noted in 31.3% at baseline. Staphylococcus aureus was the predominant pathogen (73.8%). Procedural success was achieved in 89.4%, with a median residual vegetation size of 0.7 cm (Q1-Q3: 0.2-1.1 cm). Overall, 86.9% completed the procedure free from procedure-related complications. The primary endpoint occurred in 18% (mortality: 9.8%; new PE: 8.3%; emergency surgery: 3.1%). Among those without baseline severe TR, worsening TR occurred in 16.9%. On univariate analysis, shock (OR: 2.27; 95% CI: 1.15-4.43; P = 0.03) and hypoxia (OR: 3.62; 95% CI: 1.83-7.17; P < 0.001) were significantly associated with the primary endpoint, whereas worsening TR was not. On multivariate analysis, hypoxia (OR: 2.76; 95% CI: 1.34-5.73; P = 0.006) remained significantly associated with the primary outcome.</p><p><strong>Conclusions: </strong>PMA of RSIE is feasible with high procedural success. Adverse events were acceptable and largely driven by underlying RSIE. Randomized trials are warranted to confirm the clinical impact and safety of PMA in RSIE.</p>","PeriodicalId":17187,"journal":{"name":"Journal of the American College of Cardiology","volume":" ","pages":"846-856"},"PeriodicalIF":22.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144958681","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":"10 Issues for the Clinician in Tricuspid Regurgitation Evaluation and Management: 2025 ACC Expert Consensus Decision Pathway: A Report of the American College of Cardiology Solution Set Oversight Committee.","authors":"Patrick T O'Gara, JoAnn Lindenfeld, Rebecca T Hahn, Megan Joseph, Omar K Khalique, Prateeti Khazanie, Dharam J Kumbhani, Robert Page, Kristen K Patton, Vinod H Thourani","doi":"10.1016/j.jacc.2025.07.002","DOIUrl":"https://doi.org/10.1016/j.jacc.2025.07.002","url":null,"abstract":"","PeriodicalId":17187,"journal":{"name":"Journal of the American College of Cardiology","volume":" ","pages":""},"PeriodicalIF":22.3,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145113690","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":"Beyond Adiposity: Embracing Complexity in Diabetes-Associated HFpEF.","authors":"Harlan M Krumholz, Silvio E Inzucchi","doi":"10.1016/j.jacc.2025.08.005","DOIUrl":"10.1016/j.jacc.2025.08.005","url":null,"abstract":"","PeriodicalId":17187,"journal":{"name":"Journal of the American College of Cardiology","volume":" ","pages":""},"PeriodicalIF":22.3,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075657","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":"Is Type 2 Diabetes a Modifiable Risk Factor for the Evolution and Progression of Heart Failure With a Preserved Ejection Fraction?","authors":"Milton Packer, Carolyn S P Lam, Javed Butler, Faiez Zannad, Muthiah Vaduganathan, Barry A Borlaug","doi":"10.1016/j.jacc.2025.07.052","DOIUrl":"https://doi.org/10.1016/j.jacc.2025.07.052","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Type 2 diabetes is associated with an increased risk of heart failure with a preserved ejection fraction (HFpEF), but it is not clear whether this metabolic disorder is causal or represents a modifiable risk factor. Mechanisms by which diabetes may be associated with HFpEF can be grouped into the following: 1) those related to hyperglycemia and amenable to antihyperglycemic drugs; and 2) those related to the association of type 2 diabetes with obesity and visceral adiposity, and thus, treatable with interventions that reduce adipose tissue mass or improve adipocyte biology.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Evidence against a role for hyperglycemia: &lt;/strong&gt;Experimentally, acute and chronic hyperglycemia caused by islet cell destruction can lead to cardiac dysfunction, but these models resemble type 1 (not type 2) diabetes. Heightened levels of environmental glucose can cause enzymatic or nonenzymatic modification of proteins and signaling through the polyol pathway, but interference with these mechanisms has not produce clinical benefits in patients with heart disease and type 2 diabetes. Furthermore, lowering of blood glucose in type 2 diabetes with insulin, sulfonylureas, dipeptidyl peptidase-4 inhibitors and thiazolidinediones has not reduced the risk of heart failure.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Evidence for a mediating role for adiposity: &lt;/strong&gt;In marked contrast, experimental models that link type 2 diabetes to HFpEF are typically accompanied by excess adiposity. Epidemiological studies demonstrate that the association between type 2 diabetes and HFpEF is mediated primarily through a common link with central obesity and an expanded visceral fat mass. Changes in the biology of adipocytes as a result of visceral adiposity are sufficient to cause systemic insulin resistance and diabetes. Interestingly, the primary metabolic defect in the diabetic heart is lipid overload, not an impairment in glucose uptake or insulin resistance. Adiposity can promote HFpEF through the secretion of proinflammatory adipokines that lead to sodium retention and cardiac steatosis and fibrosis. Additionally, excess adiposity can drive the production of and enhance cardiac sensitivity to advanced glycation end products. Glucagon-like peptide receptor agonists and sodium-glucose cotransporter reduce the risk or progression of HFpEF, but this benefit is not related by the presence of diabetes or to the glucose-lowering effects of these drugs. Instead, their favorable cardiac effects may be mediated by their action to induce or mimic a state of caloric deprivation, thus restoring adipokine balance and alleviating the state of cardiac steatosis. Similarly, bariatric surgery alleviates both visceral adiposity and type 2 diabetes and reduces the risk of HFpEF.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;Taken together, these findings suggest that diabetes-associated HFpEF is mediated primarily through its association with excess adiposity. Diabetes is a modifiable risk factor i","PeriodicalId":17187,"journal":{"name":"Journal of the American College of Cardiology","volume":" ","pages":""},"PeriodicalIF":22.3,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075646","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}