JACC advances最新文献

{"title":"Sex-Specific Coronary Artery Calcium Percentiles Across South Asian Adults","authors":"Erfan Tasdighi MD ,&nbsp;Zeina Dardari MS ,&nbsp;Seamus P. Whelton MD ,&nbsp;Jaideep Patel MD ,&nbsp;Alka M. Kanaya MD ,&nbsp;Matthew J. Budoff MD ,&nbsp;Aamir Javaid MD ,&nbsp;Saneel Kulkarni PharmD, MPH ,&nbsp;Tsung-wei Ma PhD ,&nbsp;Javed Butler MD, MPH, MBA ,&nbsp;Nilay S. Shah MD, MPH ,&nbsp;Michael J. Blaha MD, MPH ,&nbsp;Anandita Agarwala MD","doi":"10.1016/j.jacadv.2025.101779","DOIUrl":"10.1016/j.jacadv.2025.101779","url":null,"abstract":"<div><h3>Background</h3><div>Coronary artery calcium (CAC) testing is guideline-recommended to enhance atherosclerotic cardiovascular disease (ASCVD) risk prediction, yet there are no sex-specific CAC reference data for South Asians in the United States (SAUS) across their adult lives.</div></div><div><h3>Objectives</h3><div>The purpose of this study was to determine the sex-specific distribution of CAC scores across the adult lifespan of SAUS.</div></div><div><h3>Methods</h3><div>We studied 2743 SAUS adults (ages 33-75 years old) free of known ASCVD from the MASALA (Mediators of Atherosclerosis in South Asians Living in America), a community-based cohort study, and the DILWALE (DIL Wellness and Arterial health Longitudinal Evaluation), a clinic-based study. We estimated the likelihood of CAC &gt;0 and calculated sex-specific CAC percentiles as a function of age, employing nonparametric methods.</div></div><div><h3>Results</h3><div>Participants had a mean age of 52 ± 9 years, with 37.8% women. The probability of CAC &gt;0 for women and men was 20% and 45% at age 50 years, 40% and 70% at age 60 years, and 70% and 90% at 70 years old, respectively. The 75th and the 90th percentiles of CAC at age 60 years were 26 and 115 for SAUS women and 186 and 580 for SAUS men. A CAC score of 100 was at approximately the 75th percentile for a 55-year-old man or a 65-year-old woman.</div></div><div><h3>Conclusions</h3><div>These data address the current knowledge gap regarding the distribution of CAC scores among SAUS adults. Utilizing these CAC percentiles in the clinical assessment of ASCVD risk may enhance personalized interpretation of CAC scoring and guide ASCVD prevention efforts in SAUS.</div></div>","PeriodicalId":73527,"journal":{"name":"JACC advances","volume":"4 6","pages":"Article 101779"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144120155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Historical Redlining and Cardio-Kidney-Metabolic Disease Risk Factors, Prevalence, and Outcomes","authors":"Ramzi Ibrahim MD ,&nbsp;Dwani Patel MD, PhD ,&nbsp;Hoang Nhat Pham MD ,&nbsp;Mahmoud Abdelnabi MBBCh, MSc ,&nbsp;Girish Pathangey MD ,&nbsp;Issam Motairek MD ,&nbsp;Khurram Nasir MD, MSc, MPH ,&nbsp;Sadeer Al-Kindi MD","doi":"10.1016/j.jacadv.2025.101830","DOIUrl":"10.1016/j.jacadv.2025.101830","url":null,"abstract":"<div><h3>Background</h3><div>Cardio-kidney-metabolic (CKM) diseases impact a large portion of the U.S. population each year, particularly among racial minorities and socially disadvantaged groups. Social factors contribute to this disparity, including barriers to healthcare access, structural racism, and sociocultural influences.</div></div><div><h3>Objectives</h3><div>This scoping review aimed to assess the understanding of how historical redlining has affected the prevalence and outcomes of CKM diseases.</div></div><div><h3>Methods</h3><div>We conducted a scoping review of multiple databases to identify studies examining the relationship between historical redlining and the risk factors, prevalence, and outcomes associated with CKM diseases. Data extraction focused on the type of study, linked databases, research questions, primary outcomes, and study quality.</div></div><div><h3>Results</h3><div>From an initial pool of 176 studies identified, 13 were included. Among these, 6 studies explored the impact of historical redlining on cardiovascular disease risk factors, prevalence, and metabolic disorders; 2 studies examined historical redlining in relation to heart failure; 2 studies focused on kidney disease; and 3 studies investigated atherosclerotic disease. Our findings indicate an association between historically redlined regions and increased prevalence of cardiovascular disease risk factors, heart failure events, metabolic disease burden, and kidney failure incidence. The appraisal of these studies showed that the majority met 20 to 22 of the criteria outlined in the STROBE (Strengthening the Reporting of Observational Studies in Epidemiology) checklist.</div></div><div><h3>Conclusions</h3><div>This scoping review highlighted significant associations between historically redlined neighborhoods in the United States and the prevalence and outcomes of CKM diseases. These findings have revealed the potential impact of structural racism and discriminatory practices on healthcare inequities.</div></div>","PeriodicalId":73527,"journal":{"name":"JACC advances","volume":"4 6","pages":"Article 101830"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144481146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sodium-Glucose Cotransporter Inhibition Preserves Apolipoprotein M During Acute Inflammation in Mice and Humans","authors":"Carla Valenzuela Ripoll MD ,&nbsp;Aynaz Lotfinaghsh MD ,&nbsp;Zhen Guo PhD ,&nbsp;Tripti Kumari PhD ,&nbsp;Kana N. Miyata MD ,&nbsp;Alireza Sargazi MD ,&nbsp;Mualla Ozcan MD ,&nbsp;Ahmed Diab MD ,&nbsp;Anahita Ataran MD ,&nbsp;Hamidreza Hajirezaei MD ,&nbsp;Omid Rashidi MD ,&nbsp;Wenjing Yu PhD ,&nbsp;Yoonje Cho BS ,&nbsp;Attila Kovacs MD ,&nbsp;Carla Weinheimer MS ,&nbsp;Jess Nigro BS ,&nbsp;Olivier Cases PhD ,&nbsp;Renata Kozyraki PhD ,&nbsp;Jan Oscarsson MD, PhD ,&nbsp;Russell Esterline PhD ,&nbsp;Ali Javaheri MD, PhD","doi":"10.1016/j.jacadv.2025.101839","DOIUrl":"10.1016/j.jacadv.2025.101839","url":null,"abstract":"<div><h3>Background</h3><div>Sodium-glucose cotransporter inhibitors (SGLT2is) reduce inflammation and maintain vascular integrity. Apolipoprotein M (ApoM) is crucial for vascular integrity via sphingosine-1-phosphate (S1P) signaling and is inversely linked with mortality in sepsis and COVID-19.</div></div><div><h3>Objectives</h3><div>The authors tested if SGLT2i (dapagliflozin [Dapa]) increases ApoM in mice using lipopolysaccharide (LPS) and in humans with COVID-19.</div></div><div><h3>Methods</h3><div>Diet-induced obese mice (n = 14-15/group), proximal tubule-specific knockout of the multiligand protein receptor Lrp2 (<em>Lrp2</em>^<em>KO</em>) mice (n = 5-8/group), <em>Ly6G-Cre LoxP-STOP-TdTomato</em> mice (n = 3-5/group), <em>Apom</em>^<em>KO</em> mice (n = 3-5/group), and <em>Apom</em>^<em>TG</em> mice (n = 3-5/group) were randomized to receive either vehicle or Dapa (1.25 mg/kg daily) for 4 days before LPS (10 mg/kg IP). Outcomes included ApoM protein levels (Western and enzyme-linked immunosorbent assay) and intravital microscopy to assess endothelial leak and neutrophil behavior. Plasma samples from ACTIV-4a participants (standard of care, n = 37; standard of care + SGLT2i, n = 15) were analyzed for circulating ApoM by enzyme-linked immunosorbent assay. Statistical analyses included two-way analysis of variance for mice and <em>t</em>-test or Mann-Whitney test for humans.</div></div><div><h3>Results</h3><div>Dapa restored circulating ApoM levels in LPS-treated mice (0.017 vs 0.035 [a.u./μL], <em>P</em> = 0.0489) and increased ApoM levels in patients randomized to SGLT2i (0.5240 vs 0.6537 [μM], <em>P</em> = 0.0101). LRP2 knockout blocked Dapa's effect on ApoM. In vitro, Dapa stimulated Lrp2-dependent uptake of ApoM-GFP. Dapa attenuated vascular leak induced by LPS in an ApoM-dependent manner.</div></div><div><h3>Conclusions</h3><div>SGLT2i maintains Lrp2 levels, preserving ApoM and promoting endothelial barrier integrity in acute inflammation, indicating a novel protective mechanism of SGLT2i through ApoM preservation.</div></div>","PeriodicalId":73527,"journal":{"name":"JACC advances","volume":"4 6","pages":"Article 101839"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144481147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatocyte Growth Factor","authors":"Margrethe Flesvig Holt MD ,&nbsp;Annika E. Michelsen PhD ,&nbsp;August Flø MD ,&nbsp;Yusuf Khan PhD ,&nbsp;Vilde Karoline Bjørnø RN ,&nbsp;Mona Skjelland MD, PhD ,&nbsp;Vigdis Bjerkeli BSc ,&nbsp;Benedicte Paus MD, PhD ,&nbsp;John-Peder Escobar Kvitting MD, PhD ,&nbsp;Bente Halvorsen PhD ,&nbsp;Tale Norbye Wien MD, PhD ,&nbsp;Melinda Raki MD, PhD ,&nbsp;Lars Gullestad MD, PhD ,&nbsp;Pål Aukrust MD, PhD ,&nbsp;Kaspar Broch MD, PhD ,&nbsp;Thor Ueland PhD ,&nbsp;Einar Gude MD, PhD","doi":"10.1016/j.jacadv.2025.101828","DOIUrl":"10.1016/j.jacadv.2025.101828","url":null,"abstract":"<div><h3>Background</h3><div>It is important to reduce diagnostic delays for patients with cardiac amyloidosis (CA). Plasma biomarkers could streamline the diagnostic process and enhance prognostic accuracy.</div></div><div><h3>Objectives</h3><div>The authors aimed to identify circulating biomarkers capable of differentiating patients with CA from patients with heart failure (HF) and no amyloidosis. Additionally, we assessed whether these markers were associated with patient outcomes.</div></div><div><h3>Methods</h3><div>We performed focused protein screening in 12 patients with transthyretin CA, 5 patients with HF, and 16 healthy controls (HCs). To validate the findings, we used immunoassays to measure levels of differentially regulated proteins in a larger sample of 86 patients with transthyretin CA, 15 patients with light-chain CA, 16 patients with HF, and HCs. We compared protein levels between groups using multivariable general linear models. Associations between protein levels and all-cause mortality were assessed by receiver operating characteristic analysis.</div></div><div><h3>Results</h3><div>We identified 99 candidate proteins by proteomic screening. In the validation sample, 4 of these markers were higher in CA than in HCs. Levels of C-X-C motif chemokine ligand 9 and hepatocyte growth factor (HGF) were also higher in CA than in HF. HGF correlated with measures of cardiac function in patients with transthyretin and light chain CA. HGF had a good discriminatory ability for predicting all-cause mortality (area under the curve = 0.80, <em>P</em> &lt; 0.001), similar to those of N-terminal pro-B-type natriuretic peptide and troponin T.</div></div><div><h3>Conclusions</h3><div>Plasma HGF is a promising screening tool for CA. Higher levels of HGF are associated with more severe HF and worse prognosis in patients with CA.</div></div>","PeriodicalId":73527,"journal":{"name":"JACC advances","volume":"4 6","pages":"Article 101828"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144481493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effect of 12-Week e-Cigarette Use on Smoking Abstinence at 1 Year","authors":"Kristian B. Filion PhD ,&nbsp;Tetiana Zolotarova MD ,&nbsp;Andréa Hébert-Losier MSc ,&nbsp;Sarah B. Windle MPH ,&nbsp;Pauline Reynier MSc ,&nbsp;Todd Greenspoon MD ,&nbsp;Tim Brandys MD ,&nbsp;Tamàs Fülöp MD ,&nbsp;Thang Nguyen MD ,&nbsp;Stéphane Elkouri MD ,&nbsp;Igor Wilderman MD ,&nbsp;Olivier F. Bertrand MD ,&nbsp;Joanna Alexis Bostwick MD ,&nbsp;Yves Lacasse MD ,&nbsp;Smita Pakhale MD ,&nbsp;Mark J. Eisenberg MD, MPH","doi":"10.1016/j.jacadv.2025.101833","DOIUrl":"10.1016/j.jacadv.2025.101833","url":null,"abstract":"<div><h3>Background</h3><div>The current evidence regarding the long-term efficacy of electronic cigarettes (e-cigarettes) for smoking cessation is unclear.</div></div><div><h3>Objectives</h3><div>The purpose of this study was to assess the efficacy, safety, and tolerability of nicotine and non-nicotine e-cigarettes for smoking cessation in the general population.</div></div><div><h3>Methods</h3><div>We randomized 376 adults who smoked ≥10 cigarettes/day and were motivated to quit at 17 Canadian sites to 12 weeks of nicotine (15 mg/mL) e-cigarettes (n = 128), non-nicotine e-cigarettes (n = 127), or no e-cigarettes (n = 121). All groups received individual counseling. The primary endpoint was point prevalence abstinence (7-day recall, biochemically validated using expired carbon monoxide) at 12 weeks. The 52-week follow-up results are reported here.</div></div><div><h3>Results</h3><div>Participants (mean age 52 ± 13 years; 47% female) smoked a mean of 21 ± 11 cigarettes/day at baseline. Compared to individual counseling alone, participants randomized to nicotine e-cigarettes plus counseling had higher rates of point prevalence (23.6% vs 9.9%; difference: 13.7%; 95% CI: 4.6%-22.8%) and continuous abstinence (3.1% vs 0.0%; difference: 3.1%; 95% CI: 0.1%-6.2%) and greater reductions in the number of cigarettes smoked (−9.5 ± 10.5 vs −5.6 ± 9.5; difference: −3.9; 95% CI: −6.5 to −1.4) at 52 weeks. Benefits were also observed among participants randomized to non-nicotine e-cigarettes plus counseling vs counseling alone. No differences in abstinence or reduction were found between nicotine and non-nicotine e-cigarettes.</div></div><div><h3>Conclusions</h3><div>Compared to individual counseling alone, short-term use of standardized nicotine and non-nicotine e-cigarettes plus counseling is efficacious at increasing smoking abstinence at 52 weeks.</div></div>","PeriodicalId":73527,"journal":{"name":"JACC advances","volume":"4 6","pages":"Article 101833"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Critical Appraisal of Lipid Management in the Post-Statin Era","authors":"Jared Spitz MD ,&nbsp;Jaideep Patel MD ,&nbsp;Anandita Agarwala MD ,&nbsp;Garima Sharma MD ,&nbsp;Anurag Mehta MD ,&nbsp;Pradeep Natarajan MD ,&nbsp;Khurram Nasir MD, MPH ,&nbsp;Pamela Morris MD ,&nbsp;Roger S. Blumenthal MD ,&nbsp;Michael D. Shapiro DO, MCR","doi":"10.1016/j.jacadv.2025.101823","DOIUrl":"10.1016/j.jacadv.2025.101823","url":null,"abstract":"<div><div>The role of low-density lipoprotein-cholesterol in the pathogenesis of atherosclerotic cardiovascular disease (ASCVD) is well established. Lipid management remains the cornerstone of addressing ASCVD. In addition to statin therapy, there is a large and growing number of nonstatin therapies available to manage elevated cholesterol levels. This expert panel seeks to review current international recommendations regarding lipid management. In addition, complex yet commonly encountered lipid-management cases are provided. Guidance on applying guideline-based recommendations as well as newer evidence to the evaluation and management of ASCVD-risk lipid management is then provided.</div></div>","PeriodicalId":73527,"journal":{"name":"JACC advances","volume":"4 6","pages":"Article 101823"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gestational Diabetes Mellitus and Heart Failure","authors":"Eric K. Broni MD, MPH ,&nbsp;Sebhat Erqou MD, PhD ,&nbsp;Ravi Retnakaran MD ,&nbsp;Allison G. Hays MD ,&nbsp;Justin B. Echouffo-Tcheugui MD, PhD","doi":"10.1016/j.jacadv.2025.101807","DOIUrl":"10.1016/j.jacadv.2025.101807","url":null,"abstract":"<div><h3>Background</h3><div>The extent of the association between gestational diabetes mellitus (GDM) and the incidence of heart failure (HF) largely remains unclear.</div></div><div><h3>Objectives</h3><div>The aim of the study was to synthesize the evidence on the association of GDM and risk of HF.</div></div><div><h3>Methods</h3><div>This study is a systematic review and meta-analysis. We searched PubMed and Embase through July 24, 2024, for cohort studies reporting on the GDM and HF association. We pooled adjusted relative risk (RR) estimates of the association of GDM and HF using a random-effects model meta-analysis.</div></div><div><h3>Results</h3><div>In a meta-analysis of 8 observational studies, a total of 6,371,877 participants (weighted averages—age: 28.7 years, 89.7% White, body mass index 25.6 kg/m², 310,351 with GDM) were assessed and experienced 12,409 incident HF events over ∼8.6 years (weighted average). The pooled adjusted RR for the GDM and HF association was 1.54 (95% CI: 1.24-1.92). There was heterogeneity across the studies (<em>I</em>² = 86.9%, <em>P</em> &lt; 0.001). Sensitivity analyses, excluding the smallest and largest studies, did not appreciably change the significance and magnitude of the overall RR estimate of the risk of HF related to GDM.</div></div><div><h3>Conclusions</h3><div>The observed independent association of GDM with HF suggests a potential causal role of GDM in adverse myocardial remodeling. A history of GDM should be considered as a risk factor in the efforts to prevent HF.</div></div>","PeriodicalId":73527,"journal":{"name":"JACC advances","volume":"4 6","pages":"Article 101807"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevalence and Mortality Association of Different Stages of Cardiovascular-Kidney-Metabolic Syndrome","authors":"Yongming Chen PhD, MD ,&nbsp;Xiaoying Wu PhD ,&nbsp;Tianxin Long PhD ,&nbsp;Yuxiao Jiang MS ,&nbsp;Miao Wang PhD, MD ,&nbsp;Zhengtong Lv PhD, MD ,&nbsp;Huimin Hou PhD, MD ,&nbsp;Ziang Li PhD ,&nbsp;Ming Liu PhD, MD","doi":"10.1016/j.jacadv.2025.101843","DOIUrl":"10.1016/j.jacadv.2025.101843","url":null,"abstract":"<div><h3>Background</h3><div>The cardiovascular-kidney-metabolic (CKM) syndrome, introduced by the American Heart Association, underscores the interplay among metabolic, renal, and cardiovascular dysfunctions.</div></div><div><h3>Objectives</h3><div>This study aimed to evaluate the prevalence and mortality risk across CKM syndrome stages in the UK population.</div></div><div><h3>Methods</h3><div>This prospective cohort study included 110,933 participants from the UK Biobank. The primary outcome was all-cause mortality, with cardiovascular disease (CVD)-specific mortality as a secondary outcome. Kaplan-Meier and Cox proportional hazards models were used to estimate survival and mortality risks.</div></div><div><h3>Results</h3><div>Among the 110,933 participants, 9.16% were classified as CKM stage 0, 13.53% as stage 1, 44.15% as stage 2, 26.25% as stage 3, and 6.91% as stage 4. Over a median follow-up of 14.7 years, 13,012 all-cause deaths and 1,613 CVD-specific deaths were recorded. All-cause mortality rates increased progressively across CKM stages: 6.32% (stage 0), 7.47% (stage 1), 10.12% (stage 2), 13.67% (stage 3), and 30.09% (stage 4). Similarly, CVD-specific mortality rates increased from 0.43% to 5.43%. Compared to stage 0, the adjusted HRs for all-cause mortality were 1.14 for stage 2, 1.25 for stage 3, and 2.13 for stage 4. For CVD-specific mortality, the adjusted HRs were 1.48 for stage 2, 1.99 for stage 3, and 3.46 for stage 4.</div></div><div><h3>Conclusions</h3><div>Nearly 80% of individuals were classified into poor CKM stages (stages 2-4), which were strongly associated with significantly elevated risks of both all-cause and CVD-specific mortality. These findings emphasize the urgent need for early detection and targeted interventions in high-risk cardiometabolic populations.</div></div>","PeriodicalId":73527,"journal":{"name":"JACC advances","volume":"4 6","pages":"Article 101843"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144481152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mediating Effect of Established Risk Factors on Association Between Social Determinants and Cardiovascular Disease Mortality","authors":"William J. He MHS ,&nbsp;Siyi Geng MS ,&nbsp;Ling Tian MPH, PhD ,&nbsp;Frank B. Hu MD, PhD","doi":"10.1016/j.jacadv.2025.101744","DOIUrl":"10.1016/j.jacadv.2025.101744","url":null,"abstract":"<div><h3>Background</h3><div>Social determinants of health (SDOH) contribute to increased cardiovascular disease (CVD) mortality.</div></div><div><h3>Objectives</h3><div>The authors investigated the mediating effects of behavioral and clinical risk factors in the association between SDOH and CVD mortality.</div></div><div><h3>Methods</h3><div>A total of 50,808 National Health and Nutrition Examination Survey participants aged ≥20 years were included in this analysis. Data on social, behavioral, and clinical risk factors were collected in each National Health and Nutrition Examination Survey, and CVD deaths were ascertained through linkage to the National Death Index with follow-up through 2019. Multiple mediation analysis was used to examine the contributions of behavioral and clinical risk factors to the SDOH-CVD mortality association.</div></div><div><h3>Results</h3><div>The mean age of participants was 47.2 years, and 48.8% were male. A dose-response association between the number of SDOH and CVD mortality was identified. Individuals with a composite SDOH score ≥ median have a 2.13-fold increased risk of CVD mortality (95% CI: 1.91-2.37) compared to those with a score &lt; median. After adjusting for behavioral and clinical risk factors, the HR was reduced to 1.67 (95% CI: 1.50-1.86). Current smoking (relative contribution 11.4%; 95% CI: 8.1%-14.8%), physical inactivity (7.7%; 95% CI: 4.9%-10.6%), chronic kidney disease (5.5%; 95% CI: 3.8%-7.1%), diabetes (2.0%; 95% CI: 1.1%-2.9%), and unhealthy sleep duration (1.8%; 95% CI: 0.3%-3.3%) significantly mediated the association between CVD mortality and unfavorable SDOH. In aggregate, behavioral and clinical risk factors mediated 30.8% (95% CI: 24.2%-37.5%) of the overall CVD mortality attributable to unfavorable SDOH.</div></div><div><h3>Conclusions</h3><div>Behavioral and clinical risk factors partially mediate the association between unfavorable SDOH and increased CVD mortality.</div></div>","PeriodicalId":73527,"journal":{"name":"JACC advances","volume":"4 6","pages":"Article 101744"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144025085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association Between Life's Essential 8 and Cardiovascular, Cancer, and Other Cause Mortality","authors":"Katherine M. Huether MD ,&nbsp;Laura C. Pinheiro PhD, MPH ,&nbsp;Suzanne E. Judd PhD, MPH ,&nbsp;D. Leann Long PhD ,&nbsp;Monika M. Safford MD ,&nbsp;Donald M. Lloyd-Jones MD, ScM ,&nbsp;Timothy B. Plante MD, MHS","doi":"10.1016/j.jacadv.2025.101731","DOIUrl":"10.1016/j.jacadv.2025.101731","url":null,"abstract":"<div><h3>Background</h3><div>Cardiovascular disease (CVD) and cancer are leading causes of death in adults. Life's Essential 8 (LE8) estimates cardiovascular health (CVH) and includes body mass index, blood pressure, blood sugar, cholesterol, diet, physical activity, sleep, and smoking. CVD, cancer, and other mortality are competing risks.</div></div><div><h3>Objectives</h3><div>The purpose of this study was to determine the risk of CVD mortality, cancer mortality, and other mortality by LE8-quantified CVH in a competing risk framework.</div></div><div><h3>Methods</h3><div>REGARDS (REasons for Geographic and Racial Differences in Stroke) study recruited 30,239 Black and White adults from the 48 contiguous U.S. states from 2003 to 2007. We excluded prevalent CVD or cancer, missing LE8, or no follow-up. LE8 scores were categorized as low (&lt;50), moderate (50-79), or high CVH (≥80). Adjusted cause-specific hazard models estimated relative hazard of CVD mortality, cancer mortality, and non-CVD, noncancer mortality as competing risks.</div></div><div><h3>Results</h3><div>Among 11,385 included participants (mean age 65 ± 9 years, 52% female, 44% Black adults), 24%, 66%, and 10% had low, moderate, and high CVH, respectively. Over a median (IQR) follow-up of 14 (IQR: 8-17) years, 8% died from CVD, 7% from cancer, and 17% from other causes. Higher CVH was associated with significantly lower HRs for CVD (0.37; 95% CI: 0.28-0.49), cancer (0.48; 95% CI: 0.36-0.66), and non-CVD, noncancer (0.39; 95% CI: 0.32-0.48) mortality compared to low CVH levels.</div></div><div><h3>Conclusions</h3><div>Better LE8-quantified CVH was associated with lower CVD and cancer mortality in a competing risk framework. These findings underscore the significance of lifestyle modifications in mortality risk reduction, advocating for their incorporation into clinical guidelines and preventive counseling.</div></div>","PeriodicalId":73527,"journal":{"name":"JACC advances","volume":"4 6","pages":"Article 101731"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144060672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}