Journal of the American Heart Association最新文献

{"title":"Palliative Care Needs Assessment Using the Surprise Question in Hospitalized Patients With Heart Failure.","authors":"Yasuhiro Hamatani, Yurika Ikeyama, Atsuko Kunugida, Kenjiro Ishigami, Kimihito Minami, Mina Takamoto, Mitsuyo Yamaguchi, Misaki Sakai, Tae Kinoshita, Moritake Iguchi, Masaharu Akao","doi":"10.1161/JAHA.124.037769","DOIUrl":"https://doi.org/10.1161/JAHA.124.037769","url":null,"abstract":"<p><strong>Background: </strong>The surprise question \"Would I be surprised if this patient dies within 1 year?\" is a simple tool to identify patients who may benefit from palliative care. We aimed to investigate the usefulness of the surprise question to identify palliative care needs among patients hospitalized with heart failure (HF).</p><p><strong>Methods and results: </strong>This study used a prospective observational registry that includes consecutive patients hospitalized with HF using the surprise question on admission. Patients were classified as surprised or not surprised according to the surprise question. Backgrounds, symptom burdens, and clinical outcomes were compared between groups. Of 601 patients hospitalized with HF, 181 (30%) were classified as not surprised. Patients classified as not surprised were older (86±8 versus 76±12 years, <i>P</i><0.001), had a lower prevalence of men (76 [42%] versus 238 [57%], <i>P</i>=0.001), and had a lower left ventricular ejection fraction (41±19% versus 45±17%, <i>P</i>=0.015) than those classified as surprised. There were no significant differences in symptom burdens evaluated at discharge or their temporal change from admission to discharge between groups (all <i>P</i>>0.05). Among 489 patients followed until death or 1 year after admission, 108 (22%) all-cause deaths and 90 (18%) HF rehospitalizations occurred within 1 year. The multivariable Cox model demonstrated the independent association between the not surprised classification and higher risk of all-cause death (hazard ratio [HR], 3.34 [95% CI, 2.03-5.49]; <i>P</i><0.001), whereas there was no association with HF rehospitalization (HR, 1.36 [95% CI, 0.79-2.34]; <i>P</i>=0.27).</p><p><strong>Conclusions: </strong>The surprise question was significantly associated with a higher risk of all-cause death, suggesting its prognostic usefulness in identifying patients suitable for advance care planning.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e037769"},"PeriodicalIF":5.0,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143755721","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":"Daily Heart Rate Per Step (DHRPS): A Wearables Metric Associated with Cardiovascular Disease in a Cross-Sectional Study of the All of Us Research Program.","authors":"Zhanlin Chen, Charles T Wang, Carolyn J Hu, Kendra Ward, Abel Kho, Gregory Webster","doi":"10.1161/JAHA.124.036801","DOIUrl":"https://doi.org/10.1161/JAHA.124.036801","url":null,"abstract":"<p><strong>Background: </strong>Simple biometrics such as peak heart rate and exercise duration remain core predictors of cardiovascular disease (CVD). Commercial wearable devices track physical and cardiac electrical activity. Detailed, longitudinal data collection from wearables presents a valuable opportunity to identify new factors associated with CVD.</p><p><strong>Methods: </strong>This cross-sectional study analyzed 6,947 participants in the Fitbit Bring-Your-Own-Device Project, a subset of the <i>All of Us</i> Research Program. The primary exposure Daily Heart Rate Per Step (DHRPS) was defined as the average daily heart rate divided by steps per day. Our analysis correlated DHRPS with established CVD factors (type 2 diabetes, hypertension, stroke, heart failure, coronary atherosclerosis, myocardial infarction) as primary outcomes. We also performed a DHRPS-based phenome-wide association study (PheWAS) on the spectrum of human disease traits for all 1,789 disease codes across 17 disease categories. Secondary outcomes included maximum metabolic equivalents (METs) achieved on cardiovascular treadmill exercise stress testing.</p><p><strong>Results: </strong>We examined 5.8 million person-days and 51 billion total steps of individual-level Fitbit data paired with electronic health record data. Elevated DHRPS was associated with type 2 diabetes (OR 2.03 [95% CI 1.70-2.42]), hypertension (OR 1.63 [95% CI 1.32-2.02]), heart failure (OR 1.77 [95% CI 1.00-3.14]), and coronary atherosclerosis (OR 1.44 [95% CI 1.14-1.82]), even after adjusting for daily heart rate and step count. DHRPS also had stronger correlations with max METs achieved on exercise stress testing compared to steps per day (∆ρ=0.04, p<0.001) and heart rate (∆ρ=0.31, p<0.001). Lastly, DHRPS-based PheWAS demonstrated stronger associations with CVD factors (p<1×10^-55) compared to daily heart rate or step count.</p><p><strong>Conclusions: </strong>In the <i>All of Us</i> Research Program Fitbit Bring-Your-Own-Device Project, DHRPS was an easy-to-calculate wearables metric and was more strongly associated with cardiovascular fitness and CVD outcomes than daily heart rate and step count.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e036801"},"PeriodicalIF":5.0,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744438","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":"Cardiovascular Health in the Transition From Adolescence to Emerging Adulthood: A Scientific Statement From the American Heart Association.","authors":"Jewel Scott, Anandita Agarwala, Carissa M Baker-Smith, Matthew J Feinstein, Karen Jakubowski, Jill Kaar, Niyati Parekh, Kershaw V Patel, Janna Stephens","doi":"10.1161/JAHA.124.039239","DOIUrl":"https://doi.org/10.1161/JAHA.124.039239","url":null,"abstract":"<p><p>Cardiovascular disease remains a leading cause of death in the United States, with an alarming rise in the proportion of young adults experiencing cardiovascular events. Many adolescents enter adulthood with significant cardiovascular disease risk factors. This scientific statement addresses the critical need for cardiovascular health promotion during emerging adulthood, a transitional stage between the ages of 18 and 25 or 29 years of age. We discuss the significance of social determinants of health and the interplay between individual-level risk factors and developmental changes, including shifts in substance use, social connections, and emotional well-being. We conclude by outlining strategies for optimizing cardiovascular health promotion and disease prevention, underscoring the importance of primordial prevention, early intervention, and tailored approaches to address the unique needs of emerging adults. Addressing these multifaceted factors is crucial for mitigating the burden of cardiovascular disease risk factors among emerging adults and promoting long-term cardiovascular well-being.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e039239"},"PeriodicalIF":5.0,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710636","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":"Hydrochlorothiazide Is America's Most Popular Thiazide, But Should It Be?","authors":"Peter S Natov, Amy R Schwartz","doi":"10.1161/JAHA.124.035573","DOIUrl":"https://doi.org/10.1161/JAHA.124.035573","url":null,"abstract":"","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":"14 6","pages":"e035573"},"PeriodicalIF":5.0,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143652011","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":"Inhibition of Sodium/Hydrogen Exchanger-1 in the Right Ventricle and Lung Dysfunction Induced by Experimental Pulmonary Arterial Hypertension in Rats.","authors":"Giuseppina Milano, Melanie Reinero, Julien Puyal, Piergiorgio Tozzi, Michele Samaja, Florence Porte-Thomé, Maurice Beghetti","doi":"10.1161/JAHA.124.036859","DOIUrl":"10.1161/JAHA.124.036859","url":null,"abstract":"<p><strong>Background: </strong>Life-threatening pulmonary arterial hypertension (PAH) still lacks a direct therapeutic approach targeted to the molecular defects associated with the disease. Here, we focus on the impaired regulation of intracellular acidity and sodium/calcium overload by testing the hypothesis that inhibiting NHE-1 (sodium/hydrogen exchanger isoform 1) with rimeporide enables the recovery of pulmonary and right ventricular dysfunctions in the Sugen5416/hypoxia PAH model in rats.</p><p><strong>Methods and results: </strong>Adult Sprague-Dawley male rats (n=44) rats were divided into 2 broad groups: control and Sugen5416/hypoxia. After verifying PAH insurgence in the Sugen5416/hypoxia group by transthoracic echocardiography and pulse-wave Doppler analysis, rats were treated with either 100 mg/kg per day rimeporide or placebo in drinking water for 3 weeks. The functional, morphological (fibrosis and hypertrophy), and biochemical (inflammation, signaling pathways) dysfunctions caused by PAH were partially reverted by rimeporide in both the lungs and myocardium, where the most striking effects were observed in the right ventricle. Rimeporide improved hemodynamics in the pulmonary circulation and in the right ventricle, with decrease in right ventricle hypertrophy, pulmonary vascular remodeling, inflammation, and fibrosis. No effect of rimeporide was detected in control rats. The protective effect of rimeporide was accompanied by decreased p-Akt/Akt (phosphorylated protein kinase B/protein kinase B) ratio and increased autophagy flux mainly in the right ventricle.</p><p><strong>Conclusions: </strong>By specifically inhibiting NHE-1, rimeporide at the selected dosage revealed remarkable anti-PAH effects by preventing the functional, morphological, and biochemical deleterious effects of PAH on the right ventricle and lungs. Rimeporide should be considered as a potential treatment for PAH.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e036859"},"PeriodicalIF":5.0,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143588097","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":"Genetic Susceptibility to Type 2 Diabetes, Television Viewing, and Atherosclerotic Cardiovascular Disease Risk.","authors":"Mengyao Wang, Paul James Collings, Felix R Day, Ken K Ong, Soren Brage, Stephen J Sharp, Haeyoon Jang, Siyeon Suh, Shan Luo, Shiu Lun Au Yeung, Youngwon Kim","doi":"10.1161/JAHA.124.036811","DOIUrl":"10.1161/JAHA.124.036811","url":null,"abstract":"<p><strong>Background: </strong>Type 2 diabetes (T2D) is a major risk factor for atherosclerotic cardiovascular disease (ASCVD). This study examined the interplay between watching television and T2D genetic risk for risk of ASCVD.</p><p><strong>Methods: </strong>We included 346 916 White British individuals from UK Biobank. A weighted polygenic risk score for T2D was calculated on the basis of 138 genetic variants associated with T2D. Time spent watching television was self-reported and categorized into 2 groups: ≤1 h/d and ≥2 h/d. Over a median 13.8-year follow-up, 21 265 incident ASCVD events were identified. Models using Cox regression with age as the underlying time scale adjusted for potential confounders (demographic, anthropometric, lifestyle factors, and medication use) were fit.</p><p><strong>Results: </strong>Compared with watching television for ≤1 h/d, watching ≥2 h/d was associated with 12% (95% CI, 1.07-1.16) higher hazards of ASCVD, independently of T2D genetic risk. Joint analyses (with low T2D genetic risk and ≤1 h/d of television viewing as reference) indicated that medium and high T2D genetic risk was not associated with higher hazards of ASCVD as long as television viewing was ≤1 h/d. The <i>P</i> values for multiplicative and additive interactions between T2D genetic risk and television viewing were 0.050 and 0.038, respectively. The 10-year absolute risk of ASCVD was lower for high T2D genetic risk combined with ≤1 h/d of television viewing (2.13%) than for low T2D genetic risk combined with ≥2 h/d of television viewing (2.46%).</p><p><strong>Conclusions: </strong>Future clinical trials of lifestyle-modification interventions targeting specific types of screen-based sedentary activities could be implemented to individuals at high genetic risk of T2D for primary prevention of ASCVD.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e036811"},"PeriodicalIF":5.0,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143607098","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":"Identification of Long Noncoding RNA Candidate Disease Genes Associated With Clinically Reported Copy Number Variants in Congenital Heart Disease.","authors":"Jacqueline S Penaloza, Blythe Moreland, Jeffrey B Gaither, Benjamin J Landis, Stephanie M Ware, Kim L McBride, Peter White","doi":"10.1161/JAHA.124.039177","DOIUrl":"10.1161/JAHA.124.039177","url":null,"abstract":"<p><strong>Background: </strong>Copy number variants (CNVs) contribute to 3% to 10% of isolated congenital heart disease (CHD) cases, yet their pathogenic roles remain unclear. Diagnostic efforts have focused on protein-coding genes, largely overlooking long noncoding RNAs (lncRNAs), which play key roles in development and disease.</p><p><strong>Methods and results: </strong>We systematically analyzed lncRNAs overlapping clinically validated CNVs in 743 patients with CHD from the Cytogenomics of Cardiovascular Malformations Consortium. We identified heart-expressed lncRNAs, constructed a gene regulatory network using weighted gene coexpression network analysis, and identified gene modules associated with heart development. Functional enrichment and network analyses were used to identify lncRNAs that may be involved in heart development and potentially contribute to CHD. The code is stably archived at https://doi.org/10.5281/zenodo.13799779. We identified 18 lncRNA candidate genes within modules significantly correlated with heart tissue, highlighting their potential involvement in CHD pathogenesis. Notably, lncRNAs such as <i>lnc-STK32C-3, lnc-TBX20-1</i>, and <i>CRMA</i> demonstrated strong associations with known CHD genes. Strikingly, although only 7.6% of known CHD genes were affected by a CNV, 68.8% of the CNVs contained a lncRNA expressed in the heart.</p><p><strong>Conclusions: </strong>Using weighted gene coexpression network analysis, we identified CNV-associated lncRNAs with potential relevance to CHD, underscoring the complexities of noncoding regions in disease pathogenesis. These findings suggest that lncRNAs may play a greater role in CHD than previously recognized, highlighting the need for broader genomic analyses that extend beyond protein-coding genes. This study provides a foundation for further exploration of lncRNAs in CHD, with potential implications for improved genetic characterization and diagnosis.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e039177"},"PeriodicalIF":5.0,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143626822","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":"Myocardial Proteome in Human Heart Failure With Preserved Ejection Fraction.","authors":"Vivek P Jani, Edwin J Yoo, Aleksandra Binek, Alina Guo, Julie S Kim, Jennifer Aguilan, Mohammad Keykhaei, Sydney R Jenkin, Simone Sidoli, Kavita Sharma, Jennifer E Van Eyk, David A Kass, Virginia S Hahn","doi":"10.1161/JAHA.124.038945","DOIUrl":"10.1161/JAHA.124.038945","url":null,"abstract":"<p><strong>Background: </strong>Heart failure with preserved ejection fraction (HFpEF) constitutes more than half of all HF but has few effective therapies. Recent human myocardial transcriptomics and metabolomics have identified major differences between HFpEF and controls. How this translates at the protein level is unknown.</p><p><strong>Methods and results: </strong>Myocardial tissue from patients with HFpEF and nonfailing donor controls was analyzed by data-dependent acquisition (n=10 HFpEF, n=10 controls) and data-independent acquisition (n=44 HFpEF, n=5 controls) mass spectrometry-based proteomics. Differential protein expression analysis, pathway overrepresentation, weighted coexpression network analysis, and machine learning were integrated with clinical characteristics and previously reported transcriptomics. Principal component analysis (data-dependent acquisition-mass spectrometry) found HFpEF separated into 2 subgroups: one similar to controls and the other disparate. Downregulated proteins in HFpEF versus controls were enriched in mitochondrial transport/organization, translation, and metabolism including oxidative phosphorylation. Proteins upregulated in HFpEF were related to immune activation, reactive oxygen species, and inflammatory response. Ingenuity pathway analysis predicted downregulation of protein translation, mitochondrial function, and glucose and fat metabolism in HFpEF. Expression of oxidative phosphorylation and metabolism genes (higher) versus proteins (lower) was discordant in HFpEF versus controls. Data-independent acquisition-mass spectrometry proteomics also yielded 2 HFpEF subgroups; the one most different from controls had a higher proportion of patients with severe obesity and exhibited lower proteins related to fuel metabolism, oxidative phosphorylation, and protein translation. Three modules of correlated proteins in HFpEF that correlated with left ventricular hypertrophy and right ventricular load related to (1) proteasome; (2) fuel metabolism; and (3) protein translation, oxidative phosphorylation, and sarcomere organization.</p><p><strong>Conclusions: </strong>Integrative proteomics, transcriptomics, and pathway analysis supports a defect in both metabolism and translation in HFpEF. Patients with HFpEF with more distinct proteomic signatures from control more often had severe obesity, supporting therapeutic efforts targeting metabolism and translation, particularly in this subgroup.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e038945"},"PeriodicalIF":5.0,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143626915","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":"Exploration of Conserved Human Adipose Subpopulations Using Targeted Single-Nuclei RNA Sequencing Data Sets.","authors":"Christian M Potts, Xuehui Yang, Matthew D Lynes, Kimberly Malka, Lucy Liaw","doi":"10.1161/JAHA.124.038465","DOIUrl":"10.1161/JAHA.124.038465","url":null,"abstract":"<p><strong>Background: </strong>Smooth-muscle cells and pericytes are mural cells. Pericytes can differentiate into myofibroblasts, chondrocytes, vascular smooth-muscle cells, and adipocytes, marking them as a distinct progenitor population. Our goal was to molecularly define the progenitor cell populations in human adipose tissues and test the adipogenic potential of human mural cells.</p><p><strong>Methods: </strong>We used informatic analysis of single-cell RNA sequencing data from human tissues to identify and define pericytes and adipose progenitor cells found in human adipose tissues, including perivascular, brown, and white adipose tissues.</p><p><strong>Results: </strong>We established tissue-specific patterns of gene expression in pericytes and other putative human adipocyte progenitor cells. <i>PPARG</i>-expressing pericytes were present in multiple human adipose depots with consistent expression of <i>COL25A1</i>, <i>MYO1B</i>, and <i>POSTN</i>. We also found evidence of tissue-specific pericyte markers. Although there is some conservation between human and mouse adipose tissues, human pericyte populations have unique, depot-specific gene expression signatures. Immunofluorescence staining of human adipose tissue revealed the presence of pericytes both distant from and adjacent to vasculature in human adipose tissue. Additionally, we demonstrated the potential of human brain pericytes and aortic vascular smooth-muscle cells to differentiate into adipocytes in vitro on the basis of intracellular lipid accumulation and expression of adipocyte markers.</p><p><strong>Conclusions: </strong>Human adipose cell populations are distinct from mice, and the pericyte subpopulation in human adipose tissues are present across adipose depots. Given that vascular mural cells, including pericytes and smooth-muscle cells, can undergo adipogenesis, we postulate that they are a novel source of adipocytes in the vascular microenvironment.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":"14 6","pages":"e038465"},"PeriodicalIF":5.0,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143652008","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":"Years of Potential Life Lost for Children and Adults With Congenital Heart Defects: United States, 2007 to 2017.","authors":"Wendy N Nembhard, Suman Maity, Emine Bircan, Maria D Politis, Elijah H Bolin, Jun Ying","doi":"10.1161/JAHA.124.037164","DOIUrl":"10.1161/JAHA.124.037164","url":null,"abstract":"<p><strong>Background: </strong>Although most children with congenital heart defects (CHDs) live into adulthood, many have increased mortality risk across the lifespan. Little is known about years lost due to premature CHD-related deaths. We estimated the years of potential life lost (YPLL) among individuals with CHDs in the United States.</p><p><strong>Methods: </strong>We used 2007 to 2017 death records from the US National Center for Health Statistics to identify decedents with a CHD listed as the underlying or contributing cause of death. We calculated the average percent change in YPLL and the total, mean, crude, and age-standardized YPLL overall, by sex, race and ethnicity, and age group.</p><p><strong>Results: </strong>Of 28.35 million deaths, 42 158 were CHD-related. The premature deaths attributed to CHD for individuals younger than 65 years was almost 2.1 million years; of those 169 756 and 124 067 years were lost prematurely for children and adolescents, respectively. Men and women with CHDs had 1.13 million and 941 115 years lost prematurely, respectively. Non-Hispanic Black individuals and men had the highest age-standardized YPLL (per 100 000) (95.5 [95% CI, 93.2-97.7] and 74.1 [95% CI, 73.0-75.1]). The overall mean YPLL was 70 years (per 100 000) and non-Hispanic Black men and women had the highest mean YPLL. During 2007 to 2017, the YPLL average percent change declined by 17.8% overall, but the YPLL for non-Hispanic Black individuals aged 1 to 4 years (-31.6%) and 35 to 49 years (-24.3%) had the greatest decline.</p><p><strong>Conclusions: </strong>Children with CHDs experience significant premature deaths. Non-Hispanic Black and male individuals experienced the highest burden of premature deaths associated with CHDs. Further research is needed to elucidate these disparities.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e037164"},"PeriodicalIF":5.0,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143626692","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}