Tiange Liu, Jakob Stokholm, Mingyu Zhang, Rebecca Vinding, Søren J Sørensen, Ni Zhao, Noel T Mueller
{"title":"Infant Gut Microbiota and Childhood Blood Pressure: Prospective Associations and the Modifying Role of Breastfeeding.","authors":"Tiange Liu, Jakob Stokholm, Mingyu Zhang, Rebecca Vinding, Søren J Sørensen, Ni Zhao, Noel T Mueller","doi":"10.1161/JAHA.124.037447","DOIUrl":"https://doi.org/10.1161/JAHA.124.037447","url":null,"abstract":"<p><strong>Background: </strong>Germ-free mice experiments indicate that human gut microbiota influence blood pressure (BP), but no studies have prospectively examined if infant gut microbiota affects their future childhood BP. We aim to investigate prospective associations of infant gut microbiota diversity and composition with childhood BP, examining effect measure modification by breastfeeding and mediation by a child's body mass index.</p><p><strong>Methods and results: </strong>In the Copenhagen Prospective Studies on Asthma in Childhood 2010 cohort, we measured infant gut microbiota (16S rRNA V4) at 1 week, 1 month, and 1 year and child BP at 3 and 6 years. We assessed α diversity-BP, β diversity-BP, and microbe abundances-BP associations using linear regression, permutational multivariate analysis of variance, and beta-binomial count regression, respectively. Data from 526 children showed that α diversity and several <i>Bifidobacterium</i> spp. had protective associations with BP but only in children breastfed for ≥6 months. For instance, a 1-unit increment in 1 month Shannon index was associated with 1.86 mm Hg (95% CI, 0.66-3.05) lower 6-year systolic BP in children breastfed ≥6 months but a 0.73 (95% CI, -1.00 to 2.45) higher 6-year systolic BP in those breastfed <6 months (<i>P</i>-interaction=0.02). Greater abundance of 2 <i>Bifidobacterium</i> microbes at 1 week was negatively associated with 6-year systolic BP when breastfeeding ≥6 months (<i>P</i>-interaction<0.1). Further, abundance of 8 microbes at 1week or 1 month was linked to 3-year or 6-year BP (false discovery rate <i>P</i><0.05), with 5 of them independent of a child's body mass index. Lastly, 1-week unweighted UniFrac distance and 1-year weighted UniFrac distance were associated with BP after adjustment (<i>P</i><0.05).</p><p><strong>Conclusions: </strong>Gut microbiota features at 1 week and 1 month of life were associated with BP at 6 years. Breastfeeding duration modified key associations including those for α diversity and <i>Bifidobacteria</i>.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e037447"},"PeriodicalIF":5.0,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143517519","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}
Zeel Thakkar, Yan Wu, Mohammed Khan, Xinran Qi, George A Hung, Nicholas Kikuta, Armaan Jamal, Malathi Srinivasan, Robert J Huang, Karina Kim, Gloria Kim, Latha Palaniappan, Adrian M Bacong
{"title":"Evaluating the Reliability and Robustness of Racial and Ethnic Health Disparities in Cardiometabolic Disease in NHANES, NHIS, and BRFSS (2015-2021).","authors":"Zeel Thakkar, Yan Wu, Mohammed Khan, Xinran Qi, George A Hung, Nicholas Kikuta, Armaan Jamal, Malathi Srinivasan, Robert J Huang, Karina Kim, Gloria Kim, Latha Palaniappan, Adrian M Bacong","doi":"10.1161/JAHA.124.040029","DOIUrl":"https://doi.org/10.1161/JAHA.124.040029","url":null,"abstract":"<p><strong>Background: </strong>The United States uses the National Health Interview Survey (NHIS), Behavioral Risk Factor Surveillance System (BRFSS), and National Health and Nutrition Examination Survey to monitor disease trends and inform clinical care/prevention research. These 3 surveys share similar national estimates. However, the consistency of each survey's estimates by race has not been examined. Here, we compare prevalence estimates and disparities in cardiometabolic diseases across 5 aggregated racial and ethnic groups.</p><p><strong>Methods: </strong>We examined the age- and fully-adjusted prevalence of cardiovascular disease and diabetes among non-Hispanic White, non-Hispanic Black, Hispanic, non-Hispanic Asian, and \"Other\" race respondents aged 30 years or older. Cardiovascular disease included self-reported physician diagnosis of heart attack, stroke, and coronary heart disease.</p><p><strong>Results: </strong>Although overall national population estimates were similar, there was heterogeneity in estimates by survey. For heart attack and diabetes, each racial group had a higher prevalence in BRFSS than NHIS (eg, Heart Attack: Hispanic BRFSS: 3.4% [95% CI, 3.2-3.6], NHIS: 2.0% [95% CI, 1.8, 2.2]; non-Hispanic Black BRFSS: 3.8% [95% CI, 3.6, 3.9]; NHIS: 3.0% [95% CI, 2.7, 3.2]). Non-Hispanic Asian people had the lowest general cardiovascular disease prevalence across all 3 data sets (NHIS: 5.9%, National Health and Nutrition Examination Survey: 5.3%, BRFSS: 6.9%), while Other/multi-racial respondents had the highest prevalence (NHIS: 9.9%, National Health and Nutrition Examination Survey: 13.1%, BRFSS: 10.7%). However, the magnitude of these differences across data sets was small.</p><p><strong>Conclusions: </strong>Prevalence estimates for heart attack and diabetes were heterogeneous by race across surveys. These results highlight the importance of improving the representation of racially minoritized groups within national surveys to produce more precise estimates.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e040029"},"PeriodicalIF":5.0,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143505901","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}
Ke-Wei Chen, Ju-Hsin Chang, Agata Sularz, Gerardo V Lo Russo, Ghasaq Saleh, Shih-Sheng Chang, Chia-Hao Liu, Mohamad Alkhouli
{"title":"Immediate Reduction in Left Ventricular Contractility After Mitral Transcatheter Edge-to-Edge Repair Is Associated With Lower Rates of Heart Failure Hospitalizations.","authors":"Ke-Wei Chen, Ju-Hsin Chang, Agata Sularz, Gerardo V Lo Russo, Ghasaq Saleh, Shih-Sheng Chang, Chia-Hao Liu, Mohamad Alkhouli","doi":"10.1161/JAHA.124.037545","DOIUrl":"https://doi.org/10.1161/JAHA.124.037545","url":null,"abstract":"","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e037545"},"PeriodicalIF":5.0,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143506018","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}
Yao Qi, Han Jiang, Yu Lun, Qingwei Gang, Shikai Shen, Han Zhang, Mingyu Liu, Yixian Wang, Jian Zhang
{"title":"Protein Drug Targets for Abdominal Aortic Aneurysm and Proteomic Associations Between Modifiable Risk Factors and Abdominal Aortic Aneurysm.","authors":"Yao Qi, Han Jiang, Yu Lun, Qingwei Gang, Shikai Shen, Han Zhang, Mingyu Liu, Yixian Wang, Jian Zhang","doi":"10.1161/JAHA.124.037802","DOIUrl":"https://doi.org/10.1161/JAHA.124.037802","url":null,"abstract":"<p><strong>Background: </strong>Abdominal aortic aneurysm (AAA) is a severe aortic disease for which no pharmacological interventions have yet been developed. This investigation focused on identifying protein-based therapeutic targets and assessing how proteins mediate the interplay between modifiable risk factors and AAA development.</p><p><strong>Methods: </strong>Causal inferences between plasma proteins and AAA were drawn using 2-sample Mendelian randomization, followed by comprehensive sensitivity testing, colocalization, and replication efforts. Further analyses included database interrogation, single-cell RNA data analysis, enrichment analysis, protein-protein interaction networks, and immunohistochemistry to map the tissue-specific expression of these proteins, their expression within AAA tissues, and their biological roles. Mediation Mendelian randomization was employed to evaluate the mediating effects of AAA-related proteins on the associations between AAA and 3 risk factors: hypertension, smoking, and obesity.</p><p><strong>Results: </strong>A total of 43 proteins were identified as having causal links to AAA. Colocalization analysis pinpointed 13 proteins with strong evidence of colocalization with AAA. Of these, the causal involvement of 10 proteins was substantiated by external validation data. Consistent evidence for PCSK9 (proprotein convertase subtilisin/kexin type 9), IL6R (interleukin-6R), ECM1 (extracellular matrix protein 1), and ANGPTL4 (angiopoietin-related protein 4) was further validated through tissue immunohistochemistry and blood data. Moreover, Mendelian randomization analysis identified 10 proteins as mediators of the influence of hypertension, smoking, and obesity on AAA development.</p><p><strong>Conclusions: </strong>This analysis identifies 4 proteins (PCSK9, IL6R, ECM1, and ANGPTL4) as high-priority therapeutic targets for AAA and emphasizes the intermediary role of plasma proteins in linking hypertension, smoking, obesity, and AAA. Further investigations are needed to clarify the specific roles of these proteins in AAA pathology.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e037802"},"PeriodicalIF":5.0,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143506029","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}
Yang Yu, Baojian Xue, Lei Tong, Alexander G Bassuk, Alan K Johnson, Shun-Guang Wei
{"title":"RORγt Mediates Angiotensin II-Induced Pressor Responses, Microglia Activation, and Neuroinflammation by Disrupting the Blood-Brain Barrier in Rats.","authors":"Yang Yu, Baojian Xue, Lei Tong, Alexander G Bassuk, Alan K Johnson, Shun-Guang Wei","doi":"10.1161/JAHA.124.040461","DOIUrl":"https://doi.org/10.1161/JAHA.124.040461","url":null,"abstract":"<p><strong>Background: </strong>The RORγt (nuclear receptor retinoid-related orphan receptor γt) has been identified as a master transcription factor critical for the differentiation of T helper 17 cells, the primary source of IL-17A (interleukin-17A). We previously demonstrated that IL-17A promotes neuroinflammation and sympathetic excitation, contributing to cardiac dysfunction in heart failure and angiotensin II (ANG II)-induced hypertension. The present study sought to determine whether inhibiting RORγt, thereby reducing IL-17A production, could attenuate microglial activation, neuroinflammation, and sympathetic excitation by preserving the integrity of the blood-brain barrier (BBB) in ANG II-induced hypertensive rats.</p><p><strong>Methods: </strong>Rats underwent a 2-week subcutaneous infusion of ANG II, with concurrent daily subcutaneous administration of the RORγt inhibitor digoxin or vehicle.</p><p><strong>Results: </strong>Compared with controls, ANG II-infused rats exhibited elevated IL-17A levels in both the periphery and brain, along with increased blood pressure and sympathetic tone-effects that were significantly attenuated by inhibiting RORγt with digoxin. ANG II-infused rats also displayed heightened BBB permeability, decreased expression of the BBB regulator Mfsd2a (major facilitator superfamily domain-containing protein 2a), increased caveolar transcytosis, and degradation of tight junction proteins in BBB endothelial cells within the hypothalamic paraventricular nucleus, a key autonomic regulatory brain center, all of which were alleviated by digoxin. Additionally, ANG II-infused rats showed marked microglial activation and elevated expression of proinflammatory cytokines within the paraventricular nucleus, both of which were mitigated by digoxin.</p><p><strong>Conclusions: </strong>These findings suggest that RORγt inhibition reduces neuroinflammation and sympathetic activation to ameliorate ANG II-induced hypertension, likely by mitigating IL-17A-induced BBB disruption and microglial activation in the paraventricular nucleus.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e040461"},"PeriodicalIF":5.0,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143506068","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}
Abulikemu Amuti, You Ran Li, He Yuan, Shuo Feng, Guan Poh Tay, Si Yi Tang, Xin Rui Wu, Le Yuan Tao, Lin Lu, Rui Yan Zhang, Chen Die Yang, Xiao Qun Wang
{"title":"Suboptimal Control of Small Dense Low-Density Lipoprotein Cholesterol Is Associated With Coronary Plaque Progression: An Intravascular Ultrasound Study.","authors":"Abulikemu Amuti, You Ran Li, He Yuan, Shuo Feng, Guan Poh Tay, Si Yi Tang, Xin Rui Wu, Le Yuan Tao, Lin Lu, Rui Yan Zhang, Chen Die Yang, Xiao Qun Wang","doi":"10.1161/JAHA.124.038580","DOIUrl":"https://doi.org/10.1161/JAHA.124.038580","url":null,"abstract":"<p><strong>Background: </strong>Plaque progression (PP) is critical between subclinical atherosclerosis and plaque rupture. Small dense low-density lipoprotein cholesterol (sdLDL-C) is considered as the most atherogenic lipoprotein. This study aims to investigate the relationship between sdLDL-C level and PP in patients with stable coronary artery disease.</p><p><strong>Methods: </strong>We conducted a retrospective analysis of 146 lesions in 86 patients by repeat intravascular ultrasound examinations from January 2020 to May 2023. PP was determined by increases in percent atheroma volume, defined as the atheroma volume in proportion to the volume occupied by the entire vascular wall, ≥5% during follow-up. Time-averaged values were calculated for all cardiometabolic parameters including sdLDL-C. Multivariate logistic regression analysis was performed to interrogate the association between time-averaged sdLDL-C and PP.</p><p><strong>Results: </strong>During a median follow-up of 12.6 months, PP was found in 65 lesions (44.5%), and mean changes in percent atheroma volume were 4.1%±10.2%. A positive correlation was observed between time-averaged sdLDL-C and changes in total atheroma volume (Pearson <i>r</i>=0.29, <i>P</i>=0.006), especially in diabetic patients (Pearson <i>r</i>=0.58, <i>P</i><0.001). After multivariate adjustment, every 0.1-mmol/L increase in time-averaged sdLDL-C conferred a 1.2-fold increased risk of PP.</p><p><strong>Conclusions: </strong>Our findings suggest that sdLDL-C is an independent risk factor of PP in patients with coronary artery disease. Intensive control of sdLDL-C along with other risk factors should be considered to mitigate PP and improve cardiovascular outcomes.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e038580"},"PeriodicalIF":5.0,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143505228","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}
Graham Nichol, Neal W Dickert, Jacob E Moeller, Judith S Hochman, Carie Facemire, Karen N Adams, Gregg W Stone, David A Morrow, Holger Thiele, Timothy D Henry, Chuck Simonton, Sunil V Rao, William O'Neill, Ian Gilchrist, Ryan Egelund, Alastair Proudfoot, Ron Waksman, Nick E J West, John S Sapirstein, Mitchell W Krucoff
{"title":"A Framework for Exception From Informed Consent in Trials Enrolling Patients With ST-Segment-Elevation Myocardial Infarction and Cardiogenic Shock.","authors":"Graham Nichol, Neal W Dickert, Jacob E Moeller, Judith S Hochman, Carie Facemire, Karen N Adams, Gregg W Stone, David A Morrow, Holger Thiele, Timothy D Henry, Chuck Simonton, Sunil V Rao, William O'Neill, Ian Gilchrist, Ryan Egelund, Alastair Proudfoot, Ron Waksman, Nick E J West, John S Sapirstein, Mitchell W Krucoff","doi":"10.1161/JAHA.124.037946","DOIUrl":"https://doi.org/10.1161/JAHA.124.037946","url":null,"abstract":"<p><p>Cardiogenic shock (CS) is critical end-organ hypoperfusion attributable to reduced cardiac output. Acute ST-segment-elevation myocardial infarction with CS (AMI-CS) has high mortality. Clinical research is challenging in such patients as they often cannot provide consent, lack available legal representatives, and require initiation of therapy. Multiple trials have enrolled patients with AMI-CS outside the United States under deferred consent. Trials in the United States have enrolled patients with out-of-hospital cardiac arrest under exception from informed consent (EFIC). However, AMI-CS has a longer therapeutic window to initiate treatment than out-of-hospital cardiac arrest, and more patients or their representatives can engage in treatment decisions. We provide a rationale for how a trial enrolling patients with AMI-CS could qualify for conduct using EFIC by meeting each criterion specified in US human subject regulations. AMI-CS is a life-threatening situation, available treatments are unsatisfactory, and collection of valid evidence is necessary. Obtaining informed consent is often not feasible, and trial participation could benefit subjects. Only enrolling consented patients is impracticable and could reduce the study's generalizability. We propose a therapeutic window of 30 minutes within the study intervention must be initiated, with consent sought within 15 minutes, respecting any refusal or objection to enrollment, and otherwise enrollment under EFIC. A trial could enroll patients with AMI-CS under EFIC and can involve both patients and their representatives. Successful use of EFIC in trials of other interventions in patients with CS or enrolling patients with other acute cardiovascular conditions could increase the available evidence base to improve care.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e037946"},"PeriodicalIF":5.0,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143505226","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}
Qian Yang, Man Li, Pengcheng Chen, Naixin Dou, Mei Liu, Peng Lu, Chunxiao Yu
{"title":"Systematic Evaluation of the Impact of a Wide Range of Dietary Habits on Myocardial Infarction: A Two-Sample Mendelian Randomization Analysis.","authors":"Qian Yang, Man Li, Pengcheng Chen, Naixin Dou, Mei Liu, Peng Lu, Chunxiao Yu","doi":"10.1161/JAHA.124.035936","DOIUrl":"https://doi.org/10.1161/JAHA.124.035936","url":null,"abstract":"<p><strong>Background: </strong>Myocardial infarction is a cardiovascular disease that significantly contributes to global morbidity and disability. Given the significant role of diet in the pathogenesis and prevention of cardiovascular diseases, this study rigorously investigates the causal relationship between dietary habits and myocardial infarction.</p><p><strong>Methods and results: </strong>This study used large-scale genome-wide association studies with pooled UK Biobank data to explore associations between 9 dietary categories (83 types) and myocardial infarction. A 2-sample Mendelian randomization approach was applied to assess these associations, while multivariate Mendelian randomization and mediation analyses investigated the role of lipids in mediating the effects of diet on myocardial infarction. Univariate Mendelian analyses revealed genetic associations among 9 categories of dietary habits (83 types) and myocardial infarction. Notably, robust evidence indicates the \"tablespoons of cooked vegetables per day\" as the most significant risk factor for myocardial infarction development. \"Coffee consumption(cups per day)\" and \"frequency of adding salt to food\" were also identified as supplementary risk factors. In contrast, \"overall alcohol intake\" showed a protective effect, potentially by increasing high-density lipoprotein cholesterol (4.48% mediation) and reducing triglycerides (6.24% mediation). Cereal category, particularly \"cereal consumption (bowls per week)\" was associated with reduced myocardial infarction risk, contributing by raising high-density lipoprotein cholesterol (3.69% mediation) and lowering total cholesterol (8.33% mediation). Additionally, \"overall cheese consumption\" was also protective against myocardial infarction.</p><p><strong>Conclusions: </strong>Our findings elucidate the influence of dietary habits on myocardial infarction, showing underlying genetic mechanisms and emphasizing the regulatory role of lipids as an intermediate.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e035936"},"PeriodicalIF":5.0,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143505891","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}
Ariane Martinez Oeckel, Bjoern Misselwitz, Christian Foerch
{"title":"Incidence But Not Severity of Intracerebral Hemorrhage Shows a Strong Pattern of Seasonal Variation.","authors":"Ariane Martinez Oeckel, Bjoern Misselwitz, Christian Foerch","doi":"10.1161/JAHA.124.034077","DOIUrl":"https://doi.org/10.1161/JAHA.124.034077","url":null,"abstract":"<p><strong>Background: </strong>A strong risk factor for intracerebral hemorrhage (ICH) is elevated arterial blood pressure, which is known to vary by season, with highest values in winter months. The objective was to assess seasonal trends of ICH incidence, clinical severity, and case fatality according to demographic and clinical characteristics.</p><p><strong>Methods: </strong>This study was conducted on adult patients hospitalized for ICH between 2003 and 2022. Cases were identified from a stroke inpatient quality assurance registry covering the entire Federal State of Hesse, Germany. Population data were derived from the Hessian Bureau of Statistics. Incidence rates (IRs) per 100 000 person-years of ICH, recorded with 4-digit <i>International Statistical Classification of Diseases, Tenth Revision, German Modification</i> (<i>ICD-10-GM</i>) I61.x codes, were estimated by season, calendar month, and bleeding location. Seasonal variations and subgroup analyses were tested using Poisson distribution and the Wald test.</p><p><strong>Results: </strong>A total of 33 444 patients were included (mean age, 72.4±13.6 years, 52% men). ICH IR correlated with the season of occurrence, demonstrating a peak in winter (IR winter, 34.6 [95% CI, 33.9-35.4], IR summer, 29.4 [95% CI, 28.7-30.1]; <i>P</i><0.01). Seasonal variation was equally present in men and women but was more pronounced in older compared with younger patients (peak at age 60-90 years; <i>P</i><0.01). IR showed seasonal variation both for cortical and subcortical bleeding locations (<i>P</i><0.01). Clinical severity and case fatality did not vary between seasons (mean, 24.3±0.8%).</p><p><strong>Conclusions: </strong>This large cohort study demonstrates a seasonal incidence peak of ICH in winter. Whether ICH can be prevented by better control of arterial blood pressure in seasons with expected incidence peaks will require further studies.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e034077"},"PeriodicalIF":5.0,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143506020","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":"Role of Cardiovascular Health in the Bidirectional Progression Trajectories Between Cardiovascular Disease, Type 2 Diabetes, and Cancer.","authors":"Yu Peng, Peng Wang, Fubin Liu, Xixuan Wang, Changyu Si, Jianxiao Gong, Huijun Zhou, Fangfang Song","doi":"10.1161/JAHA.124.038180","DOIUrl":"https://doi.org/10.1161/JAHA.124.038180","url":null,"abstract":"<p><strong>Background: </strong>There existed bidirectional associations of cardiovascular disease (CVD) and type 2 diabetes (T2D) with cancer, partly attributed to their shared risk factors. We aimed to explore the role of cardiovascular health (CVH) in bidirectional transitions between CVD, T2D, and cancer.</p><p><strong>Methods: </strong>Based on the UK Biobank, we used 2 subcohorts: a disease-free cohort of 277 997 individuals without cancer, CVD, and T2D; and a disease survivor cohort consisting of 61 971 cases with cancer, CVD, and T2D at baseline. The CVH was assessed on the basis of Life's Essential 8 score. We conducted the multistate model and Cox proportional hazards model to explore the role of CVH in bidirectional transitions between CVD, T2D, and cancer in disease-free and disease survivor cohorts, respectively.</p><p><strong>Results: </strong>High CVH was significantly associated with a lower transition risk from CVD to cancer (hazard ratio, 0.822 [95% CI, 0.693-0.975]). On the other hand, increased CVH was related to reduced risks of progression from cancer to CVD and T2D (both <i>P</i> for trend<0.001), particularly in the high CVH group. For disease survivor cohorts, per 10-point increase in CVH was associated with >10% lower cancer risk in CVD and T2D cases, and a 16% and 42% reduction in the risk of incident CVD and T2D among cancer survivors, respectively.</p><p><strong>Conclusions: </strong>High CVH was related to a decreased risk of bidirectional transitions between CVD, T2D, and cancer. This highlighted the significance of maintaining high CVH throughout the life span for the primary prevention of CVD, T2D, and cancer.</p>","PeriodicalId":54370,"journal":{"name":"Journal of the American Heart Association","volume":" ","pages":"e038180"},"PeriodicalIF":5.0,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143506059","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}