Air Pollution in Cardio-Oncology and Unraveling the Environmental Nexus: JACC: CardioOncology State-of-the-Art Review.

Although recent advancements in cancer therapies have extended the lifespan of patients with cancer, they have also introduced new challenges, including chronic health issues such as cardiovascular disease arising from pre-existing risk factors or cancer therapies. Consequently, cardiovascular disease has become a leading cause of non-cancer-related death among cancer patients, driving the rapid evolution of the cardio-oncology field. Environmental factors, particularly air pollution, significantly contribute to deaths associated with cardiovascular disease and specific cancers, such as lung cancer. Despite these statistics, the health impact of air pollution in the context of cardio-oncology has been largely overlooked in patient care and research. Notably, the impact of air pollution varies widely across geographic areas and among individuals, leading to diverse exposure consequences. This review aims to consolidate epidemiologic and preclinical evidence linking air pollution to cardio-oncology while also exploring associated health disparities and environmental justice issues.

Elevated myocardial extracellular volume fraction is associated with the development of conduction pathway defects following transcatheter aortic valve replacement.

BACKGROUND: Transcatheter aortic valve replacement (TAVR) has become an established method of aortic stenosis treatment but suffers from the risk of heart block and pacemaker requirement. Risk stratification for patients who may develop heart block remains imperfect. Simultaneously, myocardial fibrosis as measured by cardiac magnetic resonance imaging (CMR) has been demonstrated as a prognostic indicator of ventricular recovery and mortality following TAVR. However, the association of CMR-based measures of myocardial fibrosis with post-TAVR conduction disturbances has not yet been explored. AIMS: We evaluated whether myocardial fibrosis, as measured by late gadolinium enhancement and extracellular volume (ECV) from CMR would be associated with new conduction abnormalities following TAVR. METHODS: One hundred seventy patients who underwent CMR within 2 months before TAVR were retrospectively reviewed. Septal late gadolinium enhancement (LGE) and ECV measurements were made as surrogates for replacement and interstitial fibrosis respectively. New conduction abnormalities were defined by the presence of transient or permanent atrioventricular block, new bundle branch blocks, and need for permanent pacemaker. Association of myocardial fibrosis and new conduction derangements were tested using receiver operator curve (ROC) and regression analysis in patients with and without pre-existing conduction issues. RESULTS: Forty-six (27.1%) patients developed post-TAVR conduction deficits. ECV was significantly higher among patients who experienced new conduction defects (26.2 ± 3.45% vs. 24.7% ± 4.15%, p value: 0.020). A greater fraction of patients that had new conduction defects had an elevated ECV of ≥26% (54.3% vs. 36.3%, p value: 0.026). ECV ≥ 26% was independently associated with the development of new conduction defects (odds ratio [OR]: 2.364, p value: 0.030). ROC analysis revealed a significant association of ECV with new conduction defects with an area under the receiver operating characteristic curve (AUC) of 0.632 (95% confidence interval: 0.555-0.705, p value: 0.005). The combination of prior right bundle branch block (RBBB) and ECV revealed a greater AUC of 0.779 (0.709-0.839, p value: <0.001) than RBBB alone (Delong p value: 0.049). No association of LGE/ECV with new conduction defects was observed among patients with pre-existing conduction disease. Among patients without baseline conduction disease, ECV was independently associated with the development of new conduction deficits (OR: 3.685, p value: 0.008). CONCLUSION: The present study explored the association of myocardial fibrosis, as measured by LGE and ECV with conduction deficits post-TAVR. Our results demonstrate an association of ECV, and thereby interstitial myocardial fibrosis, with new conduction derangement post-TAVR and introduce ECV as a potentially new risk stratification tool to identify patients at higher risk for needing post-TAVR surveillance and/or permanent pacemaker.

Historical neighborhood redlining and bystander CPR disparities in out-of-hospital cardiac arrest.

BACKGROUND: Out-of-hospital cardiac arrest (OHCA) is associated with low survival rates. Bystander cardiopulmonary resuscitation (CPR) is essential for improving outcomes, but its utilization remains limited, particularly among racial and ethnic minorities. Historical redlining, a practice that classified neighborhoods for mortgage risk in 1930s, may have lasting implications for social and health outcomes. This study sought to investigate the influence of redlining on the provision of bystander CPR during witnessed OHCA. METHODS: We conducted an analysis using data from the comprehensive Cardiac Arrest Registry to Enhance Survival (CARES), encompassing 736,066 non-traumatic OHCA cases across the United States. The Home Owners' Loan Corporation (HOLC) map shapefiles were utilized to categorize census tracts of arrests into four grades (A signifying "best", B "still desirable", C "declining", and D "hazardous"). Multivariable hierarchical logistic regression models were employed to predict the likelihood of CPR provision, adjusting for various factors including age, sex, race/ethnicity, arrest location, calendar year, and state of occurrence. Additionally, we accounted for the percentage of Black residents and residents below poverty levels at the census tract level. RESULTS: Among the 43,186 witnessed cases of OHCA in graded HOLC census tracts, 37.2% received bystander CPR. The rates of bystander CPR exhibited a gradual decline across HOLC grades, ranging from 41.8% in HOLC grade A to 35.8% in HOLC grade D. In fully adjusted model, we observed significantly lower odds of receiving bystander CPR in HOLC grades C (OR 0.89, 95% CI 0.81-0.98, p = 0.016) and D (OR 0.86, 95% CI 0.78-0.95, p = 0.002) compared to HOLC grade A. CONCLUSION: Redlining, a historical segregation practice, is associated with reduced contemporary rates of bystander CPR during OHCA. Targeted CPR training in redlined neighborhoods may be imperative to enhance survival outcomes.

Air Pollution and Adverse Cardiovascular Events After Coronary Artery Bypass Grafting: A 10-Year Nationwide Study.

Background: Increased particulate matter <2.5 µm (PM2.5) air pollution is associated with adverse cardiovascular outcomes. However, its impact on patients with prior coronary artery bypass grafting (CABG) is unknown. Objectives: The purpose of this study was to evaluate the association between major adverse cardiovascular events (MACE) (defined as myocardial infarction, stroke, or cardiovascular death) and air pollution after CABG. Methods: We linked 26,403 U.S. veterans who underwent CABG (2010-2019) nationally with average annual ambient PM2.5 estimates using residential address. Over a 5-year median follow-up period, we identified MACE and fit a multivariable Cox proportional hazard model to determine the risk of MACE as per PM2.5 exposure. We also estimated the absolute potential reduction in PM2.5 attributable MACE simulating a hypothetical PM2.5 lowered to the revised World Health Organization standard of 5 µg/m3. Results: The observed median PM2.5 exposure was 7.9 µg/m3 (IQR: 7.0-8.9 µg/m3; 95% of patients were exposed to PM2.5 above 5 µg/m3). Increased PM2.5 exposure was associated with a higher 10-year MACE rate (first tertile 38% vs third tertile 45%; P < 0.001). Adjusting for demographic, racial, and clinical characteristics, a 10 µg/m3 increase in PM2.5 resulted in 27% relative risk for MACE (HR: 1.27, 95% CI: 1.10-1.46; P < 0.001). Currently, 10% of total MACE is attributable to PM2.5 exposure. Reducing maximum PM2.5 to 5 µg/m3 could result in a 7% absolute reduction in 10-year MACE rates. Conclusions: In this large nationwide CABG cohort, ambient PM2.5 air pollution was strongly associated with adverse 10-year cardiovascular outcomes. Reducing levels to World Health Organization-recommended standards would result in a substantial risk reduction at the population level.

Environmental Pollution and Cardiovascular Disease: Part 2 of 2: Soil, Water, and Other Forms of Pollution.

With a growing body of evidence that now links environmental pollution to adverse cardiovascular disease (CVD) outcomes, pollution has emerged as an important risk factor for CVD. There is thus an urgent need to better understand the role of pollution in CVD, key pathophysiological mechanisms, and to raise awareness among health care providers, the scientific community, the general population, and regulatory authorities about the CV impact of pollution and strategies to reduce it. This article is part 2 of a 2-part state-of-the-art review on the topic of pollution and CVD-herein we discuss major environmental pollutants and their effects on CVD, highlighting pathophysiological mechanisms, and strategies to reduce CVD risk.

Environmental Pollution and Cardiovascular Disease: Part 1 of 2: Air Pollution.

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide. Over the past 50 years, there has been a substantial decline in the incidence of CVD and related mortality in high-income countries, largely due to the mitigation of modifiable risk factors such as smoking, hypertension, and diabetes. However, a significant burden of CVD remains in low- to middle-income countries, despite their lower prevalence of traditional risk factors; other environmental factors, particularly pollution, play a significant role in this attributable risk. Mounting evidence underscores a strong association between pollution and adverse health effects, including CVD. This article is part 1 of a 2-part state-of-the-art review and discusses air pollution and its adverse effects on CVD, highlighting pathophysiological mechanisms and methods to reduce air pollution and exposure to these pollutants.

Deep Learning-Based Assessment of Built Environment From Satellite Images and Cardiometabolic Disease Prevalence.

Importance: Built environment plays an important role in development of cardiovascular disease. Large scale, pragmatic evaluation of built environment has been limited owing to scarce data and inconsistent data quality. Objective: To investigate the association between image-based built environment and the prevalence of cardiometabolic disease in urban cities. Design, Setting, and Participants: This cross-sectional study used features extracted from Google satellite images (GSI) to measure the built environment and link them with prevalence of cardiometabolic disease. Convolutional neural networks, light gradient-boosting machines, and activation maps were used to assess the association with health outcomes and identify feature associations with coronary heart disease (CHD), stroke, and chronic kidney disease (CKD). The study obtained aerial images from GSI covering census tracts in 7 cities (Cleveland, Ohio; Fremont, California; Kansas City, Missouri; Detroit, Michigan; Bellevue, Washington; Brownsville, Texas; and Denver, Colorado). The study used census tract-level data from the US Centers for Disease Control and Prevention's 500 Cities project. The data were originally collected from the Behavioral Risk Factor Surveillance System that surveyed people 18 years and older across the country. Analyses were conducted from February to December 2022. Exposures: GSI images of built environment and cardiometabolic disease prevalence. Main Outcomes and Measures: Census tract-level estimated prevalence of CHD, stroke, and CKD based on image-based built environment features. Results: The study obtained 31 786 aerial images from GSI covering 789 census tracts. Built environment features extracted from GSI using machine learning were associated with prevalence of CHD (R2 = 0.60), stroke (R2 = 0.65), and CKD (R2 = 0.64). The model performed better at distinguishing differences between cardiometabolic prevalence between cities than within cities (eg, highest within-city R2 = 0.39 vs between-city R2 = 0.64 for CKD). Addition of GSI features both outperformed and improved the model that only included age, sex, race, income, education, and composite indices for social determinants of health (R2 = 0.83 vs R2 = 0.76 for CHD; P <.001). Activation maps from the features revealed certain health-related built environment such as roads, highways, and railroads and recreational facilities such as amusement parks, arenas, and baseball parks. Conclusions and Relevance: In this cross-sectional study, a significant portion of cardiometabolic disease prevalence was associated with GSI-based built environment using convolutional neural networks.

Geographic proximity to cardiovascular clinical trial sites: A National analysis in the United States.

INTRODUCTION: Suboptimal geographical access to cardiovascular clinical trial sites (CV-CTS) may be a cause of inadequate demographic representation in contemporary trials. Thus, we investigate access to CV-CTS in the US. METHODS: We obtained the location of CV-CTS from Clinicaltrials.gov. We calculated the distance in kilometers from each ZIP code to the nearest CV-CTS, stratifying our results based on urban/rural setting, sex and race. RESULTS: We identified a total of 10,506 studies in 4,630 US ZIP codes (10.5 %), of those only 237 (5 %) were rural. The overall median CV-CTS distance was 5.8 km (IQR: 2.7, 15.8). For urban residents, this distance was 4.5 km (IQR: 2.3, 9.2), while for rural residents, it was 24.2 km (IQR: 13.8, 42.2). RESULTS: We revealed important disparities involving geographical proximity to cardiovascular clinical trial sites. Increasing the representation of these populations in clinical trials is paramount to improving the applicability of their findings to real-world settings.

PM2.5-induced cellular senescence drives brown adipose tissue impairment in middle-aged mice.

Airborne fine particulate matter (PM2.5) exposure is closely associated with metabolic disturbance, in which brown adipose tissue (BAT) is one of the main contributing organs. However, knowledge of the phenotype and mechanism of PM2.5 exposure-impaired BAT is quite limited. In the study, male C57BL/6 mice at three different life phases (young, adult, and middle-aged) were simultaneously exposed to concentrated ambient PM2.5 or filtered air for 8 weeks using a whole-body inhalational exposure system. H&E staining and high-resolution respirometry were used to assess the size of adipocytes and mitochondrial function. Transcriptomics was performed to determine the differentially expressed genes in BAT. Quantitative RT-PCR, immunohistochemistry staining, and immunoblots were performed to verify the transcriptomics and explore the mechanism for BAT mitochondrial dysfunction. Firstly, PM2.5 exposure caused altered BAT morphology and mitochondrial dysfunction in middle-aged but not young or adult mice. Furthermore, PM2.5 exposure increased cellular senescence in BAT of middle-aged mice, accompanied by cell cycle arrest, impaired DNA replication, and inhibited AKT signaling pathway. Moreover, PM2.5 exposure disrupted apoptosis and autophagy homeostasis in BAT of middle-aged mice. Therefore, BAT in middle-aged mice was more vulnerable to PM2.5 exposure, and the cellular senescence-initiated apoptosis, autophagy, and mitochondrial dysfunction may be the mechanism of PM2.5 exposure-induced BAT impairment.

Enhancing cardiovascular risk prediction through AI-enabled calcium-omics.

Whole-heart coronary calcium Agatston score is a well-established predictor of major adverse cardiovascular events (MACE), but it does not account for individual calcification features related to the pathophysiology of the disease (e.g., multiple-vessel disease, spread of the disease along the vessel, stable calcifications, numbers of lesions, and density). We used novel, hand-crafted calcification features (calcium-omics); Cox time-to-event modeling; elastic net; and up and down synthetic sampling methods for imbalanced data, to assess MACE risk. We used 2457 CT calcium score (CTCS) images enriched for MACE events from our large no-cost CLARIFY program (ClinicalTrials.gov Identifier: NCT04075162). Among calcium-omics features, numbers of calcifications, LAD mass, and diffusivity (a measure of spatial distribution) were especially important determinants of increased risk, with dense calcification (> 1000HU, stable calcifications) associated with reduced risk Our calcium-omics model with (training/testing, 80/20) gave C-index (80.5%/71.6%) and 2-year AUC (82.4%/74.8%). Although the C-index is notoriously impervious to model improvements, calcium-omics compared favorably to Agatston and gave a significant difference (P < 0.001). The calcium-omics model identified 73.5% of MACE cases in the high-risk group, a 13.2% improvement as compared to Agatston, suggesting that calcium-omics could be used to better identity candidates for intensive follow-up and therapies. The categorical net-reclassification index was NRI = 0.153. Our findings from this exploratory study suggest the utility of calcium-omics in improved risk prediction. These promising results will pave the way for more extensive, multi-institutional studies of calcium-omics.

Trends in tracheal, bronchial and lung cancer attributed to smoking in South America: Global Burden of Disease analysis 1990-2019.

Objective: To investigate the burden of tracheal, bronchus, and lung (TBL) cancer due to tobacco exposure in the last 30 years in 12 South American countries. Methods: We used the Global Burden of Disease (GBD) 2019 exposure-response function to analyze the total tobacco, smoking, and secondhand smoke exposure-related TBL cancer deaths and disability-adjusted life years (DALYs), for 12 South American countries, between 1990 and 2019. Metrics were described as absolute numbers or rates per 100 000 individuals. The relative change in burden was assessed by comparing the 1990-1994 to 2015-2019 periods. Results: In 2019, the all-ages number of TBL cancer deaths and DALYs associated with tobacco exposure in South America was 29 348 and 658 204 in males and 14 106 and 318 277 in females, respectively. Age-adjusted death and DALYs rates for the region in 2019 were 182.8 and 4035 in males and 50.8 and 1162 in females, respectively. In males, 10/12 countries observed relative declines in TBL death rates attributed to tobacco exposure while only 4 countries reduced their mortality in females. Conclusion: While significant efforts on tobacco control are under place in South America, substantial burden of TBL cancer persists in the region with significant sex-specific disparities. Increased country-specific primary data on TBL cancer and tobacco exposure is needed to optimize healthcare strategies and improve comprehension of regional trends.

Understanding the Cardiovascular and Metabolic Health Effects of Air Pollution in the Context of Cumulative Exposomic Impacts.

Poor air quality accounts for more than 9 million deaths a year globally according to recent estimates. A large portion of these deaths are attributable to cardiovascular causes, with evidence indicating that air pollution may also play an important role in the genesis of key cardiometabolic risk factors. Air pollution is not experienced in isolation but is part of a complex system, influenced by a host of other external environmental exposures, and interacting with intrinsic biologic factors and susceptibility to ultimately determine cardiovascular and metabolic outcomes. Given that the same fossil fuel emission sources that cause climate change also result in air pollution, there is a need for robust approaches that can not only limit climate change but also eliminate air pollution health effects, with an emphasis of protecting the most susceptible but also targeting interventions at the most vulnerable populations. In this review, we summarize the current state of epidemiologic and mechanistic evidence underpinning the association of air pollution with cardiometabolic disease and how complex interactions with other exposures and individual characteristics may modify these associations. We identify gaps in the current literature and suggest emerging approaches for policy makers to holistically approach cardiometabolic health risk and impact assessment.

Continuous glucose monitoring for glycaemic control and cardiovascular risk reduction in patients with type 2 diabetes not on insulin therapy: A clinical trial.

AIM: To evaluate the impact of the Dexcom G6 continuous glucose monitoring (CGM) device on glycaemic control and cardiometabolic risk in patients with type 2 diabetes mellitus (T2DM) at high cardiovascular risk who are not on insulin therapy. MATERIALS AND METHODS: Adults with T2DM with glycated haemoglobin (HbA1c) >7% and body mass index (BMI) ≥30 kg/m2 not using insulin were enrolled in a two-phase cross-over study. In phase 1, CGM data were blinded, and participants performed standard glucose self-monitoring. In phase 2, the CGM data were unblinded, and CGM, demographic and cardiovascular risk factor data were collected through 90 days of follow-up and compared using paired tests. RESULTS: Forty-seven participants were included (44% women; 34% Black; mean age 63 years; BMI 37 kg/m2; HbA1c 8.4%; 10-year predicted atherosclerotic cardiovascular disease risk 24.0%). CGM use was associated with a reduction in average glucose (184.0 to 147.2 mg/dl, p < .001), an increase in time in range (57.8 to 82.8%, p < .001) and a trend towards lower glucose variability (26.2 to 23.8%). There were significant reductions in HbA1c, BMI, triglycerides, blood pressure, total cholesterol, diabetes distress and 10-year predicted risk for atherosclerotic cardiovascular disease (p < .05 for all) and an increase in prescriptions for sodium-glucose cotransporter 2 inhibitors (36.2 to 83.0%) and glucagon-like peptide-1 receptor agonists (42.5 to 87.2%, p < .001 for both). CONCLUSIONS: Dexcom G6 CGM was associated with improved glycaemic control and cardiometabolic risk in patients with T2DM who were not on insulin. CGM can be a safe and effective tool to improve diabetes management in patients at high risk for adverse cardiovascular outcomes.

Public Health Relevance of US EPA Air Quality Index Activity Recommendations.

Importance: Reducing exposure to fine particulate matter (<2.5 µm [PM2.5]) air pollution improves cardiopulmonary morbidity and mortality. However, the public health relevance of air quality index (AQI) activity guidelines under present-day environmental conditions in the US has not been critically assessed. Objective: To evaluate the public health relevance of following PM2.5 AQI activity guidance in preventing serious atherosclerotic cardiovascular disease (ASCVD) and pulmonary events among adults in the US. Design, Setting, and Participants: This cross-sectional modeling study involved the general adult population and sensitive individuals as designated by the US Environmental Protection Agency (EPA), including adults with preexisting ASCVD or lung disease (asthma or chronic obstructive pulmonary disease). The study was conducted between August 1, 2023, and January 31, 2024. Exposures: Daily AQI strata for PM2.5 and the corresponding activity recommendations. Main Outcomes and Measures: The main outcome was the number needed to treat (NNT) per day by following activity guidance across daily AQI strata to prevent 1 serious ASCVD or pulmonary event among relevant populations. To calculate PM2.5-induced excess disease event rates per day, estimated baseline disease-specific daily event rates for each group were multiplied by the increase in risks due to PM2.5 levels at each AQI stratum. The number of events prevented per day was calculated by multiplying each excess disease event rate by the percentage in exposure reduction plausibly incurred by following population-specific activity guidance at each AQI level. The NNT is the reciprocal of the number of events prevented. Results: The NNT to prevent ASCVD events was high for the general population and for patients with ASCVD across all AQI strata. The range of values was comparatively lower to prevent pulmonary events among adults with lung disease. During most days (96%) when activity recommendations were promulgated due to elevated PM2.5 (AQI, 101-200), the NNT to prevent a serious disease event remained very high for the general population (>18 million), patients with ASCVD (approximately 1.6-5 million), and adults with lung disease (approximately 66 000-202 000). Conclusions and Relevance: These findings suggest that existing PM2.5 AQI activity recommendations are of questionable public health relevance in present-day conditions and merit consideration for updating to improve their potential effectiveness.

Incidence, progression, and predictors of left atrial appendage sealing after Watchman FLX device implantation with computed tomographic assessment.

BACKGROUND: Limited data exists regarding incidence, progression, and predictors of left atrial appendage (LAA) sealing after transcatheter LAA closure. We aimed to evaluate the incidence, progression, and predictive factors associated with LAA sealing after LAA closure. METHODS: This study includes patients who underwent successful LAA closure with Watchman FLX device and had both pre- and postprocedural computed tomography (CT). Postprocedural CT was performed 45 days after LAA closure and used to evaluate residual LAA patency. Patient who had residual LAA patency at 45 days underwent 1-year follow-up CT. RESULTS: A total of 105 patients (mean age: 75.2 ± 9.6 years; 53.3% female) who underwent successful LAA closure with Watchman FLX device and had pre- and postprocedural CT at 45 days were included. Residual patency was observed in 35 (33.3%) patients: 21 (20.0%) patients showed complete contrast opacification in LAA (complete LAA patency) while 14 (13.3%) patients showed contrast opacification only in the distal LAA (distal LAA patency). Among patients with residual LAA patency at 45 days, the rate of LAA sealing at 1 year was significantly higher in the distal LAA patency group than in the complete LAA patency group (75.0% vs. 16.7%; p = 0.019). Increased depth oversizing was associated with both distal LAA patency and complete LAA patency. CONCLUSION: Postprocedural CT at 45 days detected patent LAA in one-third of patients after LAA closure. LAA sealing was more frequently observed at 1 year among the distal LAA patency group than the complete LAA patency group.

Environmental Exposome and Atrial Fibrillation: Emerging Evidence and Future Directions.

There has been increased awareness of the linkage between environmental exposures and cardiovascular health and disease. Atrial fibrillation is the most common sustained cardiac arrhythmia, affecting millions of people worldwide and contributing to substantial morbidity and mortality. Although numerous studies have explored the role of genetic and lifestyle factors in the development and progression of atrial fibrillation, the potential impact of environmental determinants on this prevalent condition has received comparatively less attention. This review aims to provide a comprehensive overview of the current evidence on environmental determinants of atrial fibrillation, encompassing factors such as air pollution, temperature, humidity, and other meteorologic conditions, noise pollution, greenspace, and the social environment. We discuss the existing evidence from epidemiological and mechanistic studies, critically evaluating the strengths and limitations of these investigations and the potential underlying biological mechanisms through which environmental exposures may affect atrial fibrillation risk. Furthermore, we address the potential implications of these findings for public health and clinical practice and identify knowledge gaps and future research directions in this emerging field.

County-Level Socio-Environmental Factors Associated With Stroke Mortality in the United States: A Cross-Sectional Study.

We used machine learning methods to explore sociodemographic and environmental determinants of health (SEDH) associated with county-level stroke mortality in the USA. We conducted a cross-sectional analysis of individuals aged ≥15 years who died from all stroke subtypes between 2016 and 2020. We analyzed 54 county-level SEDH possibly associated with age-adjusted stroke mortality rates/100,000 people. Classification and Regression Tree (CART) was used to identify specific county-level clusters associated with stroke mortality. Variable importance was assessed using Random Forest analysis. A total of 501,391 decedents from 2397 counties were included. CART identified 10 clusters, with 77.5% relative increase in stroke mortality rates across the spectrum (28.5 vs 50.7 per 100,000 persons). CART identified 8 SEDH to guide the classification of the county clusters. Including, annual Median Household Income ($), live births with Low Birthweight (%), current adult Smokers (%), adults reporting Severe Housing Problems (%), adequate Access to Exercise (%), adults reporting Physical Inactivity (%), adults with diagnosed Diabetes (%), and adults reporting Excessive Drinking (%). In conclusion, SEDH exposures have a complex relationship with stroke. Machine learning approaches can help deconstruct this relationship and demonstrate associations that allow improved understanding of the socio-environmental drivers of stroke and development of targeted interventions.

The Urban Environment and Cardiometabolic Health.

Urban environments contribute substantially to the rising burden of cardiometabolic diseases worldwide. Cities are complex adaptive systems that continually exchange resources, shaping exposures relevant to human health such as air pollution, noise, and chemical exposures. In addition, urban infrastructure and provisioning systems influence multiple domains of health risk, including behaviors, psychological stress, pollution, and nutrition through various pathways (eg, physical inactivity, air pollution, noise, heat stress, food systems, the availability of green space, and contaminant exposures). Beyond cardiometabolic health, city design may also affect climate change through energy and material consumption that share many of the same drivers with cardiometabolic diseases. Integrated spatial planning focusing on developing sustainable compact cities could simultaneously create heart-healthy and environmentally healthy city designs. This article reviews current evidence on the associations between the urban exposome (totality of exposures a person experiences, including environmental, occupational, lifestyle, social, and psychological factors) and cardiometabolic diseases within a systems science framework, and examines urban planning principles (eg, connectivity, density, diversity of land use, destination accessibility, and distance to transit). We highlight critical knowledge gaps regarding built-environment feature thresholds for optimizing cardiometabolic health outcomes. Last, we discuss emerging models and metrics to align urban development with the dual goals of mitigating cardiometabolic diseases while reducing climate change through cross-sector collaboration, governance, and community engagement. This review demonstrates that cities represent crucial settings for implementing policies and interventions to simultaneously tackle the global epidemics of cardiovascular disease and climate change.

Association of Environmental Injustice and Cardiovascular Diseases and Risk Factors in the United States.

BACKGROUND: While the impacts of social and environmental exposure on cardiovascular risks are often reported individually, the combined effect is poorly understood. METHODS AND RESULTS: Using the 2022 Environmental Justice Index, socio-environmental justice index and environmental burden module ranks of census tracts were divided into quartiles (quartile 1, the least vulnerable census tracts; quartile 4, the most vulnerable census tracts). Age-adjusted rate ratios (RRs) of coronary artery disease, strokes, and various health measures reported in the Prevention Population-Level Analysis and Community Estimates data were compared between quartiles using multivariable Poisson regression. The quartile 4 Environmental Justice Index was associated with a higher rate of coronary artery disease (RR, 1.684 [95% CI, 1.660-1.708]) and stroke (RR, 2.112 [95% CI, 2.078-2.147]) compared with the quartile 1 Environmental Justice Index. Similarly, coronary artery disease 1.057 [95% CI,1.043-1.0716] and stroke (RR, 1.118 [95% CI, 1.102-1.135]) were significantly higher in the quartile 4 than in the quartile 1 environmental burden module. Similar results were observed for chronic kidney disease, hypertension, diabetes, obesity, high cholesterol, lack of health insurance, sleep <7 hours per night, no leisure time physical activity, and impaired mental and physical health >14 days. CONCLUSIONS: The prevalence of CVD and its risk factors is highly associated with increased social and environmental adversities, and environmental exposure plays an important role independent of social factors.