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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. [ABSTRACT FROM AUTHOR]

Nearly 56% of the global population lives in cities, with this number expected to increase to 6.6 billion or >70% of the world's population by 2050. Given that cardiometabolic diseases are the leading causes of morbidity and mortality in people living in urban areas, transforming cities and urban provisioning systems (or urban systems) toward health, equity, and economic productivity can enable the dual attainment of climate and health goals. Seven urban provisioning systems that provide food, energy, mobility-connectivity, housing, green infrastructure, water management, and waste management lie at the core of human health, well-being, and sustainability. These provisioning systems transcend city boundaries (eg, demand for food, water, or energy is met by transboundary supply); thus, transforming the entire system is a larger construct than local urban environments. Poorly designed urban provisioning systems are starkly evident worldwide, resulting in unprecedented exposures to adverse cardiometabolic risk factors, including limited physical activity, lack of access to heart-healthy diets, and reduced access to greenery and beneficial social interactions. Transforming urban systems with a cardiometabolic health-first approach could be accomplished through integrated spatial planning, along with addressing current gaps in key urban provisioning systems. Such an approach will help mitigate undesirable environmental exposures and improve cardiovascular and metabolic health while improving planetary health. The purposes of this American Heart Association policy statement are to present a conceptual framework, summarize the evidence base, and outline policy principles for transforming key urban provisioning systems to heart-health and sustainability outcomes. [ABSTRACT FROM AUTHOR]

The article explores the connection between human and planetary health, emphasizing the impact of environmental pollution on cardiovascular disease. It suggests that addressing environmental exposures, such as air pollution, can improve both planetary health and human well-being. Additionally, the article discusses the importance of involving developing countries in global climate change efforts, as they are often the most vulnerable to its impacts. It argues for supporting and empowering these countries to adopt sustainable practices and technologies, with assistance from developed countries. [Extracted from the article]

Since the publication of the last American Heart Association scientific statement on air pollution and cardiovascular disease in 2010, unequivocal evidence of the causal role of fine particulate matter air pollution (PM2.5, or particulate matter ≤2.5 μm in diameter) in cardiovascular disease has emerged. There is a compelling case to provide the public with practical personalized approaches to reduce the health effects of PM2.5. Such interventions would be applicable not only to individuals in heavily polluted countries, high-risk or susceptible individuals living in cleaner environments, and microenvironments with higher pollution exposures, but also to those traveling to locations with high levels of PM2.5. The overarching motivation for this document is to summarize the current evidence supporting personal-level strategies to prevent the adverse cardiovascular effects of PM2.5, guide the use of the most proven/viable approaches, obviate the use of ineffective measures, and avoid unwarranted interventions. The significance of this statement relates not only to the global importance of PM2.5, but also to its focus on the most tested interventions and viable approaches directed at particulate matter air pollution. The writing group sought to provide expert consensus opinions on personal-level measures recognizing the current uncertainty and limited evidence base for many interventions. In doing so, the writing group acknowledges that its intent is to assist other agencies charged with protecting public health, without minimizing the personal choice considerations of an individual who may decide to use these interventions in the face of ongoing air pollution exposure. [ABSTRACT FROM AUTHOR]

Air pollution involving particulate matter smaller than 2.5 μm in size (PM2.5) is the world's leading environmental risk factor contributing to mortality through cardiometabolic pathways. In this study, we modeled early life exposure using chow-fed C57BL/6J male mice that were exposed to real-world inhaled, concentrated PM2.5 (~10 times ambient levels/~60-120 μg/m3) or filtered air over a 14-week period. We investigated the effects of PM2.5 on phenotype, the transcriptome, and chromatin accessibility and compared these with the effects of a prototypical high-fat diet (HFD) as well as cessation of exposure on phenotype reversibility. Exposure to PM2.5 impaired glucose and insulin tolerance and reduced energy expenditure and 18FDG-PET uptake in brown adipose tissue. Multiple differentially expressed gene clusters in pathways involving metabolism and circadian rhythm were noted in insulin-responsive tissues. Although the magnitude of transcriptional change detected with PM2.5 exposure was lower than that observed with a HFD, the degree of alteration in chromatin accessibility after PM2.5 exposure was significant. The novel chromatin remodeler SMARCA5 (SWI/SNF complex) was regulated in response to PM2.5 exposure, the cessation of which was associated with a reversal of insulin resistance and restoration of chromatin accessibility and nucleosome positioning near transcription start sites, as well as a reversal of exposure-induced changes in the transcriptome, including SMARCA5. These changes indicate pliable epigenetic control mechanisms following cessation of exposure. [ABSTRACT FROM AUTHOR]

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Deficiencies in the care of patients with diabetes are the norm rather than the exception. We propose a reframing of diabetes care quality, which encompasses four key principles ('the 4 BEs') that together can help address deficiencies in the care of the patient with Type 2 diabetes (T2D) and eliminate these missed opportunities. [ABSTRACT FROM AUTHOR]

Fine particulate matter <2.5 μm (PM2.5) air pollution is the most important environmental risk factor contributing to global cardiovascular (CV) mortality and disability. Short-term elevations in PM2.5 increase the relative risk of acute CV events by 1% to 3% within a few days. Longer-term exposures over several years increase this risk by a larger magnitude (∼10%), which is partially attributable to the development of cardiometabolic conditions (e.g., hypertension and diabetes mellitus). As such, ambient PM2.5 poses a major threat to global public health. In this review, the authors provide an overview of air pollution and health, including assessment of exposure, impact on CV outcomes, mechanistic underpinnings, and impact of air pollution reduction strategies to mitigate CV risk. The review concludes with future challenges, including the inextricable link between air pollution and climate change, and calls for large-scale trials to allow the promulgation of formal evidence-based recommendations to lower air pollution-induced health risks. [ABSTRACT FROM AUTHOR]

An editorial is presented which discusses the threat of anthropogenic ambient air pollution to global health and well-being. It mentions that the American Heart Association (AHA) and European Society of Cardiology (ESC) has identified air pollution as an independent risk factor for cardiovascular events, such as myocardial infarction, stroke, and heart failure.

Cardiometabolic disorders including obesity, diabetes and cardiovascular disease are among the most severe health problems worldwide. DPP4 enzymatic inhibitors were first developed as anti-diabetic reagents which preserve incretin hormones and promote post-prandial insulin secretion. It's been shown in animal studies that incretin-based therapy has a beneficial effect on cardiovascular disease. Recent studies demonstrated novel non-catalytic functions of DPP4 that may play a role in cardiometabolic disease. Although the role of DPP4 inhibition-mediated incretin effects has been well-reviewed, little information of its incretin-independent actions was introduced in cardiometabolic disease. In the current review, we will summarize the catalytic dependent and independent effects of DPP4 inhibition on cardiometabolic disease. [ABSTRACT FROM AUTHOR]

The article discusses relationship between air pollution and type 2 Diabetes Mellitus (DM). It has been informed that at least six published epidemiologic studies depict association between Particulate Matter (PM) or traffic related air pollutants and DM. It has been informed that endothelial function is being altered due to air pollution in both animals and humans.

Angiotensin receptor blockers have been hypothesized to have synergistic effects with statins. We evaluated the effects of valsartan alone or combined with simvastatin on blood pressure (BP) and indexes of inflammation and oxidant stress in hypertensive patients with hyperlipidemia. In this double-blind trial, 404 patients were randomized to 12 weeks valsartan 160 mg (V) or valsartan 160 mg plus simvastatin 20 mg (V/S20) or 80 mg (V/S80). Twenty-four–hour mean ambulatory BP and biochemical marker measurements were recorded at baseline and study end. There were no statistically significant between-treatment differences for least-square mean reductions from baseline in systolic BP (V, −9.22; V/S20, −9.25; V/S80, −9.58 mm Hg; p <0.0001 for all within-treatment changes vs baseline). Plasma high-sensitivity C-reactive protein decreased with the combinations but not with V alone (least-square mean median change from baseline, −0.16, −0.20, −0.70 mg/L; p = 0.0001 for V/S80 vs baseline; p = 0.045 for V/S20 vs baseline; p = 0.0023 for V/S80 vs V/S20; p = 0.0045 for V/S80 vs V). Monocyte chemoattractant protein–1 was reduced by V, with no evidence for additional lowering with V/S combinations. In conclusion, addition of simvastatin to valsartan did not incrementally lower BP. However, V/S80 was superior to V and V/S20 in reducing high-sensitivity C-reactive protein. [Copyright &y& Elsevier]

The renin-angiotensin system (RAS) may play a role in vascular aging. The authors hypothesized that blockade of the angiotensin II type 1 receptor with an angiotensin receptor blocker in healthy elderly subjects improves vascular compliance and endothelial function. Thirty-five healthy elderly subjects were randomized to valsartan or placebo in a double-blind crossover study after baseline testing for pulse wave velocity, aortic augmentation index, and brachial artery flow-mediated dilation. Angiotensin II type 1 receptor blockade with valsartan improved vascular compliance but not flow-mediated dilation. Changes in pulse wave velocity with valsartan were correlated with change in central systolic blood pressure and pulse pressure and remained associated on multivariate analysis. Change in pulse wave velocity after adjusting for degree of blood pressure change, age, and sex remained correlated with assignment to the angiotensin receptor blocker but not placebo. These data suggest that angiotensin II type 1 receptor blockade improves aging-related vascular compliance without alterations in flow-mediated dilation. Mechanisms regulating compliance and endothelial function are complex and may not necessarily converge in aging. [ABSTRACT FROM AUTHOR]

Raynaud''s syndrome (RS), which is characterized by recurrent episodes of vasospasm with exposure to cold, may occur alone (primary RS) or in association with connective tissue diseases or other underlying conditions (secondary RS). We investigated the effect of cilostazol on vessel wall responses in RS. Patients were diagnosed (primary or secondary RS associated with connective tissue diseases) and randomized to placebo or cilostazol 100 mg twice daily for 6 weeks in a double-blind manner. Brachial artery vasoreactivity, laser Doppler fluxmetry, and cold pressor testing (CPT) were performed at study initiation and completion. Symptoms were assessed using standardized questionnaires. Forty subjects completed the study (19 with primary RS and 21 with secondary RS). Cilostazol significantly increased the mean brachial artery diameter at 6 weeks (primary RS, p = 0.006; secondary RS, p = 0.06). There was no change in median flow-mediated dilation (FMD) with cilostazol in primary RS (25th, 75th percentiles) (4.06% [2.5, 6.1] to −0.77% [−2.4, 3.4] or secondary RS (2.2% [0.05, 6.3] to 2.95% [1.7, 7.4]). There were no changes in nitroglycerin-mediated dilation or microvascular flow indexes in either cohort. In patients with primary RS, cilostazol treatment yielded a positive change in the slope of brachial responsiveness to CPT (increase of 0.32 mm/min; p = 0.002 vs placebo). Cilostazol treatment remained significantly associated with increased brachial artery diameter when controlling for baseline values (p = 0.018). Cilostazol increased conduit vessel diameter in patients with primary and secondary RS, with a favorable impact on conduit vessel responsiveness to cold in patients with primary RS without affecting microvascular flow or symptoms. [Copyright &y& Elsevier]

Critical limb ischemia (CLI) is typified by rest pain and/or tissue necrosis secondary to advanced peripheral arterial disease (PAD) and is characterized by diminution in limb perfusion at rest. We tested the safety of an angiogenic strategy with CI-1023 (Ad[sub GV]VEGF121.10), a replication-deficient adenovirus encoding human vascular endothelial growth factor isoform 121 in patients with CLI as part of a phase I trial. Fifteen subjects >35 years of age with CLI and angiographic disease involving the infra-inguinal vessels underwent intramuscular injection of CI-1023 (4 × 10[sup 8] to 4 × 10[sup 10] particle units, n = 13) or placebo (n = 2). All of the patients tolerated the injection well and there were no serious complications related to the procedure. Transient edema was noted in one patient. A total of 79 adverse events were reported over the course of one year. One death (day 136) and one malignancy (day 332) occurred in the CI-1023 group. CI-1023 appears to be well tolerated and safe for single-dose administration in patients with critical limb ischemia due to PAD. Further studies are needed to determine the efficacy of this form of therapeutic angiogenesis. [ABSTRACT FROM AUTHOR]

The long-term safety and efficacy of adenoviral delivery of growth factors in patients with peripheral arterial disease (PAD) is unknown. CI-1023 (AdGVVEGF121.10) is a replication-deficient adenovirus encoding human vascular endothelial growth factor isoform 121. In this phase I trial, we investigated the safety and efficacy of CI-1023 in subjects with advanced claudication symptoms secondary to infra-inguinal disease. Eighteen subjects >35 years of age with a median ankle brachial index (ABI) at rest of 0.525 (interquartile range 0.4) and angiographic disease involving the infra-inguinal vessels underwent intramuscular injection of CI-1023 (4 ×108 to 4 ×1010 particle units, n = 15) or placebo (n = 3). Eleven of 15 patients (73%) who received CI-1023 and 1 of 3 subjects (33%) who received placebo, completed 1 year of follow-up. Edema and rash were the most common early adverse event. One infra-inguinal bypass procedure occurred in each of the placebo and CI-1023 groups at days 29 and 104, respectively. One death (day 160) and 1 malignancy (day 274) occurred in the CI-1023 group. Conclusions on efficacy could not be made due to the small number of patients. However, there were encouraging trends in ABI at rest and peak walking time at follow-up. [Copyright &y& Elsevier]

Aging is associated with progressive deterioration in endothelial function. We hypothesized that losartan may represent a useful therapeutic strategy to ameliorate endothelial function in aged subjects. Eighteen healthy older subjects (mean age 75 ± 3 years) were prospectively randomized in a double-blind, crossover fashion to receive either losartan 50 mg/day or placebo for 6 weeks. Subjects were switched to the opposite arm after a 2- week washout period. Flow-mediated dilation (FMD) in the brachial artery and plasma levels of vascular cell adhesion molecule-1, intercellular adhesion molecule (ICAM), moncocyte chemoattractant 1 protein, and E-selectin were measured in both arms at the beginning and end of the 6-week period. Losartan resulted in a 6-mm Hg decrease in systolic blood pressure (from 130 ± 12 to 124 ± 13 mm Hg), which was no different from placebo (132 ± 12 to 127 ± 13 mm Hg). FMD increased from 3.1 ± 0.6% to 3.9 ± 0.6% after losartan, and decreased from 3.3 ± 0.3% to 2.4 ± 0.6% after placebo (p = NS for both). In contrast, losartan reduced circulating concentrations of vascular cell adhesion molecule 1 (750 ± 73 to 572 ± 39), ICAM (405 ± 26 to 196 ± 10), and moncocyte chemoattractant 1 protein (560 ± 56 to 423 ± 35) (p <0.01 for all by analysis of variance), but not E-selectin. On univariate analyses, the strongest predictor of baseline endothelial function and change in FMD with losartan was low-density lipoprotein. There was a negative correlation between baseline endothelial function and change in FMD in response to losartan (r2 = −0.75, p = 0.0003). Baseline ICAM levels alone significantly correlated with low-density lipoprotein cholesterol (r2 = 0.54, p = 0.02) and weakly correlated with total cholesterol (r2 = 0.47, p = 0.05). Thus, administration of losartan for a duration of 6 weeks has favorable effects on inflammatory markers in healthy older subjects, but does not alter peripheral conduit endothelial function. [Copyright &y& Elsevier]

Depressive illness in patients without traditional risk factors for coronary artery disease is associated with striking abnormalities of endothelial function and elevation of circulating markers of atherosclerosis propensity. Further studies are needed to define the mechanisms that underlie these observations. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Aims: To investigate high‐risk sociodemographic and environmental determinants of health (SEDH) potentially associated with adult obesity in counties in the United States using machine‐learning techniques. Materials and Methods: We performed a cross‐sectional analysis of county‐level adult obesity prevalence (body mass index ≥30 kg/m2) in the United States using data from the Diabetes Surveillance System 2017. We harvested 49 county‐level SEDH factors that were used in a classification and regression trees (CART) model to identify county‐level clusters. The CART model was validated using a 'hold‐out' set of counties and variable importance was evaluated using Random Forest. Results: Overall, we analysed 2752 counties in the United States, identifying a national median (interquartile range) obesity prevalence of 34.1% (30.2%, 37.7%). The CART method identified 11 clusters with a 60.8% relative increase in prevalence across the spectrum. Additionally, seven key SEDH variables were identified by CART to guide the categorization of clusters, including Physically Inactive (%), Diabetes (%), Severe Housing Problems (%), Food Insecurity (%), Uninsured (%), Population over 65 years (%) and Non‐Hispanic Black (%). Conclusion: There is significant county‐level geographical variation in obesity prevalence in the United States, which can in part be explained by complex SEDH factors. The use of machine‐learning techniques to analyse these factors can provide valuable insights into the importance of these upstream determinants of obesity and, therefore, aid in the development of geo‐specific strategic interventions and optimize resource allocation to help battle the obesity pandemic. [ABSTRACT FROM AUTHOR]

Examines the pressure-dependent behavior of isolated coronary resistance vessels greater than 100 micrometers in diameter. Steady-state diameter changes; Transient responses; Autoregulation.

Several letter to the editor are presented in response to the article "Vitamin D therapy and cardiac structure and function in patients with chronic kidney disease: The PRIMO randomized controlled trial," by Ravi Thadhani and colleagues in a previous issue of "The Journal of the American Medical Association."

A letter to the editor is presented on the article "Long-term exposure to air pollution and incidence of cardiovascular events in women," by K. A. Miller, D. S. Siscovisk, L. Sheppard, et al., in the February 1, 2007 issue.

Fine particulate air pollution <2.5 μm in diameter (PM2.5) is a major environmental threat to global public health. Multiple national and international medical and governmental organizations have recognized PM2.5 as a risk factor for cardiopulmonary diseases. A growing body of evidence indicates that several personal-level approaches that reduce exposures to PM2.5 can lead to improvements in health endpoints. Novel and forward-thinking strategies including randomized clinical trials are important to validate key aspects (e.g., feasibility, efficacy, health benefits, risks, burden, costs) of the various protective interventions, in particular among real-world susceptible and vulnerable populations. This paper summarizes the discussions and conclusions from an expert workshop, Reducing the Cardiopulmonary Impact of Particulate Matter Air Pollution in High Risk Populations, held on May 29 to 30, 2019, and convened by the National Institutes of Health, the U.S. Environmental Protection Agency, and the U.S. Centers for Disease Control and Prevention. [ABSTRACT FROM AUTHOR]

The author reflects on the chronic obstructive pulmonary disease (COPD) as a risk factor for cardiovascular (CV) mortality rate and efforts to made to reduce the same in Great Britain. Topics discussed include patients with COPD that have higher rehospitalisation, mortality and poorer health condition following myocardial infarction (MI) and evidence that support reduction in mortality gap with the help of secondary preventive therapies.

BACKGROUND: Previous evidence has identified exposure to fine ambient particulate matter (PM2.5) as a leading risk factor for adverse health outcomes. However, to date, only a few studies have examined the potential association between long-term exposure to PM2.5 and bone homeostasis. OBJECTIVE: We sought to examine the relationship between long-term PM2.5 exposure and bone health and explore its potential mechanism. METHODS: This research included both observational and experimental studies. First, based on human data from UK Biobank, linear regression was used to explore the associations between long-term exposure to PM2.5 (i.e., annual average PM2.5 concentration for 2010) and bone mineral density [BMD; i.e., heel BMD (푛= 37,440) and femur neck and lumbar spine BMD (푛= 29,766)], which were measured during 2014-2020. For the experimental animal study, C57BL/6 male mice were assigned to ambient PM2.5 or filtered air for 6 months via a whole-body exposure system. Micro-computed tomography analyses were applied to measure BMD and bone microstructures. Biomarkers for bone turnover and inflammation were examined with histological staining, immunohistochemistry staining, and enzyme-linked immunosorbent assay. We also performed tartrate-resistant acid phosphatase (TRAP) staining and bone resorption assay to determine the effect of PM2.5 exposure on osteoclast activity in vitro. In addition, the potential downstream regulators were assessed by real-time polymerase chain reaction and western blot. RESULTS: We observed that long-term exposure to PM2.5 was significantly associated with lower BMD at different anatomical sites, according to the analysis of UK Biobank data. In experimental study, mice exposed long-term to PM2.5 exhibited excessive osteoclastogenesis, dysregulated osteogenesis, higher tumor necrosis factor-alpha (TNF-α) expression, and shorter femur length than control mice, but they demonstrated no significant differences in femur structure or BMD. In vitro, cells stimulated with conditional medium of PM2.5-stimulated macrophages had aberrant osteoclastogenesis and differences in the protein/mRNA expression of members of the TNF-α/Traf6/c-Fos pathway, which could be partially rescued by TNF-α inhibition. DISCUSSION: Our prospective observational evidence suggested that long-term exposure to PM2.5 is associated with lower BMD and further experimental results demonstrated exposure to PM2.5 could disrupt bone homeostasis, which may be mediated by inflammation-induced osteoclastogenesis. [ABSTRACT FROM AUTHOR]

Background: The importance of type 2 diabetes mellitus (T2D) in heart failure hospitalizations (HFH) is acknowledged. As information on the prevalence and influence of social deprivation on HFH is limited, we studied this issue in a racially diverse cohort. Methods: Linking data from US Veterans with stable T2D (without prevalent HF) with a zip‐code derived population‐level social deprivation index (SDI), we grouped them according to increasing SDI as follows: SDI: group I: ≤20; II: 21‐40; III: 41‐60; IV: 61‐80; and V (most deprived) 81‐100. Over a 10‐year follow‐up period, we identified the total (first and recurrent) number of HFH episodes for each patient and calculated the age‐adjusted HFH rate [per 1000 patient‐years (PY)]. We analysed the incident rate ratio between SDI groups and HFH using adjusted analyses. Results: In 1 012 351 patients with T2D (mean age 67.5 years, 75.7% White), the cumulative incidence of first HFH was 9.4% and 14.2% in SDI groups I and V respectively. The 10‐year total HFH rate was 54.8 (95% CI: 54.5, 55.2)/1000 PY. Total HFH increased incrementally from SDI group I [43.3 (95% CI: 42.4, 44.2)/1000 PY] to group V [68.6 (95% CI: 67.8, 69.9)/1000 PY]. Compared with group I, group V patients had a 53% higher relative risk of HFH. The negative association between SDI and HFH was stronger in Black patients (SDI × Race pinteraction <.001). Conclusions: Social deprivation is associated with increased HFH in T2D with a disproportionate influence in Black patients. Strategies to reduce social disparity and equalize racial differences may help to bridge this gap. [ABSTRACT FROM AUTHOR]

This article discusses a report that revealed additional important information that strengthens the link between air pollutants and stroke further. The study, which involved patients of a stroke center in Boston, Massachusetts found that the risk for ischemic stroke was significantly increased after short-term exposure to higher levels of ambient particulate matter. The report found that as short as 6 to 24 hours of exposure can trigger ischemic stroke.

A letter to the editor is presented in response to the article "Coronary Heart Disease Mortality Declines in the United States From 1979 Through 2011: Evidence for Stagnation in Young Adults, Especially Women" by K. A. Wilmot and colleagues in the 2015 issue.

BACKGROUND Ankle-brachial pressure index (ABI) is a reliable and widely used measure of the presence and severity of peripheral arterial disease (PAD) in the lower extremities; however, the presence of diabetes or end-stage renal disease can lead to a falsely elevated ABI. OBJECTIVE To compare skin perfusion pressure (SPP) with ABI for the diagnosis of PAD in patients on hemodialysis both with and without diabetes. DESIGN AND INTERVENTION Adults receiving hemodialysis as outpatients were recruited between July and October 2005 for this single-center Japanese study. SPP in the foot and resting ABI were measured with a laser Doppler scanner and a volume plethysmographic device, respectively, either before dialysis or on a dialysis-free day. OUTCOME MEASURE The main outcome was the level of correlation between SPP and ABI, expressed as a Pearson's correlation coefficient (r). RESULTS The 59 patients enrolled (mean age 63 years; range 30-81 years) comprised 37 men (62.7%) and 22 women (37.3%). Mean dialysis vintage was 91 months (range 1-336 months) and 21 patients (35.6%) were diabetic. A total of 25 patients (42.4%) had claudication, which was accompanied by other exertional leg symptoms in 20 cases. ABI could not be measured in one limb because of leg pain and a chronic ulcer; SPP could not be measured in three limbs because of involuntary movement caused by restless leg syndrome or by previous stroke. Measurements from 114 limbs were, therefore, included in the analysis. SPP was found to be positively associated with ABI (r= 0.429; P = 0.0001); the association remained when patients with and without diabetes were analyzed separately (r = 0.461, P = 0.0036 and r= 0.372, P = 0.0009, respectively). SPP tended to decrease with age (r=-0.279; P=0.03). Limbs with a low ABI (<0.9; n=11) had a significantly lower mean SPP (+ SD) than those with a normal ABI (≥0.9 to <1.3; n=88) and those with an elevated ABI (≥1.3; n = 15): 40.9 ± 12.6 mmHg vs 71.0±25.1 mmHg and 77.7±22.9mmHg, respectively (P<0.05 for both comparisons). When each of these groups was subdivided according to whether or not patients had diabetes, only the limbs with a normal ABI showed a significant difference in mean SPP between diabetics and nondiabetics (61.3 ±23.0mmHg vs 75.3±24.9mmHg; P<0.05). Stepwise regression analysis revealed that increased ABI was a significant predictor of increased SPP (P<0.0001), and that increased age, increased dialysis vintage, and presence of diabetes were significant predictors of decreased SPP (P= 0.0003, P<0.0001 and P = 0.0011, respectively). CONCLUSION Measurement of SPP is a noninvasive means of screening for PAD and might be useful in patients on hemodialysis. [ABSTRACT FROM AUTHOR]

A response is presented to a letter to the editor on the article "Long-term air pollution exposure and acceleration of atherosclerosis and vascular inflammation in an animal model," by Sung Q. Wang et al.

To stabilise the housing market during the great depression, the government-sanctioned Home Owners' Loan Corporation (HOLC) created colour-coded maps of nearly 200 United States cities according to lending risk. These maps were largely driven by racial segregation, with the worst graded neighbourhoods coloured in red, later termed redlined neighbourhoods. We sought to investigate the association between historical redlining, and trends in environmental disparities across the US over the past few decades. We characterised environmental exposures including air pollutants (e.g. NO2 and fine particulate matter), vegetation, noise, and light at night, proximity hazardous emission sources (e.g. hazardous water facilities, wastewater discharge indicator) and other environmental and social indicators harnessed from various sources across HOLC graded neighbourhoods and extrapolated census tracts (A [lowest risk neighbourhoods] to D [highest risk neighbourhoods]). Lower graded areas (C and D) had consistently higher exposures to worse environmental factors. Additionally, there were consistent relative disparities in the exposures to PM2.5 (1981–2018) and NO2 (2005–2019), without significant improvement in the gap compared with HOLC grade A neighbourhoods. Our findings illustrate that historical redlining, a form of residential segregation largely based on racial discrimination is associated with environmental injustice over the past 2–4 decades. [ABSTRACT FROM AUTHOR]

Disparities in premature cardiovascular mortality (PCVM) have been associated with socioeconomic, behavioral, and environmental risk factors. Understanding the "phenotypes", or combinations of characteristics associated with the highest risk of PCVM, and the geographic distributions of these phenotypes is critical to targeting PCVM interventions. This study applied the classification and regression tree (CART) to identify county phenotypes of PCVM and geographic information systems to examine the distributions of identified phenotypes. Random forest analysis was applied to evaluate the relative importance of risk factors associated with PCVM. The CART analysis identified seven county phenotypes of PCVM, where high-risk phenotypes were characterized by having greater percentages of people with lower income, higher physical inactivity, and higher food insecurity. These high-risk phenotypes were mostly concentrated in the Black Belt of the American South and the Appalachian region. The random forest analysis identified additional important risk factors associated with PCVM, including broadband access, smoking, receipt of Supplemental Nutrition Assistance Program benefits, and educational attainment. Our study demonstrates the use of machine learning approaches in characterizing community-level phenotypes of PCVM. Interventions to reduce PCVM should be tailored according to these phenotypes in corresponding geographic areas. [ABSTRACT FROM AUTHOR]

T cells play a crucial role in atherosclerosis, with its infiltration preceding the formation of atheroma. However, how T‐cell infiltration is regulated in atherosclerosis remains largely unknown. Here, this work demonstrates that dipeptidyl peptidase‐4 (DPP4) is a novel regulator of T‐cell motility in atherosclerosis. Single‐cell ribonucleic acid (RNA) sequencing and flow cytometry show that CD4+ T cells in atherosclerotic patients display a marked increase of DPP4. Lack of DPP4 in hematopoietic cells or T cells reduces T‐cell infiltration and atherosclerotic plaque volume in atherosclerosis mouse models. Mechanistically, DPP4 deficiency reduces T‐cell motility by suppressing the expression of microtubule associated protein midline‐1 (Mid1) in T cells. Deletion of either DPP4 or Mid1 inhibits chemokine‐induced shape change and motility, while restitution of Mid1 in Dpp4−/− T cell largely restores its migratory ability. Thus, DPP4/Mid1, as a novel regulator of T‐cell motility, may be a potential inflammatory target in atherosclerosis. [ABSTRACT FROM AUTHOR]

Disparities in premature cardiovascular mortality (PCVM) have been associated with socioeconomic, behavioral, and environmental risk factors. Understanding the "phenotypes", or combinations of characteristics associated with the highest risk of PCVM, and the geographic distributions of these phenotypes is critical to targeting PCVM interventions. This study applied the classification and regression tree (CART) to identify county phenotypes of PCVM and geographic information systems to examine the distributions of identified phenotypes. Random forest analysis was applied to evaluate the relative importance of risk factors associated with PCVM. The CART analysis identified seven county phenotypes of PCVM, where high-risk phenotypes were characterized by having greater percentages of people with lower income, higher physical inactivity, and higher food insecurity. These high-risk phenotypes were mostly concentrated in the Black Belt of the American South and the Appalachian region. The random forest analysis identified additional important risk factors associated with PCVM, including broadband access, smoking, receipt of Supplemental Nutrition Assistance Program benefits, and educational attainment. Our study demonstrates the use of machine learning approaches in characterizing community-level phenotypes of PCVM. Interventions to reduce PCVM should be tailored according to these phenotypes in corresponding geographic areas. [ABSTRACT FROM AUTHOR]

Air particulate matter induced oxidative stress and inflammation in cardiovascular disease and atherosclerosis: the role of Nrf2 and AhR-mediated pathways. Keywords: air pollution; biomarker; chronic rhinosinusitis EN air pollution biomarker chronic rhinosinusitis 1424 1427 4 11/15/22 20221101 NES 221101 INTRODUCTION Exposure to airborne environmental pollutants including fine particulate matter (PM SB 2.5 sb ) has been linked to respiratory disease, including chronic rhinosinusitis (CRS), allergies, and anosmia.1 Recent work has established a link between PM SB 2.5 sb exposure and the development of nonallergic CRS.1 In addition, CRS symptom severity is influenced by air pollutant exposure, and chronic PM SB 2.5 sb exposure has been found to induce sinonasal epithelial barrier dysfunction and type 2 eosinophilic rhinosinusitis in a novel mouse model.2 Molecular mechanisms of airway responses to these environmental stimuli, including possible epigenomic reprogramming, remain unknown. [Extracted from the article]