Citations

Background Although micro‐ and nanoplastics are an emerging risk factor for the development of cardiovascular diseases, the association of marine microplastic levels (MMLs) with the burden of cardiometabolic diseases at a population level remains unexplored. We investigated the relationship between the mean microplastic concentration in ocean water within 200 nautical miles of the US coastline and the prevalence of type 2 diabetes, coronary artery disease, and stroke in nearby counties. Methods Microplastic concentration data within 200 nautical miles of the US coastline were geospatially analyzed to calculate mean MMLs. The coastal counties were stratified into 4 categories based on MMLs in the adjacent ocean water body: low, medium, high, or very high. The Behavioral Risk Factor Surveillance System 2019 to 2020 survey data were used to identify the prevalence of type 2 diabetes, coronary artery disease, and stroke in these counties. Univariate and population‐weighted multivariate quasi‐Poisson regression, adjusted for county‐level confounding variables, was used to evaluate the unadjusted and adjusted associations between disease prevalence and MMLs. Results The mean age of the population was 43±6 years. After adjusting for age, sex, physician access, and socioenvironmental vulnerabilities at the county level, counties with very high MMLs exhibited an 18%, 7%, and 9% higher adjusted prevalence of type 2 diabetes, coronary artery disease, and stroke, respectively, compared with those with low levels. Conclusion Marine microplastic levels were significantly associated with the prevalence of cardiometabolic diseases in coastal counties. Comprehensive studies at an individual level are needed to further investigate the health impacts of microplastic pollution.

ABSTRACTBackgroundMicroplastics are emerging as environmental pollutants with potential neurotoxic effects, yet their association with neurological disabilities remains largely unexplored.MethodsIn this cross‐sectional study comprising 218 coastal counties in the United States, we compared the self‐reported prevalence of cognitive disability, mobility disability, self‐care disability, and independent living disability in counties with very high and low marine microplastic levels (MMLs). Unadjusted and adjusted prevalence ratios (PRs) were computed using population‐weighted quasi‐Poisson regression across three different models to examine the relationship between disability prevalence and MMLs.ResultsCounties exposed to very high marine microplastic levels had a higher mean prevalence of self‐reported cognitive disability (15.2% vs. 13.9%), mobility disability (14.1% vs. 12.3%), self‐care disability (4.2% vs. 3.6%), and independent living disability (8.5% vs. 7.7%) compared to those exposed to low levels (p < 0.001). Regression analyses revealed significantly elevated adjusted prevalence ratios (PRs) for cognitive (PR: 1.09 [95% CI: 1.06–1.12], p < 0.001), mobility (PR: 1.06 [1.03–1.10], p < 0.001), self‐care (PR: 1.16 [1.11–1.20], p < 0.001), and independent living disability (PR: 1.08 [1.05–1.12], p < 0.001) in counties with very high microplastic exposure compared to those with low exposure.ConclusionsThis study highlights a significant association between marine microplastic pollution and the self‐reported prevalence of cognitive, mobility, self‐care, and independent living disabilities at the county level. While merely associative, these findings emphasize the urgent need for further investigation into the individual‐level health impacts of microplastic exposure and underscore the importance of environmental interventions to mitigate potential risks.

Background Although cardiovascular mortality (CVM) rates in the United States have been declining overall, our study evaluated whether this holds true for areas with increased social deprivation. Methods and Results We used county‐level cross‐sectional age‐adjusted CVM rates (aa‐CVM) (2000–2019) linked to the Centers for Disease Control and Prevention Social Vulnerability Index (SVI–2010). We grouped counties as per SVI (Groups I 0–0.2, II 0.21–0.4, III 0.41–0.6, IV 0.61–0.8, and V 0.81–1) and calculated the relative change in the aa‐CVM between 2000 to 2003 and 2016 to 2019. We used adjusted linear regression analyses to explore the association between a higher SVI and temporal aa‐CVM improvement; we studied this temporal change in aa‐CVM across subgroups of race, sex, and location. The median aa‐CVM rate (per 100 000) was 272.6 (interquartile range [IQR]: 237.5–311.7). The aa‐CVM was higher in men (315.6 [IQR: 273.4–363.9]) than women (221.3 [IQR: 189.6–256.7]), and in Black residents (347.2 [IQR: 301.1–391.1]; P <0.001) than White residents (258.9 [IQR: 226–299.1]; P <0.001). The aa‐CVM for SVI I (233.6 [IQR: 214.8–257.0]) was significantly lower than that of group V (323.6 [IQR: 277.2–359.2]; P <0.001). The relative reduction in CVM was significantly higher for SVI group I (32.2% [IQR: 24.2–38.4]) than group V (27.2% [IQR: 19–34.1]) counties. After multivariable adjustment, a higher SVI index was associated with lower relative improvement in the age‐adjusted CVM (model coefficient −3.11 [95% CI, −5.66 to −1.22]; P <0.001). Conclusions Socially deprived counties in the United States had higher aa‐CVM rates, and the improvement in aa‐CVM over the past 20 years was lower in these counties.

Aims Despite the common occurrence of coronary artery disease (CAD) and heart failure (HF) with preserved ejection fraction (HFpEF), there is limited evidence to guide revascularization. Methods and Results We investigated the long‐term outcomes of coronary artery bypass grafting (CABG) in patients with HF and significant CAD across the spectrum of ejection fraction, using a large national cohort of patients from the Veteran Affairs (VA) Medical Centers in the US. Patients with HF were stratified into groups, HFpEF, HF with mid‐range ejection fraction (HFmrEF), and HF with reduced ejection fraction (HFrEF) and compared to patients with no preoperative HF. We analysed 10 396 patients. Despite an increased hazard in the first year following revascularization, the long‐term survival (median follow‐up 6.6 years; interquartile range 3.7–10.1) of HFpEF post‐CABG was similar to controls (hazard ratio 0.85, 95% confidence interval 0.68‐1.06), but survival progressively declined with HFmrEF and HFrEF. Similar trends were seen with recurrent HF hospitalization with lower risk with baseline HFpEF (43.9 ± 6.9/100 patient‐years) compared to HFmrEF (65.9 ± 3.8/100 patient‐years) and HFrEF (93.4 ± 4.8/100 patient‐years). Although HFpEF patients had lower mortality and HF hospitalization post‐CABG compared to patients with a lower ejection fraction, they experienced the highest rates of future myocardial infarction. Conclusion Although HFpEF patients with CAD have greater short‐term risk post‐CABG, their long‐term survival is comparable to controls. However, they are at increased risk for HF hospitalizations and myocardial infarction. These data support the safety of CABG in HFpEF patients and suggest continuum of mortality risk for ischaemic HF when stratified by baseline ejection fraction before revascularization.

Abstract Here, we report a nanoparticle-based probe that affords facile cell labeling with cholesterol in cholesterol efflux (CE) assays. This probe, called ezFlux, was optimized through a screening of multiple nanoformulations engineered with a Förster resonance energy transfer (FRET) reporter. The physicochemical- and bio-similarity of ezFlux to standard semi-synthetic acetylated low-density lipoprotein (acLDL) was confirmed by testing uptake in macrophages, the intracellular route of degradation, and performance in CE assays. A single-step fast self-assembly fabrication makes ezFlux an attractive alternative to acLDL. We also show that CE testing using ezFlux is significantly cheaper than that performed using commercial kits or acLDL. Additionally, we analyze clinical trials that measure CE and show that ezFlux has a place in many research and clinical laboratories worldwide that use CE to assess cellular and lipoprotein function.

Abstract Vitamin A metabolite retinoic acid (RA) regulates life-sustaining differentiation processes and metabolic homeostasis. The aldehyde dehydrogenase-1 (Aldh1) family of enzymes (Aldh1a1, a2, and a3) catalyzes RA production from retinaldehyde and thereby controls concentrations of this transcriptionally active metabolite. The hierarchy of Aldh1 functions in adipose tissue has not been elucidated. We hypothesized that Aldh1 enzymes produce endogenous RA and regulate adipogenesis and fat formation in a fat depot-specific manner. We demonstrate that adipogenesis in vitro is accompanied by RA production generated primarily by Aldh1a1. In Aldh1a1-deficient adipocytes, adipogenesis is impaired compared with wild-type adipocytes due to markedly reduced expression of PPARγ regulated through zinc-finger protein 423 (ZFP423)-dependent mechanisms. These effects were recovered to some extent either by RA stimulation or overexpression of any of the Aldh1 enzymes in Aldh1a1−/− cells arguing that Aldh1a1 plays a dominant role in autocrine RA production. In vivo studies in C57/BL6 and Aldh1a1−/− mice on a regular diet revealed that multiple Aldh1 enzymes regulate differences in the formation of sc and visceral fat. In Aldh1a1−/− mice, visceral fat essentially lacked all Aldh1 expression. This loss of RA-producing enzymes was accompanied by 70% decreased expression of ZFP423, PPARγ, and Fabp4 in visceral fat of Aldh1a1−/−vs. wild-type mice and by the predominant loss of visceral fat. Subcutaneous fat of Aldh1a1−/− mice expressed Aldh1a3 for RA production that was sufficient to maintain expression of ZFP423 and PPARγ and sc fat mass. Our data suggest a paradigm for regulation of fat depots through the concerted action of Aldh1 enzymes that establish RA-dependent tandem regulation of transcription factors ZFP423 and PPARγ in a depot-specific manner.