Objective
To evaluate the role of early-life exposure to airborne fine particulate matter (diameter, <2.5 µm [PM2.5]) pollution on metabolic parameters, inflammation, and adiposity; and to investigate the involvement of oxidative stress pathways in the development of metabolic abnormalities.
Methods and Results
PM2.5 inhalation exposure (6 h/d, 5 d/wk) was performed in C57BL/6 mice (wild type) and mice deficient in the cytosolic subunit of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase p47phox (p47phox−/−) beginning at the age of 3 weeks for a duration of 10 weeks. Both groups were simultaneously fed a normal diet or a high-fat diet for 10 weeks. PM2.5-exposed C57BL/6 mice fed a normal diet exhibited metabolic abnormalities after exposure to PM2.5 or FA for 10 weeks. Consistent with insulin resistance, these abnormalities included enlarged subcutaneous and visceral fat contents, increased macrophage infiltration in visceral adipose tissue, and vascular dysfunction. Ex vivo–labeled and infused monocytes demonstrated increased adherence in the microcirculation of normal diet– or high-fat diet–fed PM2.5-exposed mice. p47phox−/− mice exhibited an improvement in parameters of insulin resistance, vascular function, and visceral inflammation in response to PM2.5.
Conclusion
Early-life exposure to high levels of PM2.5 is a risk factor for subsequent development of insulin resistance, adiposity, and inflammation. Reactive oxygen species generation by NADPH oxidase appears to mediate this risk.
A growing number of extreme climate events are occurring in the setting of ongoing climate change, with an increase in both the intensity and frequency. It has been shown that ambient temperature challenges have a direct and highly varied impact on cardiovascular health. With a rapidly growing amount of literature on this issue, we aim to review the recent publications regarding the impact of cold and heat on human populations with regard to cardiovascular disease (CVD) mortality/morbidity while also examining lag effects, vulnerable subgroups, and relevant mechanisms. Although the relative risk of morbidity/mortality associated with extreme temperature varied greatly across different studies, both cold and hot temperatures were associated with a positive mean excess of cardiovascular deaths or hospital admissions. Cause-specific study of CVD morbidity/mortality indicated that the sensitivity to temperature was disease-specific, with different patterns for acute and chronic ischemic heart disease. Vulnerability to temperature-related mortality was associated with some characteristics of the populations, including sex, age, location, socioeconomic condition, and comorbidities such as cardiac diseases, kidney diseases, diabetes, and hypertension. Temperature-induced damage is thought to be related to enhanced sympathetic reactivity followed by activation of the sympathetic nervous system, renin-angiotensin system, as well as dehydration and a systemic inflammatory response. Future research should focus on multidisciplinary adaptation strategies that incorporate epidemiology, climatology, indoor/building environments, energy usage, labor legislative perfection, and human thermal comfort models. Studies on the underlying mechanism by which temperature challenge induces pathophysiological response and CVD await profound and lasting investigation.
The aims of this analysis were to characterize the burden and timing of bleeding events in females versus males on left ventricular assist device (LVAD) support. A single-center retrospective review of 375 patients receiving continuous-flow LVADs was performed. Bleeding events included gastrointestinal, naso-oropharyngeal, gynecologic (GYN), intracranial hemorrhage (ICH), and mediastinal bleeding. Cox hazard ratios (HRs) [95% CI] and incident event rates for females versus males were calculated. Eighty-four females (22%) and 291 males (78%) received an LVAD. There were 189 patients with 406 bleeding events over a median 399 days of support. Two-year freedom from bleeding was 33 ± 6.2% in females and 46 ± 3.7% in males (p = 0.027). Correlates of bleeding included female sex (adjusted HR = 1.6 [1.1-2.2]) and older age (adjusted HR = 1.2 [1.1-1.3] per 10 years). There was no sex-associated difference in 30 day mediastinal bleeding (males 12%; females 16% at 30 days; overall p = 0.35), but incident event rates for overall bleeding and naso-oropharyngeal bleeding were higher in females (p < 0.05) and trends were noted in ICH (eppy: 0.06 male vs. 0.10 female, p = 0.14). Eight females (10%) experienced 12 GYN bleeding events; five required surgical intervention. In summary, females had a 60% higher hazard of bleeding than males with significant morbidity encountered from mucosa (including vaginal) bleeding. Future large device studies should be inclusive of sex-specific outcomes.
A 55-year-old patient was found to have complete heart block during preoperative assessment. Cardiac magnetic resonance imaging revealed an interatrial mass suggestive of primary cardiac tumor. Extensive evaluation including intracardiac biopsy and finally open resection revealed lipomatous hypertrophy masquerading as tumor. (
Level of Difficulty: Intermediate.
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