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Fine particulate matter (PM 2.5 ) air pollution is a leading contributor to the global burden of cardiovascular disease (CVD). One important underlying mechanism is an increase in blood pressure (BP). A growing number of studies have reported a beneficial effect of portable air cleaners (PACs) on systolic and diastolic BP; SBP and DBP. We conducted an updated systematic review and meta-analysis of studies using true versus sham mode filtration reporting the effects on BP. Of 214 articles identified up to February 5, 2023, seventeen (from China, USA, Canada, South Korea and Denmark) enrolling approximately 880 participants (484 female) met the inclusion criteria for meta-analyses. Aside from studies conducted in China, research on PACs and BP has been conducted in relatively low pollution settings. Mean indoor PM 2.5 concentrations during the active and sham mode purification were 15.9 and 41.2 µg/m 3 , respectively. The mean efficiency of PACs against indoor PM 2.5 was 59.8 % (ranging from 23 % to 82 %). True mode filtration was associated with a pooled mean difference of - 2.35 mmHg (95 % confidence interval [CI]: - 4.5, - 0.2) and - 0.81 mmHg (95 % CI: - 1.86, 0.24) in SBP and DBP, respectively. After removing the studies with high risk of bias, the magnitude of the pooled benefits on SBP and DBP increased to - 3.62 mmHg (95 % CI: - 6.69, - 0.56) and - 1.35 mmHg (95 % CI: - 2.29, - 0.41), respectively. However, there are several barriers to the use of PACs, specifically in low- and middle-income countries (LMICs), such as the initial purchase cost and filter replacements. There may be several avenues to help overcome these economic burdens and improve cost effectiveness, such as implementing government or other subsidized programs to distribute PACs targeting vulnerable and higher-risk individuals. We propose that environmental health researchers and healthcare providers should be better trained to educate the public regarding the use of PACs to reduce the impacts of PM 2.5 on cardiometabolic diseases globally., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. It should be noted that Ryan W. Allen has conducted studies using PACs purchased at a discounted rate from Woongjin-Coway., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Epidemiological evidence on cardiometabolic health of particulate organic matter (POM) and its sources is sparse. In a panel of 73 healthy adults in Beijing, China, daily concentrations of ambient fine particulate matter-bound polycyclic aromatic hydrocarbons (PAHs) and n-alkanes were measured throughout the study period, and Positive Matrix Factorization approach was used to identity PAHs sources. Linear mixed-effect models and mediation analyses were applied to examine the associations and potential interlink pathways between POM and biomarkers indicative of hemodynamics, insulin resistance, vascular calcification and immune inflammation. We found that significant alterations in cardiometabolic measures were associated with POM exposures. In specific, interquartile range increases in PAHs concentrations at prior up to 9 days were observed in association with significant elevations of 2.6-2.9% in diastolic blood pressure, 6.6-8.1% in soluble ST2, 10.5-14.5% in insulin, 40.9-45.7% in osteoprotegerin, and 36.3-48.7% in interleukin-17A. Greater associations were generally observed for PAHs originating from traffic emissions and coal burning. Mediation analyses revealed that POM exposures may prompt the genesis of hemodynamic abnormalities, possibly via worsening insulin resistance and calcification potential. These findings suggested that cardiometabolic health benefits would be achieved by reducing PM from combustion emissions., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Household air pollution emitted from solid-fuel cookstoves used for domestic cooking is a leading risk factor for morbidity and premature mortality globally. There have been attempts to design and distribute lower emission cookstoves, yet it is unclear if they meaningfully improve health. Using a crossover design, we assessed differences in central aortic hemodynamics and arterial stiffness following controlled exposures to air pollution emitted from five different cookstove technologies compared to a filtered air control. Forty-eight young, healthy participants were assigned to six 2-h controlled treatments of pollution from five different cookstoves and a filtered air control. Each treatment had a target concentration for fine particulate matter: filtered air control = 0 μg/m 3 , liquefied petroleum gas = 10 μg/m 3 , gasifier = 35 μg/m 3 , fan rocket = 100 μg/m 3 , rocket elbow = 250 μg/m 3 , three stone fire = 500 μg/m 3 . Pulse wave velocity (PWV), central augmentation index (AIx), and central pulse pressure (CPP) were measured before and at three time points after each treatment (0, 3, and 24 h). Linear mixed models were used to assess differences in the outcomes for each cookstove treatment compared to control. PWV and CPP were marginally higher 24 h after all cookstove treatments compared to control. For example, PWV was 0.15 m/s higher (95% confidence interval: -0.02, 0.31) and CPP was 0.6 mmHg higher (95% confidence interval: -0.8, 2.1) 24 h after the three stone fire treatment compared to control. The magnitude of the differences compared to control was similar across all cookstove treatments. PWV and CPP had no consistent trends at the other post-treatment time points (0 and 3 h). No consistent trends were observed for AIx at any post-treatment time point. Our findings suggest higher levels of PWV and CPP within 24 h after 2-h controlled treatments of pollution from five different cookstove technologies. The similar magnitude of the differences following each cookstove treatment compared to control may indicate that acute exposures from even the cleanest cookstove technologies can adversely impact these subclinical markers of cardiovascular health, although differences were small and may not be clinically meaningful., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Background: Ambient air pollution has been associated with acute cardiovascular events; however, the underlying mechanisms remain incompletely understood. We aimed to examine the impacts of ambient air pollutants on cardiac ventricular repolarization in a highly polluted urban region., Methods: Seventy-three healthy non-smoking young adults (66% female, mean age of 23.3 ± 5.4 years) were followed with four repeated 24-h electrocardiogram recordings in 2014-2016 in Beijing, China. Continuous concentrations of ambient particulates in size fractions of 5-560 nm diameter, black carbon (BC), nitrogen dioxide (NO 2 ), carbon monoxide (CO), sulfur dioxide (SO 2 ), and ozone (O 3 ) were measured at a fixed-location air pollution monitoring station. Generalized linear mixed models, with adjustment for individual risk factors, time-varying factors and meteorological parameters, were used to evaluate the effects of air pollution on 5-min segments of heart rate-corrected QT interval (QTc), an index of cardiac ventricular repolarization., Results: During the study period, the mean levels of number concentrations of particulates in size range of 5-560 nm (PNC 5-560 ) were 20,711 particles/cm 3 . Significant increases in QTc of 0.56% (95% CI: 0.27, 0.84) to 1.76% (95% CI: 0.73, 2.79) were associated with interquartile range increases in PNC 50-560 at prior 1-5 moving average days. Significant increases in QTc were also associated with increases in exposures to traffic-related air pollutants (BC, NO 2 and CO), a combustion pollutant SO 2 , and the secondary pollutant O 3 . The associations were stronger in participants who were male, overweight, with abdominal obesity, and with higher levels of high-sensitivity C-reactive protein., Conclusions: Our findings suggest that exposures to higher levels of ambient particulates in small size fractions and traffic pollutants were associated with cardiac repolarization abnormalities in healthy adults, and the cardio-metabolic risks may modify the adverse cardiac effects attributable to air pollution., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Background: Household air pollution from cooking with solid fuels affects nearly 3 billion people worldwide and is responsible for an estimated 2.5 million premature deaths and 77 million disability-adjusted life years annually. Investigating the effect of household air pollution on indicators of cardiometabolic disease, such as metabolic syndrome, can help clarify the pathways between this widespread exposure and cardiovascular diseases, which are increasing in low- and middle-income countries., Methods: Our cross-sectional study of 150 women in rural Honduras (76 with traditional stoves and 74 with cleaner-burning Justa stoves) explored the effect of household air pollution exposure on cardiovascular disease risk factors. Household air pollution was measured by stove type and 24-h average kitchen and personal fine particulate matter [PM 2.5 ] mass and black carbon concentrations. Health endpoints included non-fasting total cholesterol, high-density lipoprotein, calculated low-density lipoprotein, triglycerides, waist circumference to indicate abdominal obesity, and presence of metabolic syndrome (defined by current modified international guidelines: waist circumference ≥ 80 cm plus any two of the following: triglycerides > 200 mg/dL, HDL < 50 mg/dL, systolic blood pressure ≥ 130 mmHg, diastolic blood pressure ≥ 85 mmHg, or glycated hemoglobin > 5.6%)., Results: Forty percent of women met the criteria for metabolic syndrome. The prevalence ratio [PR] for metabolic syndrome (versus normal) per interquartile range increase in kitchen PM 2.5 and kitchen black carbon was 1.16 (95% confidence interval [CI]: 1.01-1.34) per 312 μg/m 3 increase in PM 2.5 , and 1.07 (95% CI: 1.03-1.12) per 73 μg/m 3 increase in black carbon. There is suggestive evidence of a stronger effect in women ≥ 40 years of age compared to women < 40 (p-value for interaction = 0.12 for personal PM 2.5 ). There was no evidence of associations between all other exposure metrics and health endpoints., Conclusions: The prevalence of metabolic syndrome among our study population was high compared to global estimates. We observed a suggestive effect between metabolic syndrome and exposure to household air pollution. These results for metabolic syndrome may be driven by specific syndrome components, such as blood pressure. Longitudinal research with repeated health and exposure measures is needed to better understand the link between household air pollution and indicators of cardiometabolic disease risk., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Low high-density lipoprotein cholesterol (HDL-C) can be caused by several acquired secondary causes as well as primary genetic disorders. However, only a few conditions are associated with profoundly reduced levels below 10 mg/dL. We present an unusual case of a healthy man with severely decreased HDL-C because of a novel homozygous variant causing a Proline > Arginine amino acid change at position 1412 in the ATP-binding cassette transporter A1 gene. Homozygous variations in ATP-binding cassette transporter A1 typically cause Tangier disease, a rare autosomal recessive condition linked with several other abnormalities (eg, enlarged discolored tonsils). Despite having an HDL-C below 10 mg/dL, our patient presented without any other clinical symptoms or physical signs suggestive of Tangier disease. This case of presumptive Tangier disease adds support to the growing body of evidence that this genetic disorder may have greater phenotypic heterogeneity along with a more varied presentation than traditionally considered., (Copyright © 2018 National Lipid Association. Published by Elsevier Inc. All rights reserved.)

Ambient air pollution is an independent risk factor for cardiovascular diseases. However, the underlying mechanisms have yet to be fully elucidated. We performed a panel study on 65 nonsmoking patients with metabolic syndrome, with four repeated clinical visits between 2012 and 2013 in Beijing, China. Cardiac and central aortic hemodynamic parameters were measured by pulse wave analyses as subendocardial viability ratio, ejection duration, and central aortic pressure. We also calculated rate-pressure product parameter and collected peripheral blood for analyses. High levels of ambient particulate matter with diameter ≤10 and 2.5 μm (PM 10 and PM 2.5 ), black carbon, sulfur dioxide, and nitrogen dioxide were 121.3, 99.5, 6.5, 24.5, and 59.2 μg/m 3 , respectively. Short- to medium-term exposures to high levels of ambient air pollution adversely impacted central hemodynamics-derived surrogates of myocardial perfusion and oxygen demand. Each 10 μg/m 3 increase in PM 2.5 was associated with significant decreases of 0.67% (95% confidence interval: -2.84, -0.22) in subendocardial viability ratio at moving average 35 days (MA35) and an increase of 0.31 in rate-pressure product (95% confidence interval: 0.03, 0.59) at MA5. In conclusion, our results suggest that impaired myocardial perfusion and increased myocardial oxygen demand may play importantly mechanistic roles in air pollution-attributed cardiovascular diseases., (Copyright © 2017 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Environmental temperatures influence cardiovascular physiology. However, the majority of time is spent indoors, making outdoor-ambient temperatures inaccurate estimates of true exposures encountered by most individuals. We evaluated in 50 healthy adults the associations between previous 7-day outdoor-ambient (four occasions) and prior 24-hour personal-level (two occasions) environmental temperature exposures with blood pressure, heart rate variability, sleep parameters, and endothelial-dependent vasodilatation (brachial flow-mediated dilatation [FMD]) using generalized estimating equations. Participants (34 females; age, 32.1 ± 9.6 years) had normal blood pressures (107.8 ± 13.3/70.2 ± 9.4 mm Hg), FMD (7.4 ± 2.8%), as well as sleep and heart rate variability parameters. Mean 7-day outdoor-ambient (4.6 ± 9.7°C) differed from personal-level temperature exposures (22.0 ± 3.0°C). Colder outdoor-ambient temperatures (per -10°C) over the previous 1-6 days (rolling averages) were associated with decreases in FMD: -0.57% (95% confidence interval [CI]: -1.14% to 0.01%, P = .055) to -0.62% (95% CI: -1.07% to -0.18%, P = .006). However, a 10°C decrease in personal-level temperature during the prior 24 hours was associated with a greater decrement in FMD: -2.44% (95% CI: -4.74% to -0.13%, P = .038). Both were also linearly related to FMD during all seasons and without a threshold temperature. Other end points were not significantly related to either temperature level in this study. Short-term exposures to colder environmental temperatures reduced endothelial-dependent vasodilatation, supporting the epidemiologic associations with heightened cardiovascular risk. We show here for the first time that temperature exposures characterized at the personal level may be more robust predictors of endothelial function than outdoor-ambient levels., (Copyright © 2017 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Rationale: Pneumonia risk with inhaled corticosteroid use in chronic obstructive pulmonary disease (COPD) has not been thoroughly assessed in patients with moderate airflow limitation., Objectives: To determine the incidence of pneumonia and risk factors in COPD patients with moderate airflow limitation who had, or were at high risk for cardiovascular disease., Methods: In the Study to Understand Mortality and MorbidITy in COPD (SUMMIT), 16,590 subjects with moderate airflow limitation (50% ≤ FEV 1  ≤ 70% predicted) and heightened cardiovascular risk were randomized double-blind 1:1:1:1 to inhaled once-daily vilanterol 25 μg (VI), fluticasone furoate 100 μg (FF), vilanterol 25 μg combined with 100 μg fluticasone furoate (FF/VI), or matched placebo. In a pre-specified analysis, we assessed investigator-reported adverse pneumonia events, and independently-adjudicated fatal events., Measurements and Main Results: The safety population comprised 16,568 subjects who actually received study medication. There were 1017 pneumonia events reported from 842 subjects. For placebo, FF, VI and FF/VI, reported pneumonia incidence was 5%, 5%, 4% and 6%, respectively. When adjusted for time on treatment, event rates were similar in the placebo, FF and FF/VI containing arms (3.84, 4.24 and 3.95/100 treatment years, respectively) but lower in the VI group (2.77/100 treatment years). Risk factors for pneumonia risk included: greater degree of airflow limitation (i.e. FEV 1 <60% predicted), prior exacerbation history, and BMI <25 kg/m 2 ., Conclusions: In contrast to previous studies in patients with severe disease, increased pneumonia risk with inhaled corticosteroid use was not evident in COPD subjects with moderate airflow limitation and heightened cardiovascular risk., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

A host of environmental factors can significantly increase arterial blood pressure (BP) including cold temperature, high altitude, loud noises, and ambient air pollutants. Although brief exposures acutely elevate BP, over the long term, chronic exposures may be capable of promoting the development of sustained hypertension. Given their omnipresent nature, environmental factors may play a role in worsening BP control and heightening overall cardiovascular risk at the global public health level., (Copyright © 2016 Elsevier Inc. All rights reserved.)

While laboratory studies show that air pollutants can potentiate insulin resistance, the epidemiologic evidence regarding the association of air pollution with diabetes incidence is conflicting. The purpose of the present study was to assess the association of the traffic-related nitrogen dioxide (NO2) with the incidence of diabetes in a longitudinal cohort study of African American women. We used Cox proportional hazards models to calculate hazard ratios and 95% confidence intervals (CI) for diabetes associated with exposure to NO2 among 43,003 participants in the Black Women's Health Study (BWHS). Pollutant levels at participant residential locations were estimated with 1) a land use regression model for participants living in 56 metropolitan areas, and 2) a dispersion model for participants living in 27 of the cities. From 1995 to 2011, 4387 cases of diabetes occurred. The hazard ratios per interquartile range of NO2 (9.7 ppb), adjusted for age, metropolitan area, education, vigorous exercise, body mass index, smoking, and diet, were 0.96 (95% CI 0.88-1.06) using the land use regression model estimates and 0.94 (95% CI 0.80, 1.10) using the dispersion model estimates. The present results do not support the hypothesis that exposure to NO2 contributes to diabetes incidence in African American women., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Background: Chronic obstructive pulmonary disease (COPD) often coexists with cardiovascular disease. Treatments for airflow limitation might improve survival and both respiratory and cardiovascular outcomes. The aim of this study was to assess whether inhaled treatment with a combined treatment of the corticosteroid, fluticasone furoate, and the long-acting β agonist, vilanterol could improve survival compared with placebo in patients with moderate COPD and heightened cardiovascular risk., Methods: In this double-blind randomised controlled trial (SUMMIT) done in 1368 centres in 43 countries, eligible patients were aged 40-80 years and had a post-bronchodilator forced expiratory volume in 1 s (FEV1) between 50% and 70% of the predicted value, a ratio of post-bronchodilator FEV1 to forced vital capacity (FVC) of 0·70 or less, a smoking history of at least 10 pack-years, and a score of 2 or greater on the modified Medical Research Council dyspnoea scale. Patients had to have a history, or be at increased risk, of cardiovascular disease. Enrolled patients were randomly assigned (1:1:1:1) through a centralised randomisation service in permuted blocks to receive once daily inhaled placebo, fluticasone furoate (100 μg), vilanterol (25 μg), or the combination of fluticasone furoate (100 μg) and vilanterol (25 μg). The primary outcome was all-cause mortality, and secondary outcomes were on-treatment rate of decline in forced expiratory volume in 1 s (FEV1) and a composite of cardiovascular events. Safety analyses were performed on the safety population (all patients who took at least one dose of study drug) and efficacy analyses were performed on the intention-to-treat population (safety population minus sites excluded with Good Clinical Practice violations). This study is registered with ClinicalTrials.gov, number NCT01313676., Findings: Between Jan 24, 2011, and March 12, 2014, 23 835 patients were screened, of whom 16 590 were randomised. 16 485 patients were included in the intention-to-treat efficacy population; 4111 in the placebo group, 4135 in the fluticasone furoate group, 4118 in the vilanterol group, and 4121 in the combination group. Compared with placebo, all-cause mortality was unaffected by combination therapy (hazard ratio [HR] 0·88 [95% CI 0·74-1·04]; 12% relative reduction; p=0·137) or the components (fluticasone furoate, HR 0·91 [0·77-1·08]; p=0·284; vilanterol, 0·96 [0·81-1·14]; p=0·655), and therefore secondary outcomes should be interpreted with caution. Rate of decline in FEV1 was reduced by combination therapy (38 mL per year [SE 2·4] vs 46 mL per year [2·5] for placebo, difference 8 mL per year [95% CI 1-15]) with similar findings for fluticasone furoate (difference 8 mL per year [95% CI 1-14]), but not vilanterol (difference -2 mL per year [95% CI -8 to 5]). Combination therapy had no effect on composite cardiovascular events (HR 0·93 [95% CI 0·75-1·14]) with similar findings for fluticasone furoate (0·90 [0·72-1·11]) and vilanterol (0·99 [0·80-1·22]). All treatments reduced the rate of moderate and severe exacerbation. No reported excess risks of pneumonia (5% in the placebo group, 6% in the combination group, 5% in the fluticasone furoate group, and 4% in the vilanterol group) or adverse cardiac events (17% in the placebo group, 18% in the combination group, and 17% in the fluticasone furoate group, and 17% in the vilanterol group) were noted in the treatment groups., Interpretation: In patients with moderate COPD and heightened cardiovascular risk, treatment with fluticasone furoate and vilanterol did not affect mortality or cardiovascular outcomes, reduced exacerbations, and was well tolerated. Fluticasone furoate, alone or in combination with vilanterol, seemed to reduce FEV1 decline., Funding: GlaxoSmithKline., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Particulate matter (PM) air pollution is a leading global risk factor for cardiovascular mortality. Although exposure to fine PM <2.5 μm raises arterial blood pressure (BP), few studies have evaluated the impact of coarse PM which differs in size (2.5-10 μm), sources, and chemistry. Twenty-nine healthy adults (30.4 ± 8.2 years) underwent a randomized double-blind crossover study involving 2-hour exposures to concentrated ambient coarse PM (164.2 ± 80.4 μg/m(3)) at an urban location (Dearborn, Michigan) versus filtered air. Cardiovascular outcomes were measured during, immediately, and 2 hours after exposures. Both systolic (1.9 mm Hg; 95% confidence interval: 0.96, 2.8; P < .001) and diastolic (1.9 mm Hg; 95% confidence interval: 1.1, 2.7; P < .001) BP levels were higher throughout coarse PM compared with filtered air exposures by mixed-model analyses. Heart rate variability, endothelial function, and arterial compliance were not significantly affected. Brief exposure to coarse PM in an urban environment raises arterial BP. These findings add mechanistic support to the contention that coarse PM may be capable of promoting cardiovascular events., (Copyright © 2016 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Coronary artery calcium (CAC) is a powerful independent predictor of future cardiovascular events. However, the clinical utility of calcium score testing specifically among patients with hypertension is not well defined. We performed a review of studies involving both high blood pressure (BP) and CAC to assess several aspects of the interrelationship. Among four specific topics evaluated, the main objective was to assess the independent association of CAC with cardiovascular risk among patients with hypertension. From 6822 identified publications, 21 studies met criteria for inclusion. All studies (n = 14) that reported the relationship between BP values and the presence or extent of coronary calcium found positive associations. The results from two studies linking coronary calcium with the risk for developing hypertension were mixed. Each of the five studies that evaluated the relationships between CAC score in regard to future cardiovascular events and/or all-cause mortality in patients with high BP reported independent positive associations. The inclusion of calcium score results into prediction models improved risk stratification when statistically evaluated. The findings of this review demonstrate that CAC testing is likely to be of clinical utility for tailoring the medical management of patients with high BP, particularly among individuals with mild or prehypertension. Future trials testing the clinical effectiveness of a calcium score-based treatment algorithm should be considered., (Copyright © 2015 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Background: Patients with refractory severe hypertriglyceridemia are at risk of pancreatitis and cardiovascular disease. The role of individualized nutrition therapy in these patients independent of pharmaceutical treatment has not been documented., Objective: To document the effect of nutrition intervention on severe hypertriglyceridemia regardless of medication status or prior nutrition counseling., Methods: Outcomes of new patients with triglycerides ≥ 500 mg/dL presenting to a Lipid Management Program over a 6-year period were tracked. Patients received comprehensive laboratory assessment, nutrition assessment, and initiation of an individualized diet intervention before seeing the lipidologist. Clinical and behavioral outcomes were recorded., Results: In all, 168 patients (117 men; mean age, 49.03 ± 11.22 years; body mass index, 32.61 ± 5.85 kg/m(2); 110 (65.5%) on lipid-lowering medications) returned for assessment of nutrition intervention. Triglycerides were reduced from median (interquartile range) 961.5 (611.5-1785.3) to 493.0 (337-736.3) mg/dL (P < .0001 for log transformation of triglycerides). There was no difference in median percentage reduction in triglycerides after nutrition intervention between those not on lipid-lowering medication, on a fibric acid derivative, on other lipid-lowering medication, or on a combination of lipid-lowering medications (P = .376) in a median (interquartile range) of 5 (3-7) weeks. Effect was independent of prior nutrition counseling (P = .260). Reported percentage fat in the diet at second visit correlated with log-transformed triglycerides achieved, independent of initial triglycerides level (r = 0.290; P = .001)., Conclusions: Individualized nutrition therapy results in changes in eating behavior and reductions in triglyceride levels in patients with refractory severe hypertriglyceridemia independent of lipid-lowering medication(s) and prior nutrition counseling., (Copyright © 2015 National Lipid Association. Published by Elsevier Inc. All rights reserved.)

Hypertension guidelines recommend following published standardized protocols to obtain accurate blood pressure (BP) readings in clinical practice. However, the various measurement techniques among clinical trials that provide the basis for evidence-based management have not been evaluated or compared with guideline recommendations. We reviewed published information regarding BP measurement in clinical trials (n = 64) from 1990-2014 by searching PubMed and Google Scholar databases. Every trial failed to provide published information regarding at least one of the 10 methodological aspects we evaluated. Details regarding the health-care provider(s) performing measurement(s), temporal-relation to last medication dosage, number of readings, resting time before (and between recordings), and the device(s) used varied among the trials and often differed from clinical recommendations. Most studies did evaluate ≥2 BP readings in a seated position, presumably from the upper arm (although explicit acknowledgment of this latter detail was rare). When indicated, "trough" BP levels were most commonly obtained (15 of 16 trials), whereas the usage of automated devices increased over time. Numerous aspects of BP measurement varied considerably across trials and often from most recent guideline recommendations. The lack of uniform methodologies in outcome studies that form the foundation of evidence-based guidelines may have significant clinical implications., (Copyright © 2014 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Epidemiological studies suggest that fine particulate matter (PM2.5) may increase the risk for developing diabetes mellitus (DM). To evaluate possible mechanisms explaining these associations, we investigated if sub-acute ambient-level exposures can impair insulin sensitivity. Twenty-five healthy adults living in rural Michigan were transported to an urban location for 5 consecutive days (exposure-block) of daily 4- to 5-hour-long ambient air pollution exposures. Health outcomes, including the homeostasis model assessment of insulin resistance (HOMA-IR) the primary outcome of insulin sensitivity, were measured at 3 time points in relation to exposure-blocks: 7days prior to start; on the last exposure-day; and 7days after completion. PM2.5 was monitored at the urban exposure site and at community monitors near subjects' residences. We calculated 3 "sub-acute" exposure periods (approximately 5-days-long) starting retrospective from the time of health outcome measurements (PM2.5 ranges: 9.7±3.9 to 11.2±3.9μg·m(-3)). A 10μg·m(-3) increase in sub-acute PM2.5 exposures was associated with increased HOMA-IR (+0.7, 95% confidence interval (CI) 0.1 to 1.3; p=0.023) and reduced heart rate variability (standard deviation of normal-to-normal intervals [-13.1ms, 95%CI -25.3 to -0.9; p=0.035]). No alterations in other outcomes (inflammatory markers, vascular function) occurred in relation to PM2.5 exposures. Our findings suggest that ambient PM2.5, even at low levels, may reduce metabolic insulin sensitivity supporting the plausibility that air pollution could potentiate the development of DM., (Copyright © 2012 Elsevier B.V. All rights reserved.)

There is a paucity of prospective cohort studies investigating the impact of environmental factors on the development of cardiometabolic (CM) disorders like type II diabetes (T2DM). The objective of the Air-Pollution and Cardiometabolic Diseases (AIRCMD) study is to investigate the impact of personal level air pollution measures [personal black carbon (BC)/sulfate measures] and ambient fine particulate matter [(PM2.5)/NO2] levels on propensity to type II diabetes in Beijing, China. Subjects with metabolic syndrome will undergo four repeated study visits within each season over a one year period following an initial screening visit. At each study visit, subjects will be monitored for sub-acute exposure to personal and ambient measures of air-pollution exposure and will undergo a series of functional CM outcomes. The primary endpoints include independent associations between integrated 5-day mean exposure to PM2.5 and BC and homeostasis model assessment of insulin resistance (HOMA-IR) measures, 24-hour mean diastolic and mean arterial pressure and endothelial-dependent vasodilatation. The secondary endpoints will explore the mechanistic explanation for a causal relationship between exposures and propensity for type II diabetes and will include additional functional outcomes such as arterial compliance, heart rate variability and plasma adipokines. The novel aspects of the study include the launch of infrastructure for future translational investigations in highly polluted urbanized environments and the creation of novel methodologies for linking personalized exposure measurements with functional CM outcomes. We believe that AIRCMD will allow for unprecedented new investigations into the association between environmental risk factors and CM disorders., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Background: Numerous studies have reported associations between air pollution and cardiovascular diseases. While several studies illustrate that exposures to air pollutants can elevate blood pressure, few have evaluated the clinical relevance of this relationship. Hence, we aimed to explore the associations between daily concentrations of several air pollutants and emergency department visits for hypertension., Methods: Odds ratios (ORs) for emergency department visits for hypertension in Edmonton, Canada, from April 1992 to March 2002 were associated with pollutant levels (CO, NO(2), SO(2), O(3), and particulate matter [PM] < 10 microns [PM(10)] and < 2.5 microns [PM(2.5)] in aerodynamic diameter, respectively) by means of a case-crossover technique with time-stratified strategy to define controls. The analysis was performed for all (N = 5365), male (N = 2069), and female (N = 3296) patients and for six air pollutants lagged by 0 to 9 days. ORs and their 95% confidence intervals (CIs) were reported for an increase in an interquartile range (IQR) for each pollutant., Results: We observed associations for all patients and levels of NO(2) (IQR = 12.8 parts per billion; OR, 1.06; 95% CI, 1.00-1.12), SO(2) (IQR = 2.3 parts per billion; OR, 1.04; 95% CI, 1.00-1.08), and PM(10) (IQR = 15.0 μg/m(3); OR, 1.06; 95% CI, 1.01-1.11) for lag day 3, as well as for PM(10) (IQR = 15.0 μg/m(3); OR, 1.06; 95% CI, 1.01-1.11) and PM(2.5) (IQR = 6.2 μg/m(3); OR, 1.07; 95% CI, 1.01-1.11) for lag day 6., Conclusions: These findings support the contention that ambient pollution can produce clinically meaningful increases in blood pressure., (Copyright © 2012 Canadian Cardiovascular Society. All rights reserved.)

Background: Lipoprotein (a) [Lp(a)] has a strong association with coronary disease (CHD). We evaluated the implications of implementing a niacin strategy in persons above low risk by the Framingham risk score (FRS)., Methods: Patients referred to a university lipid management program from January 2004 to June 2010 had an Lp(a) level measured at initial evaluation. Factors associated with an increase in Lp(a) and predictors of a high risk Lp(a) (≥50 mg/dL) were assessed. FRS and Lp(a) levels were used to assess eligibility for niacin with an Lp(a) ≥50 mg/dL., Results: A total of 692 patients (57% male, mean age 52 ± 14 years) had a mean Lp(a) of 32 ± 40 mg/dL. In a multiple logistic regression model, African-American race, female gender, presence of CHD, and lower triglyceride levels were significant predictors of high risk Lp(a). Ten percent were determined to be intermediate and 44% high risk by FRS. A total of 9% of intermediate- and 26% of high-risk patients had an Lp(a) ≥50 mg/dL, and 84% were not taking niacin. A total of 19% of moderate- and high-risk patients were eligible for initiation of niacin based upon values ≥50 mg/dL. If niacin were also used for an high-density lipoprotein cholesterol levels ≤40 mg/dL, only 5.1% additional patients would require niacin., Conclusion: High-risk levels of Lp(a) are associated with female gender, African- American race, and CHD. 19% of moderate and high risk patients would be candidates for treatment with niacin if the indication is a cutpoint Lp(a) ≥50 mg/dL., (Copyright © 2012 National Lipid Association. Published by Elsevier Inc. All rights reserved.)

Intermittent claudication (IC) due to peripheral arterial disease (PAD) causes substantial impairment in quality of life, and is strongly associated with increased cardiovascular morbidity and mortality. The overall medical approach to management focuses on reducing cardiovascular events, preventing progression of underlying PAD (eg, limb loss), and improving symptoms. Aggressive secondary prevention strategies (eg, statins and smoking cessation) are of critical importance. Cilostazol treatment should be considered for those with persistent IC symptoms despite exercise and risk factor control. Management of IC requires a comprehensive approach toward symptomatic relief of pain with strategies that prolong life and prevent limb loss., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Background: Apolipoprotein-B/A-1 (apoB/A-R) and total/high-density lipoprotein-cholesterol ratios (TC/HDL-R) outperform non-high-density lipoprotein-cholesterol (non-HDL-C) suggested by Adult Treatment Panel (ATP) III guidelines for predicting cardiovascular (CV) outcomes., Objective: To evaluate the potential effects that implementing our proposed apoB/A-R and TC/HDL-R treatment algorithms would have on clinical management., Methods: We performed a chart review of all patients referred to the University of Michigan Lipid Clinic from January 2004 to June 2010. ATP III guidelines, including Framingham Risk Scores, were used to determine whether patients met non-HDL-C goals upon referral. Next, we evaluated whether subsequent management would differ if algorithms based upon potential apoB/A-R or TC/HDL-R targets derived from the literature were followed., Results: Among patients (n = 692), mean non-HDL-C, apoB/A-R, and TC/HDL-R were 192.2 ± 85.8 mg/dL, 0.92 ± 0.64, and 6.7 ± 8.0, respectively. Although moderately well correlated with apoB (r = 0.56, P < .01), non-HDL-C was less related to apoB/A-R (r = 0.20, P < .01) and TC/HDL-R (r = 0.39, P < .01). Most low-risk patients (<2 risk factors; n = 207) at non-HDL-C goal (<190 mg/dL) also met apoB/A-R <0.9 (79%) and TC/HDL-R <6.0 (92%) targets. However, a minority of high-risk patients (Framingham Risk Score >20%, cardiovascular disease or risk equivalent; n = 307) meeting non-HDL-C goal (<130 mg/dL) achieved targets for apoB/A-R <0.5 (21%) or TC/HDL-C <3.5 (42%). The percentages of intermediate-risk patients meeting both non-HDL-C and ratio goals varied; nonetheless, few met an aggressive apoB/A-R <0.6 (36%-50%) target., Conclusions: Most high- and many intermediate-risk patients at non-HDL-C goals would require more aggressive treatment to reach the suggested apoB/A-R or TC/HDL-R targets. Whether this strategy yields superior outcomes merits future investigation., (Copyright © 2011 National Lipid Association. Published by Elsevier Inc. All rights reserved.)

A short-term increase in fine particulate matter air pollution (PM(2.5)) concentration increases the risk for myocardial infarctions, strokes, and heart failure exacerbations. An important mechanism likely contributing to these associations is an elevation in arterial blood pressure (BP). Exposure to ambient PM(2.5) even at present-day concentrations can increase BP within a period of a few days while long-term exposure might also promote the development of chronic hypertension. Controlled human and animal experiments have corroborated the veracity of these findings and elucidated plausible biological mechanisms. PM(2.5) deposition within the pulmonary tree is capable of rapidly triggering autonomic nervous system imbalance, thereby increasing BP within minutes of inhalation. In addition, fine particles can instigate a systemic pro-inflammatory response over a more prolonged period of exposure. Higher circulating levels of activated immune cells and inflammatory cytokines could consequently cause vascular endothelial dysfunction leading to an imbalance in vascular homeostatic responses. Indeed, chronic PM(2.5) exposure augments pro-vasoconstrictive pathways while blunting vasodilator capacity. Finally, certain particle constituents (e.g., metals, organic compounds, and ultra-fine particles) might also be capable of reaching the systemic circulation upon inhalation and thereafter directly impair vascular function. At the molecular level, the generation of oxidative stress with the consequent up-regulation of redox sensitive pathways appears to be a common and fundamental mechanism involved in the instigation of these pro-hypertensive responses. Due to the ubiquitous, continuous and often involuntary nature of exposure, PM(2.5) may be an important and under-appreciated worldwide environmental risk factor for increased arterial BP.

Women with systemic lupus erythematosus (SLE) are at risk for premature atherothrombosis independent of Framingham risk factors. We investigated whether endothelial cell (EC) apoptosis predicts abnormal vasomotor tone and contributes to circulating tissue factor (TF) levels in this disease. Brachial artery flow-mediated dilation (FMD) and nitroglycerin-mediated dilation were determined in women with SLE, healthy control subjects, and subjects with coronary artery disease (CAD) (n = 43/group). Quantification of circulating apoptotic ECs was performed by flow cytometry (CD146(+) cells that stained for Annexin V [CD146(AnnV+)]) and immunofluorescent microscopy. Plasma TF was measured by enzyme-linked immunosorbent assay (ELISA). Compared with healthy control and CAD subjects, patients with SLE had higher numbers of circulating CD146(AnnV+) cells (10 +/- 3, 18 +/- 5, and 89 +/- 32 cells/mL, respectively, mean +/- SEM; P <.01). Increased CD146(AnnV+) cells correlated strongly with abnormal vascular function (P =.037). After adjusting for known predictors of endothelial function, CD146(AnnV+) was the only variable that predicted FMD (beta = -4.5, P <.001). Increased CD146(AnnV+) was strongly associated with elevated levels of circulating TF (r =.46, P =.002). Circulating apoptotic ECs are elevated in young women with SLE and strongly correlate with markedly abnormal vascular function and elevated TF levels. Heightened endothelial apoptosis may represent an important mechanism for development of atherothrombosis in SLE.

Medical management of PAD is a considerable challenge. Although patients typically present with IC, there is a substantial pool of subclinical PAD patients. PAD, whether symptomatic or not, confers a marked cardiovascular risk; with affected patients dying of heart attack or stroke, identification of index patients and aggressive medical treatment can offer health benefits far in excess of improvement in IC or related symptoms. Management of risk factors, lifestyle interventions, and pharmacologic treatment with agents to provide symptomatic relief have a central role in improving function and quality of life and slowing the progression to advanced endpoints, such as the rest pain, nonhealing ulcers, gangrene, and cardiac death. Surgical or percutaneous revascularization for aorto-iliac disease provides durable treatment for individuals with disabling symptoms. Newer treatments, such as angiogenic growth factor treatments, are being tested in clinical trials and seem promising. There are limited treatment choices for individuals with predominant infra-popliteal disease. In the future, the availability of newer stents and therapies to prevent re-stenosis may extend the applicability of endovascular treatment to difficult-to-treat infra-inguinal lesions.