Acute effects of ambient particulate matter on blood pressure: differential effects across urban communities.

Recent studies have suggested a link between exposure to ambient particulate matter <2.5 microm in diameter (PM(2.5)) and adverse cardiovascular outcomes.

Ambient air pollution exaggerates adipose inflammation and insulin resistance in a mouse model of diet-induced obesity.

Background: There is a strong link between urbanization and type 2 diabetes mellitus. Although a multitude of mechanisms have been proposed, there are no studies evaluating the impact of ambient air pollutants and the propensity to develop type 2 diabetes mellitus. We hypothesized that exposure to ambient fine particulate matter (<2.

Cardiovascular effects of air pollution.

Air pollution is a heterogeneous mixture of gases, liquids and PM (particulate matter). In the modern urban world, PM is principally derived from fossil fuel combustion with individual constituents varying in size from a few nanometres to 10 microm in diameter. In addition to the ambient concentration, the pollution source and chemical composition may play roles in determining the biological toxicity and subsequent health effects.

Cardiovascular risk, obesity, and myocardial blood flow in postmenopausal women.

Background: This study was designed to determine whether overweight or obese status is independently associated with myocardial flow reserve (MFR), an established predictor of cardiovascular mortality, in a group of postmenopausal women with no previous cardiovascular disease. Postmenopausal women are the largest group of overweight and physically inactive individuals in the United States. Increased body mass index (BMI) is consistently associated with increased cardiovascular mortality in this population.

Air pollution exposure potentiates hypertension through reactive oxygen species-mediated activation of Rho/ROCK.

Objective: Fine particulate matter <2.5 microm (PM(2.5)) has been implicated in vasoconstriction and potentiation of hypertension in humans.

Blood pressure and vascular effects of leptin in humans.

Background: Leptin may play a role in mediating obesity-related hypertension. However, its effects on the vasculature and blood pressure (BP) remain poorly defined in humans.

Methods: In the first study, we performed a short-term, placebo-controlled, randomized, double-blind, cross-over experiment investigating the actions of recombinant human leptin (r-metHuLeptin) in 15 nonobese adults.

Valsartan Improves Insulin Sensitivity without Altering Vascular Function in Healthy Overweight Adults without the Metabolic Syndrome.

Background. We investigated hyperactivity of the renin-angiotensin system (RAS) as a cause of endothelial dysfunction in obese humans. Methods.

The relationship between diabetes mellitus and traffic-related air pollution.

Objective: Air pollution is associated with an increased risk for cardiovascular events. Many of the biological pathways involved could also promote diabetes mellitus (DM). We therefore investigated the association between DM prevalence and exposure to traffic-related air pollution (nitrogen dioxide [NO 2]).

Combined continuous ethinyl estradiol/norethindrone acetate does not improve forearm blood flow in postmenopausal women at risk for cardiovascular events: a pilot study.

Objective: This study sought to determine whether combined continuous ethinyl estradiol and norethindrone acetate, a postmenopausal hormone therapy (HT) combination designed to have fewer side effects than cyclical therapies and therapies using medroxyprogesterone acetate (MPA), could improve vascular endothelial function in postmenopausal women with risk factors for cardiovascular disease (CVD).

Methods: Eighteen postmenopausal women (mean age 62 +/- 11 years) participated in a randomized, placebo-controlled, crossover design trial of 10 microg estradiol/1 mg norethindrone acetate given once daily for 3 months, with a 1-month washout period between placebo and active treatment phases. Vascular reactivity was assessed at each phase of the study using high-frequency brachial artery ultrasound in response to flow-mediated hyperemia, cold pressor testing, and sublingual nitroglycerin.

Is air pollution a cause of cardiovascular disease? Updated review and controversies.

Particulate matter (PM) air pollution is associated with an increased risk of cardiovascular morbidity and mortality. The focus of this review will be on the role that both acute and chronic exposure to PM plays in causing cardiovascular disease and on the latest major new findings and controversies in this field of research. Even short-term exposure to PM2.

Why physicians who treat hypertension should know more about air pollution.

Exposure to ambient levels of particulate matter (PM) air pollution increases the risk of a host of cardiovascular diseases and events. One potential mechanism explaining this association is that acute exposure to PM at high concentrations is capable of raising blood pressure within hours to days. Epidemiologic studies confirm that even commonly encountered levels of airborne pollutants can result in a prohypertensive response in humans.

Obesity, weight loss, and vascular function.

Obesity promotes the development of several major cardiovascular risk factors. Moreover, excess adiposity may play a direct role in initiating atherosclerosis as fat cells are capable of affecting the systemic vasculature through a variety of mechanisms. Recent studies demonstrate that obesity per se may impair vascular endothelial function.

Usefulness of low-density lipoprotein particle size measurement in cardiovascular disease prevention.

Background: Cardiovascular disease is largely explained by the traditional risk factors, but there are several novel risk factors that have been shown to predict cardiovascular morbidity. The measurement of low-density lipoprotein particle size (LDLPS) is a novel cardiovascular risk factor, yet it is unknown whether this measurement provides additional information that may influence the subsequent medical treatment of patients.

Hypothesis: The measurement of LDLPS provides additional information that may influence preventive treatment for cardiovascular disease.

Long-term air pollution exposure and acceleration of atherosclerosis and vascular inflammation in an animal model.

Context: Recent studies have suggested a link between inhaled particulate matter exposure in urban areas and susceptibility to cardiovascular events; however, the precise mechanisms remain to be determined.

Objective: To test the hypothesis that subchronic exposure to environmentally relevant particulate matter, even at low concentrations, potentiates atherosclerosis and alters vasomotor tone in a susceptible disease model.

Design, Setting, And Participants: Between July 21, 2004, and January 12, 2005, 28 apolipoprotein E-/- (apoE-/-) mice were, based on randomized assignments, fed with normal chow or high-fat chow and exposed to concentrated ambient particles of less than 2.

Neutral effect on markers of heart failure, inflammation, endothelial activation and function, and vagal tone after high-dose HMG-CoA reductase inhibition in non-diabetic patients with non-ischemic cardiomyopathy and average low-density lipoprotein level.

Objectives: This study sought to determine the effect of aggressive 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor (statin) therapy on surrogate markers in non-ischemic cardiomyopathy (NICM) patients and average low-density lipoprotein (LDL) concentrations.

Background: The effects of statins may well go beyond lipid lowering, and these pleiotropic effects may be of benefit in the treatment of heart failure.

Methods: Fifteen patients with NICM on standard maximized heart failure medication were enrolled in a randomized, double-blinded, placebo-controlled, crossover trial.

You are what you breathe: evidence linking air pollution and blood pressure.

Exposure to particulate matter (PM) air pollution increases the risk for myocardial infarctions, strokes, and cardiovascular mortality. A variety of responsible mechanisms have been described, including PM-induced elevations in blood pressure. Observational studies and controlled experiments have provided evidence that PM is capable of acutely increasing blood pressure in certain scenarios.

A negative carotid plaque area test is superior to other noninvasive atherosclerosis studies for reducing the likelihood of having underlying significant coronary artery disease.

Objective: Coronary calcium score (CCS), carotid plaque area (CPA), intima-media thickness (IMT), and C-reactive protein (CRP) are independent predictors of cardiovascular prognosis. Although each test may enhance risk stratification, their comparative abilities to screen for underlying coronary stenoses in individual patients is less established.

Methods And Results: Forty-two patients who had a 16-slice coronary computed tomography angiogram (CTA) performed were invited to have CPA, IMT, and CRP measured.

Plasminogen activator inhibitor-1 is associated with impaired endothelial function in women with systemic lupus erythematosus.

Endothelial function, measured noninvasively by brachial artery flow-mediated dilatation (FMD), has been shown to be impaired in patients with systemic lupus erythematosus (SLE). We hypothesized that depressed FMD in SLE patients is associated with increased levels of plasminogen activator inhibitor-1 (PAI-1), an inhibitor of fibrinolysis and regulator of vasoactivity. In this cross-sectional study of female SLE patients under the age of 55, putative markers of cardiovascular disease (CVD) such as PAI-1 were measured in addition to lupus-related disease activity (SLEDAI).