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Insulin infusion improves myocardial blood flow (MBF) in healthy subjects. Until now, the effect of insulin on myocardial perfusion in type 2 diabetic subjects with coronary artery disease (CAD) has been unknown. We studied the effects of insulin on MBF in ischemic regions evaluated by single-photon emission-computed tomography and coronary angiography and in nonischemic regions in 43 subjects (ages 63 ± 7 years) with type 2 diabetes (Hb[A.sub.1c] 7.1 ± 0.9%). MBF was measured at fasting and during a euglycemic-hyperinsulinemic clamp at rest (n = 43) and during adenosine-induced (140 µg x [kg.sup.-1] x [min.sup.-1] for 7 min) hyperemia (n = 26) using positron emission tomography and [sup.15]O-labeled water. MBF was significantly attenuated in ischemic regions as compared with in nonischemic regions (P < 0.0001) and was increased by insulin as compared with in the fasting state (P < 0.0001). At rest, insulin infusion increased MBF by 13% in ischemic regions (P = 0.043) and 22% in nonischemic regions (P = 0.003). During adenosine infusion, insulin enhanced MBF by 20% (P = 0.018) in ischemic regions and 18% (P = 0.045) in nonischemic regions. In conclusion, insulin infusion improved MBF similarly in ischemic and nonischemic regions in type 2 diabetic subjects with CAD. Consequently, in addition to its metabolic effects, insulin infusion may improve endothelial function and thus increase the threshold for ischemia and partly contribute to the beneficial effects found in clinical trials in these subjects., Patients with type 2 diabetes are at high risk for acute cardiovascular events. In type 2 diabetes, endothelial dysfunction is a key step in the development of myocardial ischemia that [...]

In the peripheral vasculature, insulin induces time- and dose-dependent vasodilation. We have recently demonstrated that insulin potentiates adenosine-stimulated myocardial blood flow. However, it is unknown whether insulin's effects on the [...]

IMPORTANCE: Exposure to ozone has been associated with cardiovascular mortality, but the underlying biological mechanisms are not yet understood. OBJECTIVE: To examine the association between ozone exposure and cardiopulmonary pathophysiologic mechanisms. DESIGN, SETTING, AND PARTICIPANTS: A longitudinal study involving 89 healthy adult participants living on a work campus in Changsha City, China, was conducted from December 1, 2014, to January 31, 2015. This unique quasiexperimental setting allowed for better characterization of air pollutant exposure effects because the participants spent most of their time in controlled indoor environments. Concentrations of indoor and outdoor ozone, along with the copollutants particulate matter, nitrogen dioxide, and sulfur dioxide, were monitored throughout the study period and then combined with time-activity information and filtration conditions of each residence and office to estimate 24-hour and 2-week combined indoor and outdoor mean exposure concentrations. Associations between each exposure measure and outcome measure were analyzed using single-pollutant and 2-pollutant linear mixed models controlling for ambient temperature, secondhand smoke exposure, and personal-level time-varying covariates. MAIN OUTCOMES AND MEASURES: Biomarkers indicative of inflammation and oxidative stress, arterial stiffness, blood pressure, thrombotic factors, and spirometry were measured at 4 sessions. RESULTS: Of the 89 participants, 25 (28%) were women and the mean (SD) age was 31.5 (7.6) years. The 24-hour ozone exposure concentrations ranged from 1.4 to 19.4 parts per billion (ppb), corresponding to outdoor concentrations ranging from 4.3 to 47.9 ppb. Within this range, in models controlling for a second copollutant and other potential confounders, a 10-ppb increase in 24-hour ozone was associated with mean increases of 36.3% (95% CI, 29.9%-43.0%) in the level of platelet activation marker soluble P-selectin, 2.8% (95% CI, 0.6%-5.1%) in diastolic blood pressure, 18.1% (95% CI, 4.5%-33.5%) in pulmonary inflammation markers fractional exhaled nitric oxide, and 31.0% (95% CI, 0.2%-71.1%) in exhaled breath condensate nitrite and nitrate as well as a −9.5% (95% CI, −17.7% to −1.4%) decrease in arterial stiffness marker augmentation index. A 10-ppb increase in 2-week ozone was associated with increases of 61.1% (95% CI, 37.8%-88.2%) in soluble P-selectin level and 126.2% (95% CI, 12.1%-356.2%) in exhaled breath condensate nitrite and nitrate level. Other measured biomarkers, including spirometry, showed no significant associations with either 24-hour ozone or 2-week ozone exposures. CONCLUSIONS AND RELEVANCE: Short-term ozone exposure at levels not associated with lung function changes was associated with platelet activation and blood pressure increases, suggesting a possible mechanism by which ozone may affect cardiovascular health.

Objective: Hyperleptinemia, a hallmark of obesity, appears to be a risk factor for coronary artery disease. However, although leptin is a vasoactive hormone, no studies addressing leptin's effect on coronary perfusion have been performed. We examined the association between circulating leptin concentration and coronary vasoreactivity in young obese and nonobese males. Research Methods and Procedures: Myocardial blood flow was quantitated in 10 obese men (age 31 ± 7 years, BMI 34 ± 2 kg/m2) and 10 healthy matched nonobese men (age 33 ± 8 years, BMI 24 ± 2 kg/m2) using positron emission tomography and O‐15‐water. The measurements were performed basally and during adenosine infusion (140 μg/kg per minute). Results: Serum leptin was significantly higher in obese than nonobese subjects (10.3 ± 5.6 vs. 4.3 ± 2.5 ng/mL, p< 0.01). Basal myocardial blood flow was not significantly different between obese and nonobese subjects. Adenosine‐stimulated flow was blunted in obese (3.2 ± 0.6 mL/g per minute) when compared with nonobese subjects (4.0 ± 1.1 mL/g per minute, p< 0.05). Serum leptin concentration was inversely associated with adenosine‐stimulated flow in study subjects (r= −0.50, p< 0.05). This association was no longer observed after adjustment for obesity and/or hyperinsulinemia. Discussion: Hyperleptinemia and reduced coronary vasoreactivity occur concomitantly in young obese but otherwise healthy men. Moreover, the adenosine‐stimulated myocardial flow is inversely related to prevailing concentration of serum leptin. Although this relationship appears to be explained by obesity and/or hyperinsulinemia, leptin might have a role in regulation of myocardial blood supply.

Objective:Obesity is associated with increased risk for cardiovascular diseases and peripheral endothelial dysfunction. We examined whether myocardial vasoreactivity and coronary‐flow response to insulin stimulation are altered in obesity. Research Methods and Procedures:Myocardial blood flow was quantitated in 10 obese men (body mass index, 33.6 ± 1.9 kg/m2) and 10 healthy matched non‐obese men (body mass index, 24.2 ± 1.9 kg/m2), using positron emission tomography and oxygen‐15‐labeled water. The measurements were performed basally and during adenosine infusion (140 μg/kg per minute), with or without simultaneous physiological (1 mU/kg per minute) and supraphysiological (5 mU/kg per minute) hyperinsulinemia. Results:Basal myocardial blood flow was not significantly different between obese and non‐obese subjects. Adenosine‐stimulated flow was blunted in obese (3.2 ± 0.6 mL/g per minute) when compared with non‐obese subjects (4.0 ± 1.1 mL/g per minute, p< 0.05). Simultaneous physiological hyperinsulinemia increased adenosine‐stimulated myocardial flow significantly in both groups (to 4.03 ± 1.24 and 4.85 ± 1.04 mL/g per minute in obese and non‐obese men, respectively; p< 0.05 vs. adenosine). Supraphysiological hyperinsulinemia further enhanced the adenosine‐stimulated flow in non‐obese subjects (to 5.56 ± 0.98 mL/g per minute; p< 0.05) but not in obese subjects. Discussion:Young obese, healthy men have reduced myocardial vasoreactivity, which may represent an early precursor of future coronary artery disease. Additionally, insulin‐induced enhancement of myocardial blood flow is blunted in obesity. Thus, endothelial dysfunction seems to also characterize myocardial vasculature of obese subjects.

Aims We studied whether a reduced coronary flow reserve (CFR) in healthy young men independently predicts the presence of coronary artery disease as assessed by coronary artery calcification after 11 years of follow-up. Methods and results Coronary microvascular dysfunction in early stages of coronary artery disease can be detected as a reduced CFR by positron emission tomography (PET). Seventy-seven healthy, lean, normotensive, non-smoking and non-diabetic men underwent 15-Oxygen (15O) water myocardial perfusion PET at rest and during vasodilator stress at the age of 35 ± 4 years at baseline. The subjects were followed-up for 11 ± 1 years and the coronary artery calcium score (CCS) was measured with computed tomography at the end of the follow-up. At the end of the follow-up, 30 (39%) individuals had CCS >0 (average 65 ± 93), but none had clinical symptoms or evidence of ischaemia in stress echocardiography. At baseline, the average CFR was comparable in individuals with CCS >0 and CCS = 0 (4.2 ± 1.4 vs. 4.0 ± 1.2, P = 0.4). Logistic regression analysis showed no associations between CFR, serum glucose, cholesterol levels, systolic blood pressure or body mass index at baseline and CCS at the end of the follow-up (P always >0.05). The presence of CCS (CCS >0) was associated with higher systolic and diastolic blood pressures at the end of the follow-up (137 ± 18 vs. 128 ± 11 mmHg, P = 0.04 and 86 ± 12 vs. 78 ± 11 mmHg, P = 0.01). Conclusions Coronary reactivity to vasodilator-induced hyperaemia as assessed by perfusion PET was not predictive of the presence of coronary calcification after 11 years of follow-up in asymptomatic men with very low likelihood of coronary artery disease.

Background The Office Illness Project In northern Sweden, comprising both a screening questionnaire study of 4943 office workers and a case-referent study of facial skin symptoms in 163 subjects was recently completed. Previously published results from the survey showed that female gender, asthma/rhinitis, high psychosocial work load, visual display terminal (VDT) and paperwork were related to an increased prevalence of facial skin symptoms. Methods The case-referent study presented in this paper used data from the questionnaire supplemented by Information from a clinical examination, a survey of psychosocial factors at work, building data and VDT-related factors from inspection and measurements taken at the work site. Results Psychosocial conditions and exposure to electromagnetic fields or conditions associated with such factors were related to an increased occurrence of skin symptoms. The results also indicated that personal factors such as atopic dermatitis and physical exposure factors influencing indoor air quality, such as paper exposure and cleaning frequency were related to an increased prevalence of symptoms. Conclusions The results suggest that skin symptoms reported by VDT users have a multifactorial background.

Background The Office Illness Project in Northern Sweden, comprising both a screening questionnaire study of 4943 office workers and a case-referent study of Sick Building Syndrome (SBS) in 464 subjects was recently completed. Previously published results from the survey showed that female gender, asthma/rhinitis, high psychosocial work load, paper and visual display terminal (VDT) work were related to an increased prevalence of SBS symptoms. Methods The case-referent study presented in this paper used data from the questionnaire supplemented with information from a clinical examination, a survey of psychosocial factors at work and building data from inspection and measurements taken at the work sites. Results Personal factors such as atopy and photosensitive skin, psychosocial conditions and physical exposure factors influencing indoor air quality (IAQ), such as outdoor air flow rates and the presence of photocopiers were related to an increased prevalence of the reported SBS symptoms. The results were established using multivariate analysis. Conclusions The rate response relationship between actually measured ventilation rates and the prevalence of perceived SBS symptoms presents strong evidence for the association between IAQ factors and health.