Air pollution has recently been associated with the development of acute decompensated heart failure, but the underlying biological mechanisms remain unclear. A pulmonary vasoconstrictor effect of air pollution, combined with its systemic effects, may precipitate decompensated heart failure. The aim of the present study was to investigate the effects of acute exposure to diesel exhaust (DE) on pulmonary vascular resistance (PVR) under resting and stress conditions but also to determine whether air pollution may potentiate acquired pulmonary hypertension. Eighteen healthy male volunteers were exposed to ambient air (AA) or dilute DE with a particulate matter of <2.5 μm concentration of 300 μg/m(3) for 2 h in a randomized, crossover study design. The effects of DE on PVR, on the coefficient of distensibilty of pulmonary vessels (α), and on right and left ventricular function were evaluated at rest (n = 18), during dobutamine stress echocardiography (n = 10), and during exercise stress echocardiography performed in hypoxia (n = 8). Serum endothelin-1 and fractional exhaled nitric oxide were also measured. At rest, exposure to DE did not affect PVR. During dobutamine stress, the slope of the mean pulmonary artery pressure-cardiac output relationship increased from 2.8 ± 0.5 mmHg · min · l (-1) in AA to 3.9 ± 0.5 mmHg · min · l (-1) in DE (P < 0.05) and the α coefficient decreased from 0.96 ± 0.15 to 0.64 ± 0.12%/mmHg (P < 0.01). DE did not further enhance the hypoxia-related upper shift of the mean pulmonary artery pressure-cardiac output relationship. Exposure to DE did not affect serum endothelin-1 concentration or fractional exhaled nitric oxide. In conclusion, acute exposure to DE increased pulmonary vasomotor tone by decreasing the distensibility of pulmonary resistive vessels at high cardiac output.

Background: Reduced endothelial nitric oxide bioavailability, a hallmark of endothelial dysfunction, is commonly encountered in cardiovascular diseases. Intermittent fasting reduces serum markers of oxidative stress, while nitric oxide levels may rise. Whether this translates into persistent improvements in endothelial function is unknown. The aim of the study was to address the effects of intermittent «Ramadan-type» fasting on endothelial function, nitric oxide bioavailability, biological parameters and blood pressure.

BackgroundLeft Ventricular Assist Device (LVAD) is a promising therapy for patients with advanced heart failure (HF), but bleeding complications remain an important issue. Previous series show that acquired von Willebrand syndrome was present in up to 100 % of first generation LVAD recipients. We report the effects of new generation LVADs on vW factor (vWF) metabolism and activity in our center.MethodsFifteen LVAD recipients (HeartWare®, Framingham, MA, USA) were compared to 12 HF patients, matched for age and body mass index. vWF antigen and activity, as well as D-dimers, were measured on hemostasis analyzers. A vWF LVAD-induced alteration was evocated when the [vWF activity]/[vWF antigen] ratio was <0.6. ADAMTS13 and high molecular weight multimers of vWF were also assessed.ResultsLVAD recipients had similar levels of endothelial vWF production than the HF subjects (137 ± 14.5 vs. 147 ± 11.7 %; respectively, p = 0.611) but a decreased vWF activity (90 ± 11 vs. 132.6 ± 13 %; respectively, p = 0.017). [vWF activity]/[vWF antigen] ratio was 0.65 ± 0.02 in the LVAD recipients and 0.92 ± 0.06 in the subjects with HF (p = 0.001). ADAMTS13 activity was 80.3 ± 4.7 % in LVAD recipients and 96.2 ± 3.5 % in the HF patients (p = 0.016). LVAD patients disclosed markedly elevated D-dimers (3217.7 ± 735 vs. 680.6 ± 223.2 ng/mL FEU in the HF patients, p = 0.006). The LVAD patients experienced one major hemorrhagic event and one systemic thrombotic event during the median follow-up of 345 days.ConclusionsLVAD recipients achieved a new hemostatic equilibrium characterized by infrequent major hemorrhagic and thrombotic events, despite a mildly impaired vWF function and a markedly enhanced thrombin formation.Trial registrationISRCTN39517567Electronic supplementary materialThe online version of this article (doi:10.1186/s12872-016-0334-z) contains supplementary material, which is available to authorized users.

Exposure to diesel exhaust is an important cardiovascular risk factor and may promote atherothrombotic events. Some data suggest that polluted air exposure could affect haemostasis through platelet activation. The aim of the study was to investigate the effects of acute exposure to diesel exhaust on platelet activation and platelet function. We tested the hypothesis in a randomised, crossover study in 25 healthy men exposed to ambient and polluted air; 11 of the subjects also performed exercise during exposure sessions. Platelet activation was evaluated by surface expression of CD62P (P-selectin) and CD63 (dense granule glycoprotein) using flow cytometry of labelled platelets. Platelet function was measured using the PFA-100 platelet function analyser and by Multiplate whole blood impedance platelet aggregometry. Acute diesel exhaust exposure had no effect on platelet activation at rest, but exercise in polluted air increased the collagen-induced expression of CD62P and CD63 (both p< 0.05). The increase in the expression of CD62P and CD63 was related to the total amount of PM2.5 inhaled during the exercise sessions (r=+0.58 and +0.60, respectively, both p< 0.05). Platelet aggregation was not impaired after polluted air exposure at rest or during exercise. In conclusion, in healthy subjects, diesel exhaust exposure induces platelet activation as illustrated by a dose-response increase in the release of CD62P and CD63. This platelet priming effect could be a contributor to the triggering of atherothrombotic events related to air pollution exposure.

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