AimsAircraft noise disturbs sleep, and long-term exposure has been shown to be associated with increases in the prevalence of hypertension and an overall increased risk for myocardial infarction. The exact mechanisms responsible for these cardiovascular effects remain unclear.Methods and resultsWe performed a blinded field study in 75 healthy volunteers (mean age 26 years), who were exposed at home, in random order, to one control pattern (no noise) and two different noise scenarios [30 or 60 aircraft noise events per night with an average maximum sound pressure level (SPL) of 60 dB(A)] for one night each. We performed polygraphy during each study night. Noise caused a worsening in sleep quality (P < 0.0001). Noise60, corresponding to equivalent continuous SPLs of 46.3 dB (Leq) and representing environmental noise levels associated with increased cardiovascular events, caused a blunting in FMD (P = 0.016). As well, although a direct comparison among the FMD values in the noise groups (control: 10.4 ± 3.8%; Noise30: 9.7 ± 4.1%; Noise60: 9.5 ± 4.3%, P = 0.052) did not reach significance, a monotone dose-dependent effect of noise level on FMD was shown (P = 0.020). Finally, there was a priming effect of noise, i.e. the blunting in FMD was particularly evident when subjects were exposed first to 30 and then to 60 noise events (P = 0.006). Noise-induced endothelial dysfunction (ED) was reversed by the administration of Vitamin C (P = 0.0171). Morning adrenaline concentration increased from 28.3 ± 10.9 to 33.2 ± 16.6 and 34.1 ± 19.3 ng/L (P = 0.0099). Pulse transit time, reflecting arterial stiffness, was also shorter after exposure to noise (P = 0.003).ConclusionIn healthy adults, acute nighttime aircraft noise exposure dose-dependently impairs endothelial function and stimulates adrenaline release. Noise-induced ED may be in part due to increased production in reactive oxygen species and may thus be one mechanism contributing to the observed association of chronic noise exposure with cardiovascular disease.

AimsEpidemiological studies suggest the existence of a relationship between aircraft noise exposure and increased risk for myocardial infarction and stroke. Patients with established coronary artery disease and endothelial dysfunction are known to have more future cardiovascular events. We therefore tested the effects of nocturnal aircraft noise on endothelial function in patients with or at high risk for coronary artery disease.Methods60 Patients (50p 1–3 vessels disease; 10p with a high Framingham Score of 23 %) were exposed in random and blinded order to aircraft noise and no noise conditions. Noise was simulated in the patients’ bedroom and consisted of 60 events during one night. Polygraphy was recorded during study nights, endothelial function (flow-mediated dilation of the brachial artery), questionnaires and blood sampling were performed on the morning after each study night.ResultsThe mean sound pressure levels Leq(3) measured were 46.9 ± 2.0 dB(A) in the Noise 60 nights and 39.2 ± 3.1 dB(A) in the control nights. Subjective sleep quality was markedly reduced by noise from 5.8 ± 2.0 to 3.7 ± 2.2 (p < 0.001). FMD was significantly reduced (from 9.6 ± 4.3 to 7.9 ± 3.7 %; p < 0.001) and systolic blood pressure was increased (from 129.5 ± 16.5 to 133.6 ± 17.9 mmHg; p = 0.030) by noise. The adverse vascular effects of noise were independent from sleep quality and self-reported noise sensitivity.ConclusionsNighttime aircraft noise markedly impairs endothelial function in patients with or at risk for cardiovascular disease. These vascular effects appear to be independent from annoyance and attitude towards noise and may explain in part the cardiovascular side effects of nighttime aircraft noise.

Aims In a randomized, parallel, blinded study, we investigate the impact of clopidogrel, prasugrel, or ticagrelor on peripheral endothelial function in patients undergoing stenting for an acute coronary syndrome. Methods and results The primary endpoint of the study was the change in endothelium-dependent flow-mediated dilation (FMD) following stenting. A total of 90 patients (age 62 ± 9 years, 81 males, 22 diabetics, 49 non-ST elevation myocardial infarctions) were enrolled. There were no significant differences among groups in any clinical parameter. Acutely before stenting, all three drugs improved FMD without differences between groups (P = 0.73). Stenting blunted FMD in the clopidogrel and ticagrelor group (both P &lt; 0.01), but not in the prasugrel group. During follow-up, prasugrel was superior to clopidogrel [mean difference 2.13, 95% confidence interval (CI) 0.68–3.58; P = 0.0047] and ticagrelor (mean difference 1.57, 95% CI 0.31–2.83; P = 0.0155), but this difference was limited to patients who received the study therapy 2 h before stenting. Ticagrelor was not significantly superior to clopidogrel (mean difference 0.55, 95% CI −0.73 to 1.82; P = 0.39). No significant differences were seen among groups for low-flow-mediated dilation. Plasma interleukin (IL)-6 (P = 0.02 and P = 0.01, respectively) and platelet aggregation reactivity in response to adenosine diphosphate (P = 0.002 and P = 0.035) were lower in the prasugrel compared to clopidogrel and ticagrelor group. Conclusion As compared to ticagrelor and clopidogrel, therapy with prasugrel in patients undergoing stenting for an acute coronary syndrome is associated with improved endothelial function, stronger platelet inhibition, and reduced IL-6 levels, all of which may have prognostic implications. This effect was lost in patients who received the study medication immediately after stenting. EUDRACT-No 2011-005305-73

Abstract Aims Nighttime aircraft noise exposure has been associated with increased risk of hypertension and myocardial infarction, mechanistically linked to sleep disturbance, stress and endothelial dysfunction. It is unclear, whether the most widely used metric to determine noise exposure, equivalent continuous sound level (Leq), is an adequate indicator of the cardiovascular impact induced by different noise patterns. Methods and results In a randomized crossover study, we exposed 70 individuals with established cardiovascular disease or increased cardiovascular risk to two aircraft noise scenarios and one control scenario. Polygraphic recordings, echocardiography and flow-mediated dilation was determined for 3 study nights. The noise patterns consisted of 60 (Noise60) and 120 (Noise120) noise events, respectively, but with comparable Leq, corresponding to a mean value of 45 dB. Mean value of noise during control nights was 37 dB. During the control night, flow-mediated vasodilation (FMD) was 10.02±3.75%, compared to 7.27±3.21% for Noise60 nights and 7.21±3.58% for Noise120 nights (p&lt;0.001). Sleep quality was impaired after noise exposure in both noise scenario nights (p&lt;0.001). Serial echocardiographic assessment demonstrated an increase in the E/E’ ratio, a measure of diastolic function, within the three exposure nights, with a ratio of 6.83±2.26 for the control night, 7.21±2.33 for Noise60 and 7.83±3.07 for Noise120 (p=0.043). Conclusions Nighttime exposure to aircraft noise with similar Leq, but different number of noise events, results in a comparable worsening of vascular function. Adverse effects of nighttime aircraft noise exposure on cardiac function (diastolic dysfunction) seemed stronger the higher number of noise events. Translational perspective With the present field study, we tested whether 60 versus 120 simulated aircraft noise events with an equal average sound pressure level (Leq) have comparable adverse effects on endothelial and diastolic function of the heart of subjects with established cardiovascular disease or at increased cardiovascular risk. The results demonstrated that two different nighttime noise patterns with similar Leq, despite different number of noise events, results in a comparable worsening of vascular and cardiac diastolic function. These results may explain at least in part the increased incidence of coronary heart disease and heart failure being observed in response to nighttime aircraft noise.