Acute exposure to simulated nocturnal traffic noise and cardiovascular complications and sleep disturbance-results from a pooled analysis of human field studies.

OBJECTIVES: A series of human field studies demonstrated that acute exposure to simulated nocturnal traffic noise is associated with cardiovascular complications and sleep disturbance, including endothelial dysfunction, increased blood pressure, and impaired sleep quality. A pooled analysis of these results remains to be established and is of tremendous interest to consolidate scientific knowledge. METHODS: We analyzed data from four randomized crossover studies (published between 2013 to 2021 and conducted at the University Medical Center Mainz, Germany). A total of 275 subjects (40.4% women, mean age 43.03 years) were each exposed to one control scenario (regular background noise) and at least to one traffic noise scenario (60 aircraft or train noise events) in their homes during nighttime. After each night, the subjects visited the study center for comprehensive cardiovascular function assessment, including the measurement of endothelial function and hemodynamic and biochemical parameters, as well as sleep-related variables. RESULTS: The pooled analysis revealed a significantly impaired endothelial function when comparing the two different noise sequences (0-60 vs. 60-0 simulated noise events, mean difference in flow-mediated dilation -2.00%, 95% CI -2.32; -1.68, p < 0.0001). In concordance, mean arterial pressure was significantly increased after traffic noise exposure (mean difference 2.50 mmHg, 95% CI 0.54; 4.45, p = 0.013). Self-reported sleep quality, the restfulness of sleep, and feeling in the morning were significantly impaired after traffic noise exposure (all p < 0.0001). DISCUSSION: Acute exposure to simulated nocturnal traffic noise is associated with endothelial dysfunction, increased mean arterial pressure, and sleep disturbance.

Influence of Peripheral Transluminal Angioplasty Alongside Exercise Training on Oxidative Stress and Inflammation in Patients with Peripheral Arterial Disease.

In patients with intermittent claudication, exercise training ameliorates inflammation by reducing oxidative stress. A total of 41 patients with intermittent claudication (Rutherford 3) were included in the study (with 21 patients treated by endovascular revascularization (ER), and 20 patients without ER). All patients were referred to home-based exercise training. Absolute and initial claudication distance (ACD, ICD) and ABI (ankle-brachial index) were measured. ROS (reactive oxygen species) formation was measured using the luminol analogue L-012. Follow-up was performed after 3 months. ROS production after NOX2 (NAPDH oxidase 2) stimulation showed a significant reduction in both groups at follow-up (PTA group: p = 0.002, control group: p = 0.019), with a higher relative reduction in ROS in the PTA group than in the control group (p = 0.014). ABI measurements showed a significant increase in the PTA (peripheral transluminal angioplasty) group (p = 0.001), but not in the control group (p = 0.127). Comparing both groups at follow-up, ABI was higher in the PTA group (p = 0.047). Both groups showed a significant increas ACD and ICD at follow-up (PTA group: ACD: p = 0.001, ICD: p < 0.0001; control group: ACD: p = 0.041, ICD: p = 0.002). There was no significant difference between both groups at follow-up (ACD: p = 0.421, ICD: p = 0.839). Endovascular therapy in combination with exercise training leads to a lower leukocyte activation state with a reduced NOX2-derived ROS production paralleled by an improved ABI, ACD and ICD. Our data support the strategy to combine exercise training with preceding endovascular therapy.