In a cross-sectional analysis of a case-control study in 2015, we revealed the association between increased arterial stiffness (pulse wave velocity) and aircraft noise exposure. In June 2020, we evaluated the long-term effects, and the impact of a sudden decline in noise exposure during the coronavirus disease 2019 (COVID-19) lockdown, on blood pressure and pulse wave velocity, comparing 74 participants exposed to long-term day-evening-night aircraft noise level > 60 dB and 75 unexposed individuals. During the 5-year follow-up, the prevalence of hypertension increased in the exposed (42% versus 59%, P =0.048) but not in the unexposed group. The decline in noise exposure since April 2020 was accompanied with a significant decrease of noise annoyance, 24-hour systolic (121.2 versus 117.9 mm Hg; P =0.034) and diastolic (75.1 versus 72.0 mm Hg; P =0.003) blood pressure, and pulse wave velocity (10.2 versus 8.8 m/s; P =0.001) in the exposed group. Less profound decreases of these parameters were noticed in the unexposed group. Significant between group differences were observed for declines in office and night-time diastolic blood pressure and pulse wave velocity. Importantly, the difference in the reduction of pulse wave velocity between exposed and unexposed participants remained significant after adjustment for covariates (−1.49 versus −0.35 m/s; P =0.017). The observed difference in insomnia prevalence between exposed and unexposed individuals at baseline was no more significant at follow-up. Thus, long-term aircraft noise exposure may increase the prevalence of hypertension and accelerate arterial stiffening. However, even short-term noise reduction, as experienced during the COVID-19 lockdown, may reverse those unfavorable effects.

Objective: The COVID-19 lockdown caused unprecedented decline in environmental noise pollution. We aimed to evaluate the impact of aircraft noise exposure decrease during lockdown on blood pressure (BP) and selected hypertension-mediated organ damages. Design and method: As previously reported (J Hypertens. 2019; 37) in 2015 (1st observation) we examined group of inhabitants exposed to high (>60 dB) aircraft noise living near Cracow Airport (n = 101), and compared them to unexposed group (<55 dB) (n = 100). In June 2020, 4 months after COVID-19 pandemic restrictions introduction, we reassessed (2nd observation) 74 and 75 participants from previously exposed and unexposed groups, respectively, using the same study protocol. We collected medical history, office and ambulatory BP, echocardiographic and arterial stiffness data. Results: In exposed to aircraft noise group the prevalence of arterial hypertension increased from 1st to 2nd observation (P < 0.05). During lockdown in the noise exposed group office and 24 hour diastolic BP (DBP, P < 0.022) decreased significantly, which was accompanied by a significant drop in annoyance (P = 0.006). In this group in 2nd observation DBP was significantly lower than estimated DBP (i.e. calculated as a sum of DBP at 1st observation and parameter estimates of cross-sectional association of DBP and age multiplied by 5.5 year – time period between observations) (P = 0.047). The obtained decline in DBP from 1st to 2nd observation was grater in noise exposed than unexposed participants, even after adjustment for covariates. The carotid-femoral pulse wave velocity (PWV), initially higher in noise exposed group, decreased from 1st to 2nd observation in both groups, however this was more pronounced in the exposed than unexposed group (P = 0.003). In 1st observation PWV in noise exposed participants did not show any relationship with age (Parameter Estimate (PE)=0.01 m/s/year; P = 0.71), while in 2nd observation, during aircraft noise decline caused by COVID-19 lockdown, the expected positive relation of PWV with age was reinstituted (PE = 0.15 m/s/year; P < 0.001). Conclusions: As our previous study indicated, aircraft noise exposure may increase BP and accelerate arterial stiffening. The decrease in BP and PWV due to noise intensity diminution, observed during COVID-19 lockdown, in fact provides evidence for this observation.

The results from epidemiological studies suggest that environmental noise including aircraft, railway, road traffic, wind turbine, and leisure-related noise is a growing public health concern. According to the WHO, at least 100 million people in the European Union are affected by traffic noise levels above the WHO-recommended thresholds. Environmental noise can adversely affect physical and mental health, as well as wellbeing. Chronic low-level noise exposure typical for most environmental sources is associated with psychophysiological stress causing non-auditory or indirect noise effects leading ultimately to cardiovascular diseases. Among all environmental noise sources, aircraft noise is considered the most annoying, and its leading mechanism of action is autonomic system activation such as increases in heart rate and blood pressure. Previously, we observed that long-term exposure to aircraft noise was associated with increased diastolic blood pressure, arterial stiffness (as assessed by pulse wave velocity), and impaired left ventricular diastolic function. All mentioned above effects are early, subclinical, and potentially reversible changes which preceded late noise effects in the cardiovascular system, that is, established cardiovascular diseases such as myocardial infarction, stroke, and heart failure. However, even a short-term reduction in aircraft noise exposure as observed during the COVID-19 lockdown may reverse these negative effects on arterial stiffness and blood pressure and may decrease the prevalence of insomnia. In this review, we aimed to critically discuss our obtained results considering recent studies on the influence of aircraft noise (and other traffic noises) on cardiovascular diseases in the context of the WHO Environmental Noise Guidelines for the European Region.

Objectives: The pharmacological stress test with vasodilator agents is an alternative cardiological diagnostic tool for patients with contraindications to the classical stress test provided by physical activity during single-photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI). The study compared the frequency of the side effects of regadenoson and dipyridamole during a SPECT MPI. Methods: This retrospective study included data of 283 consecutive patients who underwent pharmacological stress tests in years 2015-2020. The study group consisted of 240 patients who had received dipyridamole and 43 patients who had received regadenoson. The collected data included the patients’ characteristics, the occurrence of side effects (divided into mild: headache, vertigo, nausea, vomiting, dyspnea, chest discomfort, hot flushes, general weakness and severe: bradycardia, hypotension, loss of consciousness), and blood pressure values/measurements. Results: Overall, complications occurred relatively often (regadenoson: 23.2%, dipirydamol: 26.7%, p=0.639). Procedure discontinuation was necessary in 0.7% of examinations, whereas pharmacological support was necessary in 4.7%. There was no difference in the prevalence of mild (regadenoson: 16.2%, dipirydamol: 18.3%, p=0.747) and severe complications (regadenoson: 11.6%, dipyridamole: 15.0%, p=0.563). However, regadenoson has been found to cause a significantly smaller mean decrease of systolic blood pressure (SBP) (regadenoson: -2.6±10.0 mmHg, dipyridamole: -8.7±9.6 mmHg, p=0.002), diastolic blood pressure (DBP) (regadenoson: -0.9±5.4 mmHg, dipyridamole: -3.6±6.2 mmHg, p=0.032), as well as mean arterial pressure (MAP) (regadenoson: -1.5±5.6 mmHg, dipyridamole: -5.4±6.5 mmHg, p=0.001). Conclusion: Regadenoson and dipyridamole presented a similar safety profile during SPECT MPI. However, regadenoson has been found to cause significantly smaller decreases in SBP, DBP, and MAP.