22 research outputs found

    Lärm und Herz-Kreislauf-Erkrankungen

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    Environmental noise is a significant environmental risk factor for public health. The European Environment Agency states that at least 20% of the European population are exposed to harmful day-evening-night noise levels of 55 decibels (dB), whereas the World Health Organization recommends up to 10 dB lower limit values, depending on the noise source, for the protection of the population. Chronic noise can interfere with daily activities and sleep and trigger mental and physiological stress reactions that can increase the risk of cardiovascular disease in the long term. Therefore, preventive measures at the source including noise-reducing structural changes are essential to ensure compliance with noise limits and to protect the population from the negative health effects of noise

    Effects of tobacco cigarettes, e-cigarettes, and waterpipe smoking on endothelial function and clinical outcomes

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    Tobacco smoking is a leading cause of non-communicable disease globally and is a major risk factor for cardiovascular disease (CVD) and lung disease. Importantly, recent data by the World Health Organizations (WHO) indicate that in the last two decades global tobacco use has significantly dropped, which was largely driven by decreased numbers of female smokers. Despite such advances, the use of e-cigarettes and waterpipes (shisha, hookah, narghile) is an emerging trend, especially among younger generations. There is growing body of evidence that e-cigarettes are not a harm-free alternative to tobacco cigarettes and there is considerable debate as to whether e-cigarettes are saving smokers or generating new addicts. Here, we provide an updated overview of the impact of tobacco/waterpipe (shisha) smoking and e-cigarette vaping on endothelial function, a biomarker for early, subclinical, atherosclerosis from human and animal studies. Also their emerging adverse effects on the proteome, transcriptome, epigenome, microbiome, and the circadian clock are summarized. We briefly discuss heat-not-burn tobacco products and their cardiovascular health effects. We discuss the impact of the toxic constituents of these products on endothelial function and subsequent CVD and we also provide an update on current recommendations, regulation and advertising with focus on the USA and Europe. As outlined by the WHO, tobacco cigarette, waterpipe, and e-cigarette smoking/vaping may contribute to an increased burden of symptoms due to coronavirus disease 2019 (COVID-19) and to severe health consequences

    Acute exposure to simulated nocturnal train noise leads to impaired sleep quality and endothelial dysfunction in young healthy men and women: a sex-specific analysis

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    A series of human field studies demonstrated that simulated nocturnal traffic noise exposure impaired sleep quality and endothelial function, which could be significantly improved after intake of vitamin C in case of endothelial function. However, it remains unclear whether these changes follow a sex-specific pattern. Thus, we aimed to analyze the effect of simulated nocturnal train noise exposure on sleep quality, endothelial function and its associated changes after vitamin C intake, and other hemodynamic and biochemical parameters in young healthy men and women. We used data from a randomized crossover study, wherein 70 healthy volunteers (50% women) were each exposed to one control pattern (regular background noise) and two different train noise scenarios (30 or 60 train noise events per night, with average sound pressure levels of 52 and 54 dB(A), respectively, and peak sound level of 73-75 dB(A)) in their homes for three nights. After each night, participants visited the study center for the measurement of endothelial function as well as other hemodynamic and biochemical parameters. Sleep quality measured via self-report was significantly impaired after noise 30 and noise 60 nights in both men and women (p < 0.001 vs. control). Likewise, endothelial function measured by flow-mediated dilation (FMD) was significantly impaired after noise 30 and noise 60 nights in both men and women (p < 0.001 vs. control). While in women, vitamin C intake significantly improved FMD after both noise 30 and noise 60 study nights compared to control nights, no significant changes were observed in men. Exposure to simulated nocturnal train noise impairs sleep quality and endothelial function in both men and women, whereas a significant improvement of endothelial function after noise exposure and vitamin C intake could only be observed in women. These findings suggest for the first time that in men other mechanisms such as oxidative stress causing endothelial dysfunction may come into play

    Gesundheitsrisiko Mobilfunkstrahlung? Was ändert sich mit 5G?

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    Exposure of the population to radiofrequency electromagnetic fields (RF-EMF) is dominated by the use of wireless communication devices close to the body. Exposure from transmitters far from the body is on average several orders of magnitude below the international guideline values. With increasing mobile data usage and the associated use of higher frequencies for 5G, a densification of the mobile network is to be expected. However, this will not necessarily increase the overall RF-EMF exposure of the population, as mobile phones emit less with better signal quality. 5G is a technological advancement of the previous mobile radio technology with the same biophysical properties. So far, no health effects below the guideline limits have been consistently demonstrated for RF-EMF. Biological effects such as changes of the electrical activity of the brain or the oxidative balance were observed for high local exposure in the range of the exposure guideline limits. According to current knowledge, they do not represent a health risk

    Transcatheter indirect mitral annuloplasty induces annular and left atrial remodelling in secondary mitral regurgitation

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    Aims Mitral annuloplasty using the Carillon Mitral Contour System (CMCS) reduces secondary mitral regurgitation (SMR) and leads to reverse left ventricular remodelling. The aim of this study was to evaluate the effect of the CMCS on the mitral valve annulus (MA) and left atrial volume (LAV). Methods and results We retrospectively evaluated the data of all patients treated with the CMCS at our centre. Using transthoracic echocardiography, MA diameters were assessed by measuring the anterolateral to posteromedial extend (ALPM) and the anterior to posterior (AP) dimensions, respectively. Also, LAV and left ventricular end‐diastolic volume (LVEDV) were assessed. Patients were examined at three time points: baseline, at 20–60 days (30dFUP), and at 9–15 months (1yFUP), using paired analysis. From July 2014 until March 2019, 75 cases of severe SMR were treated using CMCS. Cases in which other devices were used in combination (COMBO therapy, n = 35) or in which the device could not be implanted (implant failure, n = 3) were excluded, leaving 37 patients in the present analysis. Analysis at 30dFUP showed a significant reduction of 16% in the mean ALPM diameter (7.27 ± 5.40 mm) and 15% in the AP diameter (6.57 ± 5.33 mm). Analysis of LAV also showed a significant reduction of 21% (36.61 ± 82.67 mL), with no significant change in LVEDV. At 1yFUP, the reduction of both the mean ALPM diameter of 14% (6.24 ± 5.70 mm) and the mean AP diameter of 12% (5.46 ± 4.99 mm) remained significant and stable. The reduction in LAV was also maintained at 23% (37.03 ± 56.91 mL). LAV index was significantly reduced by 17% at 30dFUP (15.44 ± 40.98 mL/m2) and by 13% at 1yFUP (11.56 ± 31.87 mL/m2), respectively. LVEDV index showed no significant change at 30dFUP and a non‐significant 10% reduction at 1yFUP (17.75 ± 58.79 mL/m2). Conclusions The CMCS successfully treats symptomatic SMR with a stable reduction of not only the AP diameter of the MA, but the current study also demonstrates an additional reduction of the ALPM dimension at both 30dFUP and 1yFUP. We have also shown for the first time that LAV and LAV index are significantly reduced at both 30dFUP and 1yFUP and a non‐significant positive remodelling of the LVEDV. This positive left atrial remodelling has not been looked for and demonstrated in earlier randomized studies of CMCS

    Endothelial Function Assessed by Digital Volume Plethysmography Predicts the Development and Progression of Type 2 Diabetes Mellitus

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    Background Endothelial dysfunction is a consequence of type 2 diabetes mellitus, but it is unclear whether endothelial dysfunction of conductance versus resistance vessels may also precede type 2 diabetes mellitus development. Methods and Results In a population‐based cohort of 15 010 individuals from the GHS (Gutenberg Health Study) (aged 35–74 years at enrollment in 2007–2012), we identified 1610 cases of incident pre–diabetes mellitus and 386 cases of incident type 2 diabetes mellitus by hemoglobin A1c (HbA1c) and/or medical history between 2012 and 2017. Endothelial function of conductance and resistance vessels was measured by flow‐mediated dilation and digital volume plethysmography–derived reactive hyperemia index, respectively. Multivariable regression modeling was used to estimate β coefficients of HbA1c levels at follow‐up and relative risks of incident (pre–)diabetes mellitus. Reactive hyperemia index was independently associated with HbA1c after multivariable adjustment for baseline HbA1c, sex, age, socioeconomic status, arterial hypertension, waist/height ratio, pack‐years of smoking, non–high‐density lipoprotein/high‐density lipoprotein ratio, physical activity, family history of myocardial infarction/stroke, prevalent cardiovascular disease, medication use, and C‐reactive protein (β=−0.020; P=0.0029). The adjusted relative risk per SD decline in reactive hyperemia index was 1.08 (95% CI, 1.02–1.15; P=0.012) for incident pre–diabetes mellitus and 1.16 (95% CI, 1.01–1.34; P=0.041) for incident type 2 diabetes mellitus. Flow‐mediated dilation independently increased the relative risk for developing pre–diabetes mellitus by 8% (95% CI, 1.02–1.14; P=0.012), but it was not independently associated with incident type 2 diabetes mellitus (relative risk, 1.01; 95% CI, 0.86–1.19; P=0.92) and with HbA1c (β=−0.003; P=0.59). Conclusions Endothelial dysfunction of resistance rather than conductance vessels may precede the development of (pre–)diabetes mellitus. Assessment of endothelial function by digital volume plethysmography may help to identify subjects at risk for development of type 2 diabetes mellitus

    Luftverschmutzung als wichtiger Kofaktor bei COVID-19-Sterbefällen

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    Background The mortality from COVID-19 is increased in the presence of cardiopulmonary comorbidities. Air pollution is also associated with increased mortality, primarily mediated by cardiopulmonary diseases. Observations at the beginning of the COVID-19 pandemic showed that mortality from COVID-19 was increased, especially in regions with higher levels of air pollution. The influence of air pollution on the course of the disease in COVID-19 is unclear. Method A selective literature search of studies up to the beginning of April 2021 was carried out in PubMed on the association between air pollution and COVID-19 mortality using the search terms “air pollution AND/OR COVID-19/coronavirus/SARS-CoV‑2 AND/OR mortality”. Results Current research shows that around 15% of global COVID-19 deaths are due to air pollution. The proportion of COVID-19 deaths from air pollution is 19% in Europe, 17% in North America and 27% in East Asia. This role of air pollution in COVID-19 deaths has now been confirmed by various studies from the USA, Italy and England. Air pollution and COVID-19 result in similar damage to the cardiopulmonary system, which may explain the link between air pollution and increased COVID-19 mortality. Conclusion The environmental aspect of the COVID-19 pandemic shown here calls for greater efforts to be made towards effective measures to reduce anthropogenic emissions, which cause both air pollution and climate change

    Luftverschmutzung und Herz-Kreislauf-Erkrankungen: Air Pollution and Cardiovascular Diseases

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    Chronic exposure to air pollution, especially to fine particulates, is a primary public health risk factor. While in Germany air quality has improved substantially in the past three decades, and the air quality standards of the European Union are met most of the time, the stricter guidelines of the World Health Organization are still exceeded. Fine particulate matter pollution causes chronic oxidative stress in the respiratory and vascular system, which induces inflammatory responses in the lungs and vessels and beyond, even at relatively low concentrations. This leads to excess mortality by respiratory and cardiovascular diseases. In Germany, about 42000 excess deaths per year from air pollution are related to ischemic heart disease and about 6700 per year to strokes. Therefore, the mitigation of air pollution could help prevent cardiovascular diseases as effectively as the banning of tobacco smoking

    Luftverschmutzung und Herz-Kreislauf-Erkrankungen: Air pollution and cardiovascular diseases

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    Air pollution in the environment and in households is responsible worldwide for almost 9 million preventable premature deaths per year and almost 800,000 such deaths within Europe. Air pollution therefore shortens life expectancy worldwide by almost 3 years. Smoking, a proven cardiovascular risk factor, shortens the mean life expectancy by 2.2 years. Epidemiological studies have shown that air pollution from fine and coarse particulate matter is associated with increased cardiovascular morbidity and mortality. Responsible for this are mainly cardiovascular diseases, such as coronary heart disease, heart attack, heart failure, stroke, hypertension and also diabetes, which are mainly caused or aggravated by fine particulate matter. After inhalation fine particulate matter can reach the brain directly and also reach the bloodstream via a transition process. There, the particles are absorbed by the blood vessels where they stimulate the formation of reactive oxygen species (ROS) in the vascular wall. They therefore promote the formation of atherosclerotic changes and in this way increase the cardiovascular risks, especially an increase in chronic ischemic heart disease and stroke. Recent studies also reported that in coronavirus disease 2019 (COVID-19) patients a high degree of air pollution is correlated with severe disease courses with cardiovascular complications and pulmonary diseases. This necessitates preventive measures, such as lowering of the upper limits for air pollutants. Individual measures to mitigate the health consequences of fine particulate matter are also discussed

    Air pollution and cardiovascular system

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    Background Air pollution in the environment and in households is a major health problem, accounting for more than 8 million preventable premature deaths globally each year and nearly 800,000 such deaths in Europe. Objective This paper deals with the effects of air pollution on the cardiovascular system. Material and methods A literature review of epidemiological and experimental studies on the relationship between air pollution and cardiovascular diseases was carried out. Results Epidemiological studies show that airborne particulate matter (PM2.5 and PM10) is associated with increased cardiovascular morbidity and mortality. This is mainly due to fine dust-induced and/or aggravated cardiovascular diseases, such as coronary heart disease, myocardial infarction, heart failure, stroke, hypertension and also diabetes. Experimental studies show that particulate matter enters the bloodstream via a transition process and stimulates the formation of reactive oxygen species in the vascular walls, promoting atherosclerotic changes and increasing cardiovascular risk. Conclusion Air pollution is an important risk factor for the development of cardiovascular diseases, especially as a result of recent calculations. This makes preventive measures necessary, such as a reduction of air pollutant limits, in particular for PM2.5, from 25 µg/m3 to the 10 µg/m3 recommended by the World Health Organization (WHO)
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