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New Study: Aircraft Noise Can Damage the Heart

Myocardial infarction, also known as a heart attack, occurs when the blood supply to a part of the heart muscle is blocked, causing damage to the heart muscle.

New research indicates that aircraft noise exacerbates the damage caused by myocardial infarction.

Traffic noise may be a significant factor in the progression and worsening of ischemic heart disease. A recent discovery by researchers from the Cardiology Department at the University Medical Center Mainz found that exposure to noise (with an average sound pressure level of 72 dB and a peak level of 85 dB) for up to 4 days resulted in increased pro-inflammatory aortic gene expression in mice.

The researchers found that noise caused adhesion and infiltration of inflammatory cells in the vascular and cardiac tissue. This was accompanied by an increased percentage of leukocytes with a pro-inflammatory, reactive oxygen speciesA species is a group of living organisms that share a set of common characteristics and are able to breed and produce fertile offspring. The concept of a species is important in biology as it is used to classify and organize the diversity of life. There are different ways to define a species, but the most widely accepted one is the biological species concept, which defines a species as a group of organisms that can interbreed and produce viable offspring in nature. This definition is widely used in evolutionary biology and ecology to identify and classify living organisms.” data-gt-translate-attributes=”[{“attribute”:”data-cmtooltip”, “format”:”html”}]”>species (ROS)-producing phenotype and expression of the phagocytic NADPH oxidase/phospho-NFκB in peripheral blood. In order to induce myocardial infarction and worsen cardiac function, the group used the permanent LAD ligation model.

Noise-induced stress causes the release of stress hormones that trigger an inflammatory response, leading to more severe myocardial infarction, oxidative stress and endothelial dysfunction, and subsequent heart failure. Credit: Cardiovascular Research

Noise exposure before MI induced more severe endothelial dysfunction and more pronounced increases in vascular ROS and signs of inflammation in animals preconditioned with noise. Participants of the population-based Gutenberg Health Cohort Study (median follow-up:11.4y) with incident MI revealed elevated C-reactive protein (CRP) at baseline and worse LVEF after MI in case of a history of noise exposure and subsequent development of noise annoyance.

The lead and senior authors Michael Molitor and Philip Wenzel commented: “We learned from our studies that aircraft noise exposure before MI substantially amplifies subsequent cardiovascular inflammation and aggravates ischemic heart failure facilitated by pro-inflammatory vascular conditioning. Our translational results show that humans that had noise exposure in the past will have a worse outcome if they have an acute MI later in life”.

The cardiologist and noise expert Thomas Münzel concluded: “This is the first time that a translational study was performed to investigate the effects of aircraft noise on acute myocardial infarction. The results were stunning. In experimental animals and humans, aircraft noise markedly exaggerated the consequences of ischemia (left ventricular function, inflammation, and oxidative stress) in response to an acute myocardial infarction. There is no doubt anymore that transportation noise must be considered an important cardiovascular risk factor, comparable to hypercholesterolemia, hypertension, smoking, and diabetes mellitus.”

Reference: “Aircraft noise exposure induces pro-inflammatory vascular conditioning and amplifies vascular dysfunction and impairment of cardiac function after myocardial infarction” by Michael Molitor, Maria T Bayo-Jimenez, Omar Hahad, Claudius Witzler, Stefanie Finger, Venkata S Garlapati, Sanela Rajlic, Tanja Knopp, Tabea K Bieler, Melania Aluia, Johannes Wild, Jeremy Lagrange, Recha Blessing, Steffen Rapp, Andreas Schulz, Hartmut Kleinert, Susanne Karbach, Sebastian Steven, Wolfram Ruf, Philipp Wild, Andreas Daiber, Thomas Münzel and Philip Wenzel, 26 January 2023, Cardiovascular Research.
DOI: 10.1093/cvr/cvad021

The study was funded by the Boehringer Ingelheim Foundation.

Source: SciTechDaily