- Long-term exposure to noise is known to contribute to cardiovascular disease and other adverse physical effects, but the underlying mechanism isn't clear
- In a retrospective study of 498 patients, greater residential exposure to transportation noise was associated with increased metabolic activity of the amygdala, a brain region critically involved in the response to stress, and greater atherosclerotic inflammation
- Greater noise exposure was also associated with an increased risk of major adverse cardiovascular events, even after adjustment for important confounders
- The link between noise and cardiovascular events appears to be mediated in part by a multi-organ pathway that begins with activation of stress-responsive brain tissues, involves heightened arterial inflammation and culminates in clinical cardiovascular disease events
- If the findings are confirmed in a prospective trial, it may be worthwhile to find ways to lower amygdalar activity and arterial inflammation in subjects at risk of noise-associated cardiovascular disease
Long-term exposure to loud noise is known to precipitate a chronic stress reaction in the body. Epidemiologic studies have repeatedly shown that noise exposure contributes to cardiovascular disease (CVD) and other adverse physical effects, but the underlying mechanism isn't clear.
The amygdala plays a critical role in the brain's response to noise and other stressors. 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) allows simultaneous measurement of amygdalar metabolic activity and atherosclerotic inflammation, an important precursor to major adverse cardiovascular disease events (MACE).
In a previous longitudinal study published in The Lancet, Ahmed Tawakol, MD, director of nuclear cardiology in the Cardiology Division at Massachusetts General Hospital, and colleagues used 18F-FDG PET/CT to determine that upregulated amygdalar activity was associated with increased arterial inflammation and increased risk of MACE. In a recent study reported in the European Heart Journal, Dr. Tawakol, Michael T. Osborne, MD, cardiologist, Azar Radfar, MD, nuclear cardiology fellow, and colleagues extend that research to describe a biologic pathway that links higher noise exposure to MACE.
The researchers retrospectively studied 498 individuals without cancer or active CVD who underwent 18F-FDG-PET/CT imaging at Mass General between 2005 and 2008. The median age was 55 and 58% were female.
Investigators who were blinded to all clinical information quantified amygdalar activity on the 18F-FDG PET/CT images, as well as arterial inflammation. Separately, each subject's exposure to traffic and aircraft noise was quantified by entering their address into a database maintained by the U.S. Department of Transportation.
Noise Exposure and Tissue Activity
The researchers found that increasing noise exposure was significantly associated with increased amygdalar activity. This was true at all noise thresholds studied: per 5-dBA increase, the upper tertile (>45 dBA) versus others, the upper quartile (>50 dBA) versus others and >55 dBA versus others. Each 5-dBA increase in noise exposure was also significantly associated with increased arterial inflammation.
Noise Exposure, MACE and Survival
Over a median follow-up of four years, 8% of the subjects developed MACE (CVD death, myocardial infarction, coronary or peripheral artery revascularization, unstable angina, cerebrovascular accident or heart failure). The risk of MACE was significantly greater in individuals exposed to higher noise (HR per 5-dBA increase, 1.40; 95% CI, 1.20–1.62; P < .001).
At all noise thresholds studied, MACE-free survival was significantly lower among individuals with greater noise exposure. Noise exposure remained associated with MACE after accounting for traditional CVD risk factors, health care access, socioeconomic factors and air pollution.
A Proposed Biologic Pathway
Using mediation analysis, the researchers found that a pathway linking increased noise (>45 dBA) to MACE via increased metabolic activity of the amygdala and arterial inflammation in series was statistically significant.
This pathway accounted for 12% to 26% of the relationship between noise exposure and MACE after adjustment for age, sex and traditional CVD risk factors.
Several types of societal interventions would conceivably interrupt the pathway linking noise to CVD: new technologies and regulations to reduce transportation noise, better urban planning and better sound insulation of buildings. Individualized noise reduction strategies, such as earplugs, could also be evaluated.
This study further suggests, however, that the neural–arterial axis itself is a potential therapeutic target. If the findings are confirmed in a prospective trial, it may be worthwhile to find ways to lower amygdalar activity and arterial inflammation in subjects at risk of noise-associated CVD.
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