Michael T Osborne1,2, Azar Radfar1,2, Malek Z O Hassan1, Shady Abohashem1,2, Blake Oberfeld1, Tomas Patrich1, Brian Tung1, Ying Wang1,3, Amorina Ishai1, James A Scott4, Lisa M Shin5,6, Zahi A Fayad7, Karestan C Koenen8, Sanjay Rajagopalan9, Roger K Pitman6, Ahmed Tawakol1,2. 1. Department of Radiology, Cardiac Imaging Research Center, Massachusetts General Hospital, 165 Cambridge St, Suite 400, Boston, MA 02114, USA. 2. Cardiology Division, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, 55 Fruit St, Boston, MA 02114-2750, USA. 3. Department of Nuclear Medicine, First Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang 110001, Liaoning Province, China. 4. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit St, Boston, MA 02114-2750, USA. 5. Department of Psychology, Tufts University, 490 Boston Ave, Medford, MA 02115, USA. 6. Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, 55 Fruit St, Boston, MA 02114-2750, USA. 7. BioMedical Engineering and Imaging Institute, Icahn School of Medicine at Mount Sinai, 1470 Madison Ave, First Floor, New York, NY 10029, USA. 8. Department of Epidemiology, Harvard University T.H. Chan School of Public Health, 677 Huntington Ave, Boston, MA 02115, USA. 9. Department of Cardiovascular Medicine, Case Western Reserve University, 11100 Euclid Ave, Cleveland, OH 44106, USA.
Abstract
AIMS: Chronic noise exposure associates with increased cardiovascular disease (CVD) risk; however, the role of confounders and the underlying mechanism remain incompletely defined. The amygdala, a limbic centre involved in stress perception, participates in the response to noise. Higher amygdalar metabolic activity (AmygA) associates with increased CVD risk through a mechanism involving heightened arterial inflammation (ArtI). Accordingly, in this retrospective study, we tested whether greater noise exposure associates with higher: (i) AmygA, (ii) ArtI, and (iii) risk for major adverse cardiovascular disease events (MACE). METHODS AND RESULTS: Adults (N = 498) without CVD or active cancer underwent clinical 18F-fluorodeoxyglucose positron emission tomography/computed tomography imaging. Amygdalar metabolic activity and ArtI were measured, and MACE within 5 years was adjudicated. Average 24-h transportation noise and potential confounders were estimated at each individual's home address. Over a median 4.06 years, 40 individuals experienced MACE. Higher noise exposure (per 5 dBA increase) predicted MACE [hazard ratio (95% confidence interval, CI) 1.341 (1.147-1.567), P < 0.001] and remained robust to multivariable adjustments. Higher noise exposure associated with increased AmygA [standardized β (95% CI) 0.112 (0.051-0.174), P < 0.001] and ArtI [0.045 (0.001-0.090), P = 0.047]. Mediation analysis suggested that higher noise exposure associates with MACE via a serial mechanism involving heightened AmygA and ArtI that accounts for 12-26% of this relationship. CONCLUSION: Our findings suggest that noise exposure associates with MACE via a mechanism that begins with increased stress-associated limbic (amygdalar) activity and includes heightened arterial inflammation. This potential neurobiological mechanism linking noise to CVD merits further evaluation in a prospective population. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: Chronic noise exposure associates with increased cardiovascular disease (CVD) risk; however, the role of confounders and the underlying mechanism remain incompletely defined. The amygdala, a limbic centre involved in stress perception, participates in the response to noise. Higher amygdalar metabolic activity (AmygA) associates with increased CVD risk through a mechanism involving heightened arterial inflammation (ArtI). Accordingly, in this retrospective study, we tested whether greater noise exposure associates with higher: (i) AmygA, (ii) ArtI, and (iii) risk for major adverse cardiovascular disease events (MACE). METHODS AND RESULTS: Adults (N = 498) without CVD or active cancer underwent clinical 18F-fluorodeoxyglucose positron emission tomography/computed tomography imaging. Amygdalar metabolic activity and ArtI were measured, and MACE within 5 years was adjudicated. Average 24-h transportation noise and potential confounders were estimated at each individual's home address. Over a median 4.06 years, 40 individuals experienced MACE. Higher noise exposure (per 5 dBA increase) predicted MACE [hazard ratio (95% confidence interval, CI) 1.341 (1.147-1.567), P < 0.001] and remained robust to multivariable adjustments. Higher noise exposure associated with increased AmygA [standardized β (95% CI) 0.112 (0.051-0.174), P < 0.001] and ArtI [0.045 (0.001-0.090), P = 0.047]. Mediation analysis suggested that higher noise exposure associates with MACE via a serial mechanism involving heightened AmygA and ArtI that accounts for 12-26% of this relationship. CONCLUSION: Our findings suggest that noise exposure associates with MACE via a mechanism that begins with increased stress-associated limbic (amygdalar) activity and includes heightened arterial inflammation. This potential neurobiological mechanism linking noise to CVD merits further evaluation in a prospective population. Published on behalf of the European Society of Cardiology. All rights reserved.
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