Cardio-oncology & otherCohort study
A neurobiological mechanism linking transportation noise to cardiovascular disease in humans
- Retrospective cohort study
- mediation analysis
Authors' 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.
Study context
- Population
- Adults without cardiovascular disease (CVD) or active cancer who underwent clinical 18F-FDG PET/CT imaging
- Participants
- 498 adults
- Exposure
- Higher vs lower transportation noise exposure
- Outcome
- MACE
- Follow-up
- Within 5 years
Main finding
As reported in the abstract
MACE per 5 dBA increase in 24-h transportation noise · median 4.06 years
Hazard ratio
1.341
95% CI 1.147–1.567
P < 0.001
Noise exposure (per 5 dBA increase)
HR 1.341 (95% CI 1.147–1.567); P < 0.001
Per 5 dBA increase, as printed
- Individuals with MACE
- 40
Observational data: associations, not effects.
Further findings
| Outcome | standardized β (95% CI) | P value |
|---|---|---|
| Amygdalar metabolic activity (AmygA) | 0.112 (0.051–0.174) | P < 0.001 |
| Arterial inflammation (ArtI) | 0.045 (0.001–0.090) | P = 0.047 |
Mediation of noise–MACE link via AmygA and arterial inflammation (ArtI) (serial)
- Proportion of relationship accounted for
- 12-26%
Original publication
A neurobiological mechanism linking transportation noise to cardiovascular disease in humans. Eur Heart J. Published 26 November 2019. doi:10.1093/eurheartj/ehz820
Summarised from the published abstract; every number is checked against it