Depression and Anxiety Associate With Adverse Cardiovascular Events via Neural, Autonomic, and Inflammatory Pathways
Authors' conclusion
Depression and anxiety independently associate with increased MACE risk, partly mediated by heightened stress-related neural activity and autonomic-immune dysregulation. The risk is greatest among those with both conditions, underscoring shared stress-related pathophysiology.
Study context
- Population
- Participants of the Mass General Brigham Biobank (2010–2020)3,078 (3.6%) developed major adverse cardiac events (MACE)
- Participants
- 85,551 participants
- Exposure
- Depression, anxiety, or concurrent anxiety plus depression vs none
- Outcome
- MACE (ICD codes)
- Follow-up
- Median 3.4 years (IQR, 1.9-4.8)
Methodological detailsbiobank, mediation analysis
- Biobank
- Mediation analysis
Main finding
As reported in the abstract
MACE · median 3.4 years
Hazard ratio (95% CI)P value
Depression
1.24(1.14–1.34)
P < 0.001Anxiety plus depression
1.35(1.23–1.49)
P < 0.001Observational data: associations, not effects.
Further findings
Depression and amygdala-to-cortex activity ratio, HRV, CRP (subsamples)
- Higher amygdala-to-cortex activity ratio (imaging N=1123)
- β=0.16; P=0.006
- Lower heart rate variability (N=7862)
- β=−0.20; P<0.001
- Higher CRP (N=12 906)
- β=0.14; P<0.001
Mediation of depression-MACE relationship
- Indirect effect via amygdala-to-cortex activity ratio (log OR)
- 0.04
- Indirect effect via heart rate variability (log OR)
- 0.04
- Indirect effect via CRP (log OR)
- 0.02
- All P<0.05
- Similar associations for anxiety or concurrent anxiety plus depression
Original publication
Depression and Anxiety Associate With Adverse Cardiovascular Events via Neural, Autonomic, and Inflammatory Pathways. Circ Cardiovasc Imaging. Published 17 December 2025. doi:10.
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