Stress-Related Neural Activity Associates With Coronary Plaque Vulnerability and Subsequent Cardiovascular Events.
Neng Dai1, Xianglin Tang1, Xinyu Weng1
1Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China; National Clinical Research Center for Interventional Medicine, Shanghai, China.
Stress-related neural activity (SNA) predicts cardiovascular events by linking to coronary plaque vulnerability. This neural activity is mediated by bone marrow activity, inflammation, and plaque characteristics, increasing the risk of major adverse cardiovascular events (MACE).
Area of Science:
- Cardiology
- Neuroscience
- Radiology
Background:
- Stress-related neural activity (SNA), assessed via amygdalar activity, is a known predictor of cardiovascular events.
- The precise mechanisms linking SNA to coronary plaque vulnerability remain incompletely understood.
Purpose of the Study:
- To investigate the association between SNA and coronary plaque morphology and inflammation.
- To evaluate the predictive capability of SNA for major adverse cardiovascular events (MACE).
Main Methods:
- Utilized 18F-fluorodeoxyglucose positron emission tomography/computed tomography (PET/CT) and coronary computed tomographic angiography (CCTA) in 299 coronary artery disease patients.
- Assessed SNA, bone marrow activity (BMA), coronary inflammation (fat attenuation index [FAI]), and high-risk plaque (HRP) characteristics.
- Employed Cox models, log-rank tests, and mediation analyses to examine relationships and MACE prediction.
Main Results:
- SNA significantly correlated with BMA (r=0.39) and FAI (r=0.49).
- Patients with heightened SNA were more likely to exhibit HRP (40.7% vs 23.5%) and had an increased risk of MACE (adjusted HR 3.22).
- Mediation analysis revealed SNA associates with MACE through BMA, FAI, and HRP.
Conclusions:
- SNA is significantly correlated with coronary inflammation (FAI) and high-risk plaque (HRP) in patients with coronary artery disease.
- SNA is associated with MACE, with a mediating role played by bone marrow activity, coronary inflammation, and plaque vulnerability.
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