Background
Stress-related neural activity ( SNA) assessed by amygdala activity can predict cardiovascular events. However, its mechanical link to plaque vulnerability is not fully elucidated.
Goals
The authors sought to investigate the association of stress-related neuronal activity (SNA) with morphological and inflammatory characteristics of coronary plaque, as well as its ability to predict major adverse cardiovascular events (MACE).
Methods
A total of 299 patients with coronary artery disease (CAD) and no cancer underwent 18F-fluorodexoyglucose positron emission tomography/computed tomography (PET/CT) and available coronary computed tomography angiography (CCTA) between 1 January 2013 and December 31, 2020.
Stress-related neuronal activity (SNA) and bone marrow activity (BMA) were assessed with validated methods. Coronary computed tomography angiography (CCTA) assessed coronary inflammation (fat attenuation index [FAI]) and high-risk plaque (HRP) features .
The relationships between these characteristics were analyzed. Relationships between SNA and MACE were assessed with Cox models, log-rank tests, and mediation (path) analyses.
Results
Stress-related neuronal activity (SNA) was significantly correlated with bone marrow activity (BMA) (r = 0.39; P < 0.001) and FAI (r = 0.49; P < 0.001).
Patients with elevated stress-related neural activity (SNA) are more likely to have high-risk plaques (HRP) (40.7% vs. 23.5%; P = 0.002) and increased risk of MACE (17.2 % vs 5.1%, adjusted HR 3.22, 95% CI 1.31-7.93, P = 0.011).
Mediation analysis suggested that higher SNA is associated with MACE through a serial mechanism involving BMA, FAI, and HRP.
Conclusions Stress-related neural activity ( SNA) is significantly correlated with FAI and HRP in patients with coronary heart disease. Furthermore, such neuronal activity was associated with MACE, which was mediated in part by leukopoietic activity in the bone marrow, coronary inflammation and plaque vulnerability . |
