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Updated: Oct 16, 2026
Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression
Published on: January 15, 2022
Sleep-inflammation-coronary plaque phenotype axis: clinical validation and inflammation-mediated mechanisms based on
Yang Liu1, Xun-Xun Feng1, Qian-Yun Guo1
1Beijing Key Laboratory of Precision Medicine of Coronary Atherosclerotic Disease, Beijing Institute of Heart Lung and Blood Vessel Disease, Clinical Center for Coronary Heart Disease, Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Background:
The influence of sleep duration on vulnerable coronary plaques, as evaluated via optical coherence tomography (OCT), has not been clearly defined in coronary artery disease (CAD). Here, the relationships between habitual sleep duration and thin-cap fibroatheroma (TCFA) detected by OCT were investigated in individuals with CAD. We further investigated whether systemic inflammation, represented by the neutrophil-to-lymphocyte ratio (NLR), represents a mediator of this association.
Methods:
Overall, 1,178 patients with angiographically confirmed CAD who underwent OCT imaging and completed standardized sleep questionnaires were enrolled. Participants were categorized according to reported sleep duration. Multivariable logistic regression modeling was employed to assess the link between sleep duration and TCFA. Linear regression analyses assessed the association between sleep duration and NLR. Restricted cubic spline (RCS) modeling was applied as a means of detecting possible nonlinear associations between NLR and TCFA. Mediation analyses were then conducted to determine whether NLR functioned as an intermediate variable linking sleep duration and plaque vulnerability.
Results:
These results offer the first clinical evidence of the link between sleep duration and TCFA presence in individuals with CAD, with the TCFA risk in the abnormal sleep duration group being 2.16 times that of the normal group (95% CI: 1.63-2.88, P < 0.001). Sleep duration was also independently correlated with NLR, and RCS analysis highlighted a nonlinear relationship between NLR levels and TCFA risk (P < 0.001). Importantly, mediation analysis demonstrated that NLR partially mediated the effect of sleep duration on TCFA, supporting the existence of a sleep-inflammation-plaque vulnerability axis.
Conclusion:
The sleep duration has been shown to be significantly associated with the risk of developing TCFA. In addition, a partial mediating effect of NLR on this relationship has been found.
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