Abstract
A chronic inflammatory process characteristic of obstructive sleep apnea promotes vascular endothelial dysfunction and atherogenesis. This process can lead to destabilization and rupture of cardiovascular plaques, which clinically manifests as an acute coronary syndrome or stroke. The aim of this study was to investigate the inflammatory pathway leading to plaque destabilization in non-to-mild and moderate-to-severe groups of OSA patients. This prospective study involved enrollment of patients scheduled for endarterectomy. A sleep study was performed prior to surgery. Immunohistochemistry was performed on atherosclerotic plaques from carotid arteries obtained during standard open endarterectomy to determine levels of CD40, CD40L receptors, MCP-1, and MMP-9. The 46 patients included 14 controls, 13 with mild, 11 with moderate, and 8 with severe OSA. Increased expression of CD40, CD40L receptors, MCP-1, and MMP-9 were found to be proportionate with OSA severity. However, significant differences among groups were observed only for MCP-1 (p = 0.014). Increased expression of inflammatory markers (CD40, CD40L, MCP-1, MMP-9) is associated with increasing OSA severity. This suggests the CD40-CD4-L inflammatory pathway may contribute to plaque instability and rupture in OSA patients.
Highlights
IntroductionObstructive sleep apnea [1] is one of the most common sleep disorders among adults
Licensee MDPI, Basel, Switzerland.Obstructive sleep apnea [1] is one of the most common sleep disorders among adults.It is characterized by recurrent episodes of partial or complete upper airway collapse during sleep [2]
The present study demonstrated that moderate–severe OSA patients had increased levels of all measured markers of atherotic plaque vulnerability; statistically significant differences were only observed for Monocyte chemoattractant protein -1 (MCP-1)
Summary
Obstructive sleep apnea [1] is one of the most common sleep disorders among adults. It is characterized by recurrent episodes of partial or complete upper airway collapse during sleep [2]. Macrophages, lipid peroxidation, and endothelial dysfunction all lead to plaque formation [4]. Stable atherosclerotic plaques tend to transform to unstable plaques, but the mechanism of this transition is not fully understood [5]. An unstable plaque is vulnerable to rupture, which may cause acute cardiovascular episodes such as stroke or acute coronary thrombosis
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