The role of myeloperoxidase and collagen–elastin scaffold in development of unstable atherosclerotic plaques in humans

Background: Some current evidence suggest that myeloperoxidase may participate in the pathogenesis of atherosclerosis. However, its role in the development of unstable atherosclerotic lesions in humans and effects on a collagen-elastin scaffold of the vascular wall are poorly understood. Aim: This study aimed to compare the immunohistochemical assays of myeloperoxidase, smooth muscle cells, and elastic and collagen fibers in various types of human atherosclerotic lesions. Methods: Histology and immunohistochemistry tests were performed on autopsy samples obtained from 21 patients who died from acute cardiovascular failure caused by atherosclerosis. Segments of the aorta (from the arch, thoracic, and abdominal regions), coronary arteries, and the basilar artery were examined. A total of 50 tissue samples were included. We used a highly sensitive, two-step avidin–biotin assay technique to detect myeloperoxidase expression in various types of atherosclerotic vascular wall lesions. Results: Intracellular myeloperoxidase location was detected in the intima of unstable atherosclerotic plaques, and its amount increased as the lesions progressed. However, unstable plaques showed a significant decrease in smooth muscle cells and destruction of the collagen–elastin scaffold. This was accompanied by the degradation of elastic and collagen fibers, as well as the rupture of the plaque cap. Conclusion: It is hypothesized that the production of myeloperoxidase by mononuclear cells negatively affects human smooth muscle cells by promoting apoptosis and inhibiting the synthesis of elastic and collagen fibers in the vascular wall. This may destabilize atherosclerotic lesions.