Abstract

Background: Fibromascular dysplasia of internal carotid arteries (ICA) leading to their pathological deformities is one of the causes of cerebral vascular insufficiency. The structural changes of the artery wall and their causes remain poorly understood. Materials and Methods: We investigated the expression of elastin, collagen types I and III, smooth muscle cells, gelatinases degrading elastin (matrix metalloproteinases 2 and 9 (MMP2 and MMP9) and tissue inhibitors of matrix metalloproteinases 1 and 2 (TIMP1 and TIMP2) on formalin-fixed surgical samples with the methods of immunohistochemistry and confocal laser scanning microscopy. Results: We revealed the fragmentation of elastic fibers (100% of patients) and some reduction of smooth muscle cells (p 0.05). Conclusion: Our data demonstrate that the main feature of fibromuscular dysplasia underlying the pathological deformities of ICA –fragmentation of elastic fibers – is caused by the disturbance of balance between gelatinases and their inhibitors.

Highlights

  • Among the causes of cerebral vascular insufficiency one of the most important is fibromascular dysplasia of internal carotid arteries (ICA) leading to their pathological deformities.[1]

  • The histological research of ICA with fibromuscular dysplasia revealed the thickened tunica intima, the impairment of the structure of tunica media characterized by elastic fiber fragmentation, irregular collagen fiber arrangement, the formation of fibrous areas, in some places the internal elastic membrane destruction was noted (Figure 1a)

  • The expression of elastin was higher in the tunica media of ICA with pathological deformities than in the control group (p

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Summary

Introduction

Among the causes of cerebral vascular insufficiency one of the most important is fibromascular dysplasia of internal carotid arteries (ICA) leading to their pathological deformities.[1] Pathological deformities of ICA occur at 5-7% of the adult population.[2,3,4] Most investigators suppose that this is the result of congenital[5, 6] or acquired factors (arterial hypertension, atherosclerosis, ageing process),[7,8,9] but the etiology of such changes is still not completely understood. Fibromascular dysplasia of internal carotid arteries (ICA) leading to their pathological deformities is one of the causes of cerebral vascular insufficiency. With the use of confocal microscopy, we showed the decrease of elastin expression with a high MMP9 activity which correlated with low expression of TIMP-1 in the group of ICA with pathological deformities. Conclusion: Our data demonstrate that the main feature of fibromuscular dysplasia underlying the pathological deformities of ICA –fragmentation of elastic fibers – is caused by the disturbance of balance between gelatinases and their inhibitors

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