Abstract
Objectives:
Arteriovenous malformations (AVMs) are congenital vascular malformations that result from a defect in vascular morphogenesis. These lesions are slow-growing, infiltrative, and destructive resulting in significant morbidity associated with cardiac overload and increased susceptibility to massive bleeding. Recent evidence suggests a role of matrix metalloproteinases (MMPs), a family of enzymes functioning in tissue remodeling via degradation of extracellular matrix proteins and cleaving of surface molecules, in the pathogenesis of AVM development and rupture. This study sought to explore the role of MMPs, particularly MMP-9, in AVM formation and progression.
Methods:
Serum samples from patients with AVM, hemangioma, and pyogenic granuloma were collected and isolated at various stages of development. Relative quantities of MMP-2, MMP-9, and VEGF in each group were calculated and analyzed using sandwich-capture enzyme-linked immunosorbent assay.
Results:
MMP-2 concentrations were found to be decreased in AVM serum samples when compared with serum samples from the pyogenic granuloma controls (27.9 ± 5.97 vs 32.84 ± 2.20, P = 6.3 × 10–9); MMP-9 concentrations were found to be increased in AVM serum samples when compared with hemangioma serum samples (1698.81 ± 410.86 vs 1105.02 ± 239.43, P < .02); and VEGF concentrations were found to be decreased in AVM serum samples when compared with hemangioma serum samples (52.27 ± 63.02 vs 174.0 ± 9.84, P < .05).
Conclusions:
The results of this study provide support for a role of MMP-9 in AVM progression and recurrence. Specifically, an increase in MMP-9 appears to be associated with AVM formation and may play an important role in its pathogenesis.
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