Study of the changed level of angiogenesis activation factors after endovascular treatment of arteriovenous malformations depending on the type of embolizing material and the radicality of exclusion of the malformation from the blood flow
Objective ‒ тo study changes in angiogenesis factors (VEGF-A, VEGFR-1, Great Endothelin-1) in the blood plasma of patients with arteriovenous malformation (AVM) of different localization before and after endovascular treatment depending on the type of embolizing material used and the results of AVM exclusion from the bloodstream.
Materials and methods. The results of treatment in 2019–2022 were analyzed in 27 patients (11 (41.0 %) men and 16 (59.0 %) women) with AVMs of different localization who underwent endovascular treatment. The age of the patients ranged from 11 to 47 years, the average age was (32.8 ± 5.1) years. Patients with AVM were divided into two groups depending on the type of embolizing material: liquid substances (n=12) and emboli and coils (n=15). The control group was formed from 25 healthy people (10 men and 15 women) without AVM, in which the concentration of VEGF-A, VEGFR-1, Great Endothelin-1 in the blood plasma was determined for 3 months. The average age of the control group was (37.4 ± 4.8) years (from 16 to 57 years).
Results. It was proved that the concentration of VEGF-A in blood plasma in patients with AVM before endovascular treatment was statistically significantly higher by 4.5 times than in the control group, VEGFR-1 by 3.0 times, Great Endothelin-1 by 2.12 times. Within 5‒7 days after embolization, a sharp increase in the level of angiogenesis induction factors was noted by 2.5–3.0 times compared to the initial indicator and a slow decrease during 3 months. However, with the use of liquid embolizing substances, no increase in VEGFR-1 concentration was registered. A comparison of the level of angiogenesis factors before and after endovascular surgical interventions revealed that the total exclusion of AVMs from the bloodstream contributes to the reduction or normalization of the content of angiogenesis factors, while the partial exclusion of AVMs from the bloodstream leads to an increase in their level due to the preservation of the source of production in the AVM structure.
Conclusions. It was established that AVMs remain physiologically active during the life of the organism and undergo vascular remodeling as a result of constant pathological neoangiogenesis. Factors of angiogenesis actively respond to endovascular interventions by changing the expression of VEGF-A, VEGFR-1 and Great Endothelin-1 in the blood plasma, depending on the type of embolizing material and the radicality of AVM exclusion from the bloodstream. This is one of the main reasons for remission or further growth of AVMs and recurrences.
Richter GT, Friedman AB. Hemangiomas and vascular malformations: current theory and management. Int. J. Pediatr. 2012;7:645-58. Doi: 10.1155/2012/645678.
Orlov M Ju, Orlov JuA, Jarockij JuJa. Ostrye narushenija mozgovogo krovoobrashhenija kak manifestacija arteriovenoznyh malformacij golovnogo mozga u detej. Zb. nauk. prac spіvrobіt. NMAPO і m. P.L. Shupika. 2013;22(1):177-81. (in Russian)
Shheglov DV, Barkanov AV, Svyrydjuk OJe ta in. Arteriovenozni malformacii golovnogo mozku. Suchasni pogljady na problemu Zb. nauk. prac spivrobit. NMAPO im. P.L. Shupyka. 2013;22(1):264-71. (in Ukrainian)
Hartmann A, Pile-Spellman J, Stapf С, et al. Risk of endovascular treatment of brain arteriovenous malformations. Stroke. 2002;33(7):1816-20. https://doi.org/10.1161/01. STR.0000020123.80940.B2
Weil AG, Li S, Zhao JZ. Recurrence of a cerebral arteriovenous malformation following complete surgical resection: a case report and review of the literature. Surg. Neurol. Int. 2011;2:175. Doi: 10.4103/2152- 7806.90692.
Sandalcioglu IE, Wende D, Eggert A., et al. Vascular endothelial growth factor plasma levels are significantly elevated in patients with cerebral arteriovenous malformations. Cerebrovasc. Dis. 2006;21(3):154-58. Doi: 10.1159/000090526.
Pavlov KA, Gershtein ES, Dubova EA, Shchegolev AI. Vascular endothelial growth factor and type 2 receptor for this factor in vascular malformations. Bull. Exp. Biol. Med. 2011;150(4):481-84. Doi: 10.1007/S10517-011-174–6.
Mullan S, Mojtahedi S, Johnson DL, Macdonald RL. Embryological basis of some aspects of cerebral vascular fistulas and malformations. J Neurosurg. 1996;85(1):1-8. PMID: 8683257. DOI:10.3171/jns.1996.85.1.0001.
Kim H, Su H, Weinsheimer S, Pawlikowska L, Young WL. Brain arteriovenous malformation pathogenesis: a response-to-injury paradigm. Acta Neurochir. Suppl. 2011;111:83-92. Doi: 10.1136/jnnp.2009.191767.
Leblanc GG, Golanov E, Awad IA, Young WL. Biology of vascular malformations of the brain. Stroke. 2009;40(12):e694-e702. doi: 10.1161/STROKEAHA. 109.563692.
Vemimmen FJAI. Vascular endothelial growth factor blockade: A potential new therapy in the management of cerebral arteriovenous malformations. J. Medical Hypotheses and Ideas. 2014;8(2):57-61. Doi 10.1016/j.jmhi.2013.10.001.
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