Angiographic contribution to the problem of enlargement of cerebral arteriovenous malformations

Krayenbuhl, H

doi:10.1007/bf01405393

Cited by 54 publications

(20 citation statements)

References 17 publications

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“…The initial hypothesis of the congenital origin and growth tendency of AVMs is presently a matter of debate. Enlargement of AVMs or regrowth after negative postoperative angiograms argue for AVMs as dynamic lesions [6,7,8,9,11,12,13,15,26,27]. These observations are supported by several immunohistochemical studies demonstrating the involvement of angiogenic factors.…”

Section: Discussionsupporting

confidence: 68%

Proliferation Activity Is Significantly Elevated in Partially Embolized Cerebral Arteriovenous Malformations

Sandalcioglu¹,

Asgari²,

Wende³

et al. 2010

Cerebrovasc Dis

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Background: The natural history of cerebral arteriovenous malformations (AVMs) is yet to be determined. It has been shown that angiogenic factors are involved in the pathogenesis of AVMs, in particular in partially embolized lesions. This study was conducted to investigate the expression of angiogenic and proliferative factors in relation to different clinical conditions and treatment modalities. Methods: Immunohistochemistry was performed for 145 consecutive cases of cerebral AVMs. The specimens were stained with antibodies against VEGF, bFGF, Ki 67, CD 34 and CD 31. Expression was correlated with clinical presentation (haemorrhage, seizures or other symptoms), AVM localization, size, eloquence and venous drainage, as well as with preoperative AVM embolization. Results: Whereas no correlation was found between the expression of angiogenic factors and different clinical conditions, we observed a significantly increased proliferation activity as shown by Ki 67 expression in patients with intracerebral haemorrhage (p = 0.02) and in patients with preoperative embolization (p = 0.02). Conclusions: Increased proliferation activity in partially embolized AVMs supports a ‘no-touch’ strategy and clinical observation in high-risk AVMs and demands complete AVM elimination in treatable lesions.

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Section: Discussionsupporting

confidence: 68%

Proliferation Activity Is Significantly Elevated in Partially Embolized Cerebral Arteriovenous Malformations

Sandalcioglu¹,

Asgari²,

Wende³

et al. 2010

Cerebrovasc Dis

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“…Unfortunately, although the clinical risks of untreated AVMs are well documented, the angiographic natural history is less well known. Reports of serial angiography in patients with untreated AVMs are mostly limited to case reports of 1 or 2 patients [1, 2, 8], and the few series have small numbers [3, 6, 24, 33]. In total, we identified only 48 cases with delayed angiography at least 1 year after diagnosis.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to these cases with coincidental imaging prior to diagnosis of an AVM, there are numerous cases, including the first 3 presented here, in which no AVM is evident on angiography and then abnormal nidus vessels subsequently appear [1, 3, 21, 22,24,25,26,27,28,29,30,31]. …”

Section: Discussionmentioning

confidence: 99%

Postnatal Development of Arteriovenous Malformations

Jeffree¹,

Stoodley²

2009

Pediatr Neurosurg

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Background: Arteriovenous malformations (AVMs) are commonly thought to be congenital malformations; however, patients usually present in adolescence or adulthood. This study was carried out to better understand the development of AVMs between birth and presentation. Methods: A retrospective review was performed of the medical records of all patients under 25 presenting to a single institution with an AVM or spontaneous intracerebral hemorrhage from 2000 to 2007. Results: Out of a total of 34 cases, 3 children were identified with delayed de novo appearance of an AVM after an intracerebral hemorrhage and normal initial angiography. The clinical and angiographic features are presented for these 3 patients and for an additional patient with AVM recurrence after complete surgical excision. Conclusions: In the light of these cases and a review of the literature, we suggest a hypothesis that AVMs develop postnatally, undergoing a period of growth in childhood or early adulthood, and that they may become symptomatic from the time of their earliest development. The trigger to growth may be shear stress stimulating growth factor expression by endothelial cells lining an arteriovenous fistula. Alternative stimuli, such as venous hypertension, cannot be ruled out.

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“…18,24,27,47,64,72,75,76,80,81,85,86,90,112,116,118 One series of 106 patients with AVMs has demonstrated that > 50% of the lesions increased in size, whereas 9% decreased over a mean period of 8 years without intervention. Remodeling within these lesions can lead to changes in their angiographic appearance over time.…”

mentioning

confidence: 99%

Cerebral arteriovenous malformations. Part 1: cellular and molecular biology

Moftakhar

Hauptman

Malkasian

et al. 2009

FOC

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Object The scientific understanding of the nature of arteriovenous malformations (AVMs) in the brain is evolving. It is clear from current work that AVMs can undergo a variety of phenomena, including growth, remodeling, and/or regression—and the responsible processes are both molecular and physiological. A review of these complex processes is critical to directing future therapeutic approaches. The authors performed a comprehensive review of the literature to evaluate current information regarding the genetics, pathophysiology, and behavior of AVMs. Methods A comprehensive literature review was conducted using PubMed to reveal the molecular biology of AVMs as it relates to their complex growth and behavior patterns. Results Growth factors involved in AVMs include vascular endothelial growth factor, fibroblast growth factor, transforming growth factor β, angiopoietins, fibronectin, laminin, integrin, and matrix metalloproteinases. Conclusions Understanding the complicated molecular milieu of developing AVMs is essential for defining their natural history. Growth factors, extracellular matrix proteins, and other molecular markers will be the key to unlocking novel targeted drug treatments for these brain malformations.

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Angiographic contribution to the problem of enlargement of cerebral arteriovenous malformations

Cited by 54 publications

References 17 publications

Proliferation Activity Is Significantly Elevated in Partially Embolized Cerebral Arteriovenous Malformations

Proliferation Activity Is Significantly Elevated in Partially Embolized Cerebral Arteriovenous Malformations

Postnatal Development of Arteriovenous Malformations

Cerebral arteriovenous malformations. Part 1: cellular and molecular biology

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