Risk of spontaneous haemorrhage after diagnosis of cerebral arteriovenous malformation

Mast, H.; Young, William L.; Hc, Koennecke; Sciacca, Robert R.; Osipov, A; Pile‐Spellman, John; Hacein‐Bey, Lotfi; Duong, Huy; Stein, Bennett M.; Mohr, J. P.

doi:10.1097/00008506-199804000-00013

Cited by 94 publications

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“…Reported yearly hemorrhage rates may be as low as 2% or as high as 32.6%. [2][3][4][5]7,22,23 The appropriate management of patients with AVMs can therefore vary from simple observation to aggressive multimodality treatment aimed at total AVM obliteration. 6 Because risks of treatment must be weighed against those of conservative management of bAVMs, we sought to obtain a better understanding of the natural history and factors predictive of hemorrhage in bAVM patients.…”

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confidence: 99%

The Natural History and Predictive Features of Hemorrhage From Brain Arteriovenous Malformations

Costa

Wallace

Brugge

et al. 2009

Stroke

397

264

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Background and Purpose-Patients harboring brain arteriovenous malformations (bAVMs) are at a lifelong risk for hemorrhagic strokes, but the natural history is poorly understood. We examined the impact of demographic and angiographic features on the likelihood of future hemorrhage. Methods-A prospectively accrued database of bAVM patients maintained at the Toronto Western Hospital was analyzed; 678 consecutive, prospectively enrolled bAVM patients were followed for 1931.7 patient-years. The rate of hemorrhage over long-term follow-up was recorded. The impact of baseline clinical and radiographic features and partial treatment on time to hemorrhage were analyzed using survival analysis. Neurological outcome after hemorrhage was assessed using the Glasgow Outcome Score. Results-Hemorrhage rates were 4.61% per year for the entire cohort (nϭ678), 7.48% per year for bAVMs with initial hemorrhagic presentation (nϭ258), 4.16% per year for initial seizure presentation (nϭ260)

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confidence: 99%

The Natural History and Predictive Features of Hemorrhage From Brain Arteriovenous Malformations

Costa

Wallace

Brugge

et al. 2009

Stroke

397

264

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“…The usual symptoms are hemorrhage (about 50% of the cases), seizures (30%), headaches (20%), progressive neurological deficit (5%), and other less common presentations (5%) 1 . The risk of hemorrhage varies from 2 to 4% per year, and may reach 18% after a first bleeding episode [1][2][3][4] . Hemorrhage is usually associated with 10 to 15% morbidity in cAVM, and this rate increases after each recurrence [4][5][6] .…”

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confidence: 99%

“…The factors that are known to predispose to the occurrence of hemorrhage are smallsized lesions, deep or posterior fossa location, deep venous drainage, venous stenosis, elevated per-fusion pressure, and presence of aneurysms 2,3,[10][11][12][13] . Some investigators claim that presentation with seizures may be a protective factor against hemorrhage in untreated cAVMs.…”

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confidence: 99%

“…Some investigators claim that presentation with seizures may be a protective factor against hemorrhage in untreated cAVMs. 1,3,14 Hemorrhage can only be prevented by total obliteration or excision of the lesion, since residual pathologic vessels may cause bleeding 8,15 . Several studies have also reported that embolization in cAVM may be useful in the management of patients presenting hard-to-control seizures, progressive neurological deficit, and headaches, and to improve cerebral perfusion 8,9,16 .…”

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confidence: 99%

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Does treatment with N-butyl cyanoacrylate embolization protect against hemorrhage in cerebral arteriovenous malformations?

Raupp

Fernandes

2005

Arq. Neuro-Psiquiatr.

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OBJECTIVE: To assess the role of this procedure to prevent hemorrhage in cerebral arteriovenous malformations (cAVM). METHOD: Between 1992 and 2000, we studied 104 patients submitted to embolization as the main treatment. Patients were followed until hemorrhage or death. RESULTS: Follow-up ranged from 1.6 months to 8 years. The most frequent presentations were hemorrhage (50%) and seizures (38%). In addition, 40% were small (<30 mm); 56% were medium (30-60 mm). Obliteration was <1/3 in 11% of the cases; from 1/3 to <2/3 in 49%; >2/3 in 36%; complete in 5%. The risk of death was 1%/year, and of bleeding, 5.4%/year. Presentation with hemorrhage and low obliteration rate were the main factors associated with hemorrhage. CONCLUSION: cAVM embolization provides limited protection against hemorrhage with obliteration rates below 2/3. Presentation with hemorrhage is the main factor for predicting hemorrhage.

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“…Therefore, given the total AVM population prevalence of 10-18 per 100,000 adults [3,7], the fraction of HHT-AVMs in large referral series should be approximately 5-10%. Interestingly, HHT accounts for less than 1% of the UCSF [31] and Columbia [39] AVM databases (unpublished data), suggesting that systematic underestimation of undiagnosed HHT may occur in the large referral cohorts.…”

Section: Mendelian Diseasementioning

confidence: 99%

Genetic considerations relevant to intracranial hemorrhage and brain arteriovenous malformations

Kim

Marchuk

Pawlikowska

et al.

Acta Neurochirurgica Supplementum

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SUMMARYBrain arteriovenous malformations (AVM) cause intracranial hemorrhage (ICH), especially in young adults. Molecular characterization of lesional tissue provides evidence for involvement of both angiogenic and inflammatory pathways, but the pathogenesis remain obscure and medical therapy is lacking. Abnormal expression patterns have been observed for proteins related to angiogenesis (e.g., VEGF, Angiopoietin-2, MMP-9), and inflammation (e.g., IL-6 and MPO). Macrophage and neutrophil invasion has also been observed in the absence of prior ICH. Candidate gene association studies have identified a number of germline variants associated with clinical ICH course and AVM susceptibility. A single nucleotide polymorphism (SNP) in ALK-1 is associated with AVM susceptibility, and SNPs in IL-6, TNF-α and APOE are associated with AVM rupture. These observations suggest that even without a complete understanding of the determinants of AVM development, the recent discoveries of downstream derangements in vascular function and integrity may offer potential targets for therapy development. Further, biomarkers can now be established for assessing ICH risk. Finally, these data will generate hypotheses that can be tested mechanistically in model systems, including surrogate phenotypes, such as vascular dysplasia and/or models recapitulating the clinical syndrome of recurrent spontaneous ICH. Keywords angiogenesis; inflammation; vascular malformationsBrain arteriovenous malformations (AVM) represent a relatively infrequent but important source of neurological morbidity in relatively young adults [4]. Brain AVMs have a population prevalence of 10-18 per 100,000 adults [3,7], and a new detection rate of ~1.3 per 100,000 person-years [58]. The basic morphology is of a vascular mass, called the nidus, that directly shunts blood between the arterial and venous circulations without a true capillary bed. There is usually high flow through the feeding arteries, nidus and draining veins. The nidus is a

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Risk of spontaneous haemorrhage after diagnosis of cerebral arteriovenous malformation

Cited by 94 publications

References 0 publications

The Natural History and Predictive Features of Hemorrhage From Brain Arteriovenous Malformations

The Natural History and Predictive Features of Hemorrhage From Brain Arteriovenous Malformations

Does treatment with N-butyl cyanoacrylate embolization protect against hemorrhage in cerebral arteriovenous malformations?

Genetic considerations relevant to intracranial hemorrhage and brain arteriovenous malformations

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