Cerebral arteriovenous malformations and associated aneurysms: analysis of 305 cases from a series of 662 patients.

OBJECTIVE

Spontaneous intracranial hemorrhage is the primary danger for patients with cerebral arteriovenous malformations (AVMs). Associated aneurysms are considered weak points that increase the risk of intracranial hemorrhage. Aneurysms are classified as proximal aneurysms (PROXs) or intranidal aneurysms (INs).

METHODS

The present study was based on a series of 662 patients who presented with AVMs between 1985 and 1995. Its purpose was to evaluate prestated hypotheses using prospectively collected data. In 305 of these 662 patients, 372 INs and 313 PROXs were observed and analyzed with respect to their shapes, locations, and sizes. Partial targeted endovascular treatment with n-butylcyanoacrylate was performed for 450 of the 662 patients (68%) in this series, using a standard protocol. Of 450 treated patients, 181 (40%) had at least one IN and 138 (30.7%) had at least one PROX. Analysis of changes in the sizes of PROXs was based on the follow-up data for 83 treated patients, with a total of 149 PROXs. Changes in the sizes of PROXs in treated patients were analyzed with respect to PROX shapes, PROX locations, and treated AVM occlusion rates. Univariate and multivariate event data analyses were used to study factors influencing aneurysm shrinkage. False aneurysms were excluded from the series.

RESULTS

Presentation with intracranial hemorrhage was not correlated with any type of aneurysm. However, INs demonstrated a higher rebleeding rate (P < 0.002) before treatment. Among 181 patients, 92.2% of INs were occluded, together with the related portions of the AVM nidi. In cases of PROXs, embolization of the cerebral AVM compartment fed by the artery with the aneurysm was a priority. During follow-up monitoring of 83 treated patients with 149 PROXs, 100% shrinkage was observed for 12 PROXs and more than 50% shrinkage was observed for 33 PROXs. The median time required for more than 50% shrinkage was 3.5 years. The shrinkage of PROXs was influenced by the degree of AVM occlusion (P = 0.027) and occurred faster for PROXs on midline structures, such as the anterior cerebral artery and the circle of Willis, compared with arteries distal to the circle of Willis (P = 0.004). No rupture of untreated PROXs was observed after partial targeted treatment of AVMs.

CONCLUSION

PROXs are not primary treatment targets, compared with AVMs themselves. INs should be primary targets of endovascular therapy, because of their increased risk of rebleeding.