Outcome analysis of preoperative embolization with N-butyl cyanoacrylate in cerebral arteriovenous malformations.

PURPOSE: To determine the influence of preoperative N-butyl cyanoacrylate embolization on outcome in the treatment of cerebral arteriovenous malformations. METHODS: Two groups were compared: 30 patients who underwent surgery and embolization versus 41 patients who underwent surgery only. Both groups were categorized by Spetzler-Martin grade and evaluated with the Glasgow Outcome Scale at various intervals. The long-term follow-up in months was, for surgery only, mean of 35 and range of 4 to 59, and for surgery and embolization, mean of 10 and range of 1 to 19). RESULTS: The arteriovenous malformations in the surgery and embolization group had a larger average greatest diameter (4.2 +/- 1.5 cm versus 3.4 +/- 1.8 cm) and were of higher Spetzler-Martin grade (89% versus 68% grade III-V). No significant difference in the preoperative or immediate postoperative (less than 24 hours) Glasgow Outcome Scale was identified between the two groups. At I week after surgery, the surgery and embolization group displayed a significantly better outcome evaluation (70% versus 41% with Glasgow Outcome Scale score of 5). The long-term evaluation continued to favor the surgery and embolization patients (86% versus 66% with Glasgow Outcome Scale score of 5). CONCLUSION: Preoperative N-butyl cyanoacrylate embolization improves postsurgical outcome.

The effect of arteriovenous malformations on the distribution of intracerebral arterial pressures.

PURPOSE: To examine the distribution of arterial hypotension surrounding arteriovenous malformations (AVMs) using a standardized system of vascular zones. METHODS: Mean arterial pressures were recorded during superselective cerebral angiography in 96 patients with AVMs (before they underwent liquid polymer embolization) with the use of a system of vascular zones: E = extracranial internal carotid or vertebral artery; I = intracranial internal carotid or basilar artery; T = transcranial Doppler insonation site (A1, P1, M1); H = halfway to feeder, perfusing normal tissue and shunt; and F = feeder at site of N-butyl cyanoacrylate injection. Distal arterial pressure was measured contralateral to the AVM in an additional 12 patients (zone Hc). RESULTS: Zone pressures (mm Hg +/- SD) were E = 76 +/- 16, I = 69 +/- 15, T = 59 +/- 16, H = 47 +/- 13, and F = 39 +/- 15 mm Hg. Vessel/systemic ratios for the zones were E = 0.97 +/- 0.05, I = 0.86 +/- 0.08, T = 0.75 +/- 0.12, H = 0.61 +/- 0.13, and F = 0.50 +/- 0.18. Measurements were obtained in 29 patients in all five zones and all had similar mean values. Zone Hc pressure was 66 +/- 17 mm Hg and the ratio was 0.78 +/- 0.12, both greater than zone H values. CONCLUSION: Using a standardized system of anatomic vascular zones, we found a progressive and significant decrease in intracerebral arterial pressure in patients with AVMs that proceeded from the circle of Willis to the nidus. Large areas of parenchyma sharing the same parent arterial supply may be subject to chronic hypotension.

Adenosine-induced cardiac pause for endovascular embolization of cerebral arteriovenous malformations: technical case report.

OBJECTIVE: Extremely high flow through arteriovenous malformations (AVMs) may limit the safety and effectiveness of endovascular glue therapy. To achieve a more controlled deposition of glue, we used transient but profound systemic hypotension afforded by an intravenously administered bolus of adenosine to induce rapidly reversible high-degree atrioventricular block. METHODS AND CASE REPORT: A patient with a large high-flow occipital AVM fed primarily by the posterior cerebral artery underwent n-butyl cyanoacrylate glue embolization. Nitroprusside-induced systemic hypotension did not adequately reduce flow through the nidus, as determined by contrast injection in the feeding artery. In a dose-escalation fashion, boluses of adenosine were administered to optimize the dose and verify that there was no flow reversal in the AVM and no other unexpected hemodynamic abnormalities by arterial pressure measurements and transcranial Doppler monitoring of the posterior cerebral artery feeding the AVM. Thereafter, 64 mg of adenosine was rapidly injected as a bolus to provide 10 to 15 seconds of systemic hypotension (approximately 20 mm Hg). Although there were conducted beats and some residual forward flow through the AVM during this time, the mean systemic and feeding artery pressures were roughly similar and remained relatively constant. A slow controlled injection of n-butyl cyanoacrylate glue was then performed, with excellent filling of the nidus. CONCLUSION: Adenosine-induced cardiac pause may be a viable method of partial flow arrest in the treatment of cerebral AVMs. Safe, deep, and complete embolization with a permanent agent may increase the likelihood of endovascular therapy's being curative or may further improve the safety of microsurgical resection.

Adenosine-induced ventricular asystole to induce transient profound systemic hypotension in patients undergoing endovascular therapy. Dose-response characteristics.

BACKGROUND: Adenosine-induced asystole has been used to induce transient systemic hypotension for various vascular procedures. Dose-response characteristics of adenosine-induced ventricular asystole have not been determined. METHODS: During endovascular embolization of cerebral arteriovenous malformations, the authors performed a series of adenosine test injections to establish a dose-response relation in each patient. After an interval of 3-10 min, the dose was escalated by 10-20 mg for each injection to achieve an end point of 20-30 s of stable mean arterial pressure (MAP) reduction to 25-30 mmHg. All patients received constant infusion of nitroprusside (approximately 1 microgram. kg-1. min-1) throughout the procedure. RESULTS: The authors studied four adult patients (age, 22-44 yr; two patients had two separate procedures) and one pediatric patient (age, 4 yr). Twenty-three adenosine injections resulted in measurable asystole. The adenosine dose was 0. 98 +/- 0.40 mg/kg (mean +/- SD), and the dose range was 0.24-1.76 mg/kg (6-90 mg). The duration of asystole, MAP < 30 mmHg, and MAP < 50 mmHg, were 8 +/- 3 s, 18 +/- 12 s, and 50 +/- 29 s, respectively. The minimum MAP and the MAP for the first 20 s were 16 +/- 3 mmHg and 30 +/- 9 mmHg, respectively. There was a linear relation between adenosine dose and the duration of hypotension with MAP < 30 mmHg and MAP < 50 mmHg. CONCLUSIONS: In the dose range studied, a series of adenosine test injections can be used to determine optimal adenosine dose for induction of transient profound hypotension.