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Indexed/Abstracted in: e-psyche, EMBASE, PubMed/MEDLINE, Neuroscience Citation Index, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,651
Lorenzo RINALDO 1, Brandon A. MCCUTCHEON 1, Kendall A. SNYDER 1, Amanda L. PORTER 2, Mohamad BYDON 1, Giuseppe LANZINO 1, 3, Alejandro A. RABINSTEIN 4
1 Department of Neurosurgery, Mayo Clinic, Rochester, MN, USA; 2 Mayo Clinic College of Medicine, Mayo Clinic, Rochester, MN, USA; 3 Interventional Neuroradiology, Department of Radiology, Mayo Clinic, Rochester, MN, USA; 4 Section of Neurocritical Care, Department of Neurology, Mayo Clinic, Rochester, MN, USA
BACKGROUND: Congenital hypoplasia or absence of the A1 segment of the anterior cerebral artery (ACA) has been associated with increased incidence of berry aneurysms at the anterior communicating artery (Acom) complex. It is not known, however, whether this anatomic variant also predisposes patients to complications after aneurysmal subarachnoid hemorrhage.
METHODS: Patients were included for analysis if they presented to our institution for clipping or coiling of an Acom aneurysm between the years of 2001 and 2013. Patients were deemed to have cerebral infarction if a new hypodensity in a vascular distribution was visualized on CT imaging. The association between A1 segmental abnormalities and radiologic infarction was subsequently evaluated in a risk-adjusted manner using stepwise multivariable logistic regression analysis.
RESULTS: Of 145 patients who presented with aneurysmal subarachnoid hemorrhage after rupture of an ACoM aneurysm, 31 (21.4%) had a hypoplastic or absent A1 segment. On univariate analysis, there was a trend toward an increased rate of radiologic infarction in patients with A1 segment abnormalities (OR 2.11, 95% CI 0.93-4.79; p=0.0757). On multivariable analysis, a hypoplastic or absent A1 segment was significantly associated with an increased rate of radiologic infarction (OR 2.54, 95% CI 1.02-6.43; p = 0.0466).
CONCLUSIONS: Our results suggest that a hypoplastic or absent A1 segment is associated with cerebral infarction following subarachnoid hemorrhage from ruptured ACoM aneurysms, indicating a potential need for heightened vigilance and a reduced threshold for therapeutic intervention in patients harboring this abnormality.