PURPOSE: Whether the posterior communicating artery (PcomA) can be safely compromised during endovascular treatment of a PcomA aneurysm is a matter of debate. Here we present clinical and radiologic outcomes, given this scenario. METHODS: From data prospectively accrued between January 2004 and December 2012, records of 44 patients harboring 46 PcomA aneurysms were retrieved. All had suffered PcomA compromise in the course of endovascular coil embolization. Patients/aneurysms were stratified into those with complete (Group A) and incomplete (Group B) compromise depending on the degree of PcomA flow limitation documented by postembolization ipsilateral internal carotid artery angiography. Clinical and radiologic outcomes were accordingly assessed. RESULTS: All affected vessels were hypoplastic PcomA variants (PcomA/P1 ratio, ≤ 1.0), with exception of a single dominant PcomA (PcomA/P1 ratio, 1.1). In Group A (23 patients, 23 aneurysms), no PcomA compromise-related infarction was evident, whereas in Group B (21 patients, 23 aneurysms), two ischemic events occurred. One patient suffered thalamic infarction, although patency of the PcomA was adequate in a follow-up angiogram, and another experienced a transient ischemic attack. CONCLUSION: Our findings suggest that obstructed flow in hypoplastic PcomA variants during coil embolization of PcomA aneurysms carries no major consequence. However, incomplete compromise of the PcomA may be a source of delayed thromboembolic infarction.
PURPOSE: Whether the posterior communicating artery (PcomA) can be safely compromised during endovascular treatment of a PcomA aneurysm is a matter of debate. Here we present clinical and radiologic outcomes, given this scenario. METHODS: From data prospectively accrued between January 2004 and December 2012, records of 44 patients harboring 46 PcomA aneurysms were retrieved. All had suffered PcomA compromise in the course of endovascular coil embolization. Patients/aneurysms were stratified into those with complete (Group A) and incomplete (Group B) compromise depending on the degree of PcomA flow limitation documented by postembolization ipsilateral internal carotid artery angiography. Clinical and radiologic outcomes were accordingly assessed. RESULTS: All affected vessels were hypoplastic PcomA variants (PcomA/P1 ratio, ≤ 1.0), with exception of a single dominant PcomA (PcomA/P1 ratio, 1.1). In Group A (23 patients, 23 aneurysms), no PcomA compromise-related infarction was evident, whereas in Group B (21 patients, 23 aneurysms), two ischemic events occurred. One patient suffered thalamic infarction, although patency of the PcomA was adequate in a follow-up angiogram, and another experienced a transient ischemic attack. CONCLUSION: Our findings suggest that obstructed flow in hypoplastic PcomA variants during coil embolization of PcomA aneurysms carries no major consequence. However, incomplete compromise of the PcomA may be a source of delayed thromboembolic infarction.
Authors: Jean Raymond; François Guilbert; Alain Weill; Stavros A Georganos; Louis Juravsky; Anick Lambert; Julie Lamoureux; Miguel Chagnon; Daniel Roy Journal: Stroke Date: 2003-05-29 Impact factor: 7.914