• Akeel Merchant, Doniel Drazin, John Dalfino, Junichi Yamamoto, and Alan S Boulos.
• Division of Neurosurgery, Albany Medical Center, Albany, New York 12208, USA.
• Neurosurg Focus. 2009 May 1; 26 (5): E23.

AbstractThe authors report a case of restenosis in the bilateral internal carotid arteries (ICAs) following angioplasty for cerebral vasospasm. This 53-year-old woman suffering subarachnoid hemorrhage due to a ruptured posterior communicating artery aneurysm had severe vasospasm and underwent angioplasty of the left and right ICAs and middle cerebral arteries. Two months later, a follow-up CT angiogram revealed bilateral ICA stenoses. Transluminal angioplasty leads to long-term connective tissue damage in the medial and adventitial layers from the disruption of the arrangement of collagen fibers due to stretching and tearing, resulting in loss of transmission of contractile forces. Furthermore, following endothelial cell denudation and stretching and rupture of internal elastic lamina from angioplasty, reendothelialization of the intimal layer composed of smooth muscle cells may also explain the contractile properties of restenosis. Other factors such as macrophage-induced inflammation and reactive oxygen species accumulation may also contribute to restenosis. This is the second reported case of restenosis following angioplasty to treat vasospasm, although restenosis is a known complication of angioplasty for treatment of atherosclerosis. In addition, this is the first case of restenosis in the bilateral ICAs following angioplasty for vasospasm. This report presents an illustrative case study and reviews the pathophysiology of angioplasty and restenosis.

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