Tyrosine kinase inhibitor induced rapidly progressive vasculopathy after intracranial stent placement

Abstract

Tyrosine kinase inhibitor (TKI) therapy for chronic myeloid leukemia (CML) has been associated with progressive peripheral arterial disease and, more recently, rare cases of intracranial vascular stenosis have been reported. We report the fourth case of TKI treatment associated intracranial vasculopathy and rapid progression of intracranial vascular stenosis following intracranial stent placement. This was a 49-year-old woman who developed right-sided weakness, paresthesias, numbness, and speech difficulties 7 years following TKI treatment for CML. Cerebral catheter angiography demonstrated 90% stenosis of the left supraclinoid internal carotid artery, for which the patient underwent intracranial stent placement with no residual stenosis and improved distal blood flow. Approximately 1 month following the procedure, the patient returned with similar symptoms. Catheter angiography demonstrated 70% and 50% stenosis just distal and proximal to the stent construct, respectively. Rapid disease progression and non-atherosclerotic vasculopathy may argue against endovascular therapy.

Vessel Wall Magnetic Resonance Imaging Findings of Bilateral Middle Cerebral Artery Stenosis Associated with Nilotinib

“…Although peripheral artery diseases are most commonly reported, 1 cerebrovascular events associated with nilotinib have also been described. [2][3][4] However, the mechanisms by which nilotinib promotes atherosclerosis remain poorly understood. According to previous studies, nilotinib induces pro-atherogenic and anti-angiogenic effects on endothelial cells by binding to discoidin domain receptor 1, platelet-derived growth factor receptor, and C-kit.…”

“…1 However, a report of nilotinib-related cerebrovascular disease (CVD) is somewhat unusual. [2][3][4] There are no previous reports of a case with serial vessel wall magnetic resonance imaging (VWI). Herein, we report a case of nilotinib-induced intracranial stenosis in a patient with recurrent transient ischemic attacks (TIAs) and discuss the results of VWI.…”