Nilotinib, a Bcr-Abl tyrosine kinase inhibitor has been associated with accelerated arterial stenosis, presumably of atherosclerotic etiology. However, reports have been limited to peripheral vascular disease especially in the lower extremities.  The mechanism of atherosclerosis by this drug is poorly understood but endothelial, perivascular factors, mast cell depletion and metabolic factors (promotion of dyslipidemia and impaired glucose metabolism) are thought to be involved. We present a patient with no significant vascular risk factors with acute stroke due to intracranial stenosis in both the symptomatic and contralateral middle cerebral artery (MCA) territory suggesting that Nilotinib may be associated with intracranial atherosclerosis as well.

A 55-year-old Caucasian male with no significant past medical history except CML on treatment with Nilotinib for two years, presented with acute onset of right hemiparesis, aphasia and dysarthria. Patient received intravenous Alteplase followed by thrombectomy with partial target vessel recanalization and subsequent re-occlusion. The underlying residual occlusive lesion was thought to have atherosclerotic plaque appearance. A follow-up brain magnetic resonance imaging study showed acute infarction in the left hemisphere.  MRA and repeat angiography confirmed re-occlusion and revealed a mirror high grade stenosis of the contralateral MCA and severe stenosis of the P2 segment of the right posterior cerebral artery. Primary and secondary vasculitis, and cardioembolic workup was negative. A fasting lipid profile and serum HbA1c levels were normal.  Given the lack of any atherosclerotic risk factors and the angiographic appearance of plaque, underlying multifocal intracranial steno-occlusive lesions were attributed to Nilotinib.