A case report with histopathological evaluation of nilotinib-associated carotid artery plaque following carotid endarterectomy.

BACKGROUND: Nilotinib, a second-generation tyrosine kinase inhibitor used to treat chronic myeloid leukemia (CML), has been associated with the development of atherosclerosis and an increased risk of cerebrovascular events. Proposed mechanisms include endothelial dysfunction, platelet activation, and metabolic disturbances that may accelerate atherosclerotic processes; however, histopathological evidence of nilotinib-associated plaque formation has not been reported.

CASE PRESENTATION: A 55-year-old woman with CML who had been treated with nilotinib for 12 years developed progressive bilateral cervical internal carotid artery stenosis. The patient had no conventional vascular risk factors at baseline. Bilateral carotid artery stenosis was initially detected after approximately 8 years of nilotinib therapy and gradually progressed despite statin and antiplatelet therapy during follow-up. Angiography demonstrated severe bilateral cervical internal carotid artery stenosis, with 75% stenosis on the right and 95% stenosis on the left. The patient underwent carotid artery stenting for the right side, followed by carotid endarterectomy (CEA) for the left-sided lesion. Histopathological evaluation of the excised plaque revealed predominantly fibrocalcific atherosclerotic changes with inflammatory cell infiltration, including CD4⁺ T cells and CD163⁺ macrophages, without features specific to vasculitis or other nonatherosclerotic vasculopathies.

CONCLUSIONS: To our knowledge, this is the first report to document histopathological evaluation of a carotid plaque obtained following CEA in a patient with long-term nilotinib therapy. This case highlights the importance of vascular monitoring in patients receiving nilotinib and provides supportive pathological findings for the hypothesis that nilotinib may accelerate atherosclerotic processes.