Statin therapy reduces vertebral artery atherosclerotic plaques: a case report with insight from vessel wall magnetic resonance imaging

他汀类药物治疗可减少椎动脉粥样硬化斑块:一例病例报告及血管壁磁共振成像的启示

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Abstract

BACKGROUND: Posterior circulation stroke accounts for a substantial proportion of ischemic cerebrovascular events, with vertebral artery (VA) atherosclerosis representing an important etiological factor. Although statin therapy is a well-established modality for stabilizing atherosclerotic plaques and reducing stroke risk, its direct effects on VA plaque regression have not been sufficiently explored, particularly through high-resolution vessel wall magnetic resonance imaging (VW-MRI). We present a case demonstrating VA atherosclerotic plaque regression on serial VW-MRI following statin therapy. CASE DESCRIPTION: A 65-year-old man with hypertension presented with right upper extremity paresthesia. Initial imaging, including VW-MRI and transfemoral cerebral angiography (TFCA), revealed approximately 80% stenosis of the right proximal VA, which was associated with a large, stable plaque characterized by an intact fibrous cap and a necrotic core. The patient was initiated on high-intensity statin therapy (atorvastatin 40 mg daily), which was later reduced to 10 mg following significant improvement in the patient's lipid profile. Serial imaging over a 3-year period demonstrated complete radiological resolution of VA stenosis and disappearance of the previously visualized plaque. The patient remained neurologically stable throughout the follow-up period. CONCLUSIONS: This case provides significant imaging-based evidence of VA plaque regression following long-term statin therapy, as demonstrated via serial VW-MRI and angiographic studies. Despite prior assumptions regarding the limited responsiveness of vertebrobasilar circulation to statins, these findings demonstrate the potential utility of intensive lipid-lowering therapy in the management of posterior circulation atherosclerosis. VW-MRI may serve as a valuable tool for monitoring plaque evolution and therapeutic responses in cerebrovascular diseases.

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