Background <p>Carotid webs are increasingly recognized as potential sources of ischemic stroke among young patients without conventional cardiovascular risk factors. However, its pathophysiological mechanism remains unclear. We report a case in which a carotid web was resected via carotid endarterectomy (CEA), allowing for histological analysis.</p> Patient presentation <p>In a 49-year-old male, stenosis of the left internal carotid artery occurred via magnetic resonance imaging for medical examination. Carotid ultrasonography revealed turbulent blood flow around a flap-like lesion, which was consistent with a carotid web. Because this hemodynamic disturbance may increase the risk of ischemic stroke, CEA was performed. Histopathological examination revealed intimal hyperplasia with the accumulation of myofibroblast-like cells.</p> Conclusion <p>Our pathological findings revealed intimal thickening and fibrosis and proliferation of SMA-positive, desmin-negative myofibroblast-like cells, suggesting that the dysregulation of myofibroblasts may underlie the pathogenesis of carotid webs.</p>

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A carotid web with accumulation of myofibroblasts: a case report

  • Saki Kotani,
  • Ryoji Yasumizu,
  • Yasuhiro Takeuchi,
  • Takumi Yamanaka,
  • Kazuyuki Kuwayama,
  • Keigo Matsumoto

摘要

Background

Carotid webs are increasingly recognized as potential sources of ischemic stroke among young patients without conventional cardiovascular risk factors. However, its pathophysiological mechanism remains unclear. We report a case in which a carotid web was resected via carotid endarterectomy (CEA), allowing for histological analysis.

Patient presentation

In a 49-year-old male, stenosis of the left internal carotid artery occurred via magnetic resonance imaging for medical examination. Carotid ultrasonography revealed turbulent blood flow around a flap-like lesion, which was consistent with a carotid web. Because this hemodynamic disturbance may increase the risk of ischemic stroke, CEA was performed. Histopathological examination revealed intimal hyperplasia with the accumulation of myofibroblast-like cells.

Conclusion

Our pathological findings revealed intimal thickening and fibrosis and proliferation of SMA-positive, desmin-negative myofibroblast-like cells, suggesting that the dysregulation of myofibroblasts may underlie the pathogenesis of carotid webs.