Acta neurochirurgica · 2026
De novo contralateral vertebral artery dissection after treatment: incidence and clinical characteristics.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Akazawa Ayumi, Isozaki Makoto, Kawajiri Satoshi, Kidoguchi Masamune, Arai Hiroshi, Yamada Shinsuke, Yamauchi Takahiro, Higashino Yoshifumi, Matsuda Ken, Arishima Hidetaka, Kikuta Kenichiro
Аннотация
BACKGROUND: De novo contralateral vertebral artery dissection (VAD) is a rare but serious complication following parent artery occlusion (PAO) for ruptured VAD. Although hemodynamic stress has been considered the primary mechanism, the potential contribution of endovascular manipulation has not been fully explored. This study highlights the possibility that microcatheter contact with the arterial wall during treatment may play a role in the development of contralateral VAD.
METHODS: We retrospectively reviewed 39 patients diagnosed with VAD between April 2009 and December 2016. Among them, 11 patients underwent surgical or endovascular treatment and were included in this analysis. Clinical data, imaging findings, treatment details, and postoperative outcomes were evaluated, with particular attention to the occurrence of de novo contralateral VAD. Procedural angiograms were carefully reviewed to assess the relationship between microcatheter trajectory and subsequent lesion development.
RESULTS: Two of the 11 treated patients (18.2%) developed de novo contralateral VAD during postoperative follow‑up. In both cases, the site of the new dissection corresponded closely to the region where the microcatheter appeared to contact the contralateral vertebral artery during the initial procedure. One lesion enlarged and required stent‑assisted coil embolization, whereas the other resolved spontaneously. No de novo dissections occurred among the 28 conservatively managed patients.
CONCLUSIONS: In addition to hemodynamic stress and underlying arterial fragility, our observations suggest that microcatheter position may warrant attention during endovascular procedures. However, the available evidence does not allow causal inference, and the mechanism underlying de novo contralateral VAD remains unclear. Larger studies are needed to clarify the factors associated with this phenomenon.
METHODS: We retrospectively reviewed 39 patients diagnosed with VAD between April 2009 and December 2016. Among them, 11 patients underwent surgical or endovascular treatment and were included in this analysis. Clinical data, imaging findings, treatment details, and postoperative outcomes were evaluated, with particular attention to the occurrence of de novo contralateral VAD. Procedural angiograms were carefully reviewed to assess the relationship between microcatheter trajectory and subsequent lesion development.
RESULTS: Two of the 11 treated patients (18.2%) developed de novo contralateral VAD during postoperative follow‑up. In both cases, the site of the new dissection corresponded closely to the region where the microcatheter appeared to contact the contralateral vertebral artery during the initial procedure. One lesion enlarged and required stent‑assisted coil embolization, whereas the other resolved spontaneously. No de novo dissections occurred among the 28 conservatively managed patients.
CONCLUSIONS: In addition to hemodynamic stress and underlying arterial fragility, our observations suggest that microcatheter position may warrant attention during endovascular procedures. However, the available evidence does not allow causal inference, and the mechanism underlying de novo contralateral VAD remains unclear. Larger studies are needed to clarify the factors associated with this phenomenon.