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  • Author or Editor: Akira Ogawa x
  • By Author: Hosoda, Kohkichi x
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Kuniaki Ogasawara, Nobuyuki Sakai, Terumasa Kuroiwa, Kohkichi Hosoda, Koji Iihara, Kazunori Toyoda, Chiaki Sakai, Izumi Nagata, Akira Ogawa and Japanese Society for Treatment at Neck in Cerebrovascular Disease Study Group

Object

Intracranial hemorrhage associated with cerebral hyperperfusion syndrome (CHS) following carotid endarterectomy (CEA) or carotid artery stenting (CAS) is a rare but potentially devastating complication. In the present study the authors evaluated 4494 patients with carotid artery stenosis who had undergone CEA or CAS to clarify the clinicopathological features and outcomes of those with CHS and associated intracranial hemorrhage.

Methods

Patients with postoperative CHS were retrospectively selected, and clinicopathological features and outcomes were studied.

Results

Sixty-one patients with CHS (1.4%) were identified, and intracranial hemorrhage developed in 27 of them (0.6%). The onset of CHS peaked on the 6th postoperative day in those who had undergone CEA and within 12 hours in those who had undergone CAS. Results of logistic regression analysis demonstrated that poor postoperative control of blood pressure was significantly associated with the development of intracranial hemorrhage in patients with CHS after CEA (p = 0.0164). Note, however, that none of the tested variables were significantly associated with the development of intracranial hemorrhage in patients with CHS after CAS. Mortality (p = 0.0010) and morbidity (p = 0.0172) rates were significantly higher in patients with intracranial hemorrhage than in those without.

Conclusions

Cerebral hyperperfusion syndrome after CEA and CAS occurs with delayed classic and acute presentations, respectively. Although strict control of postoperative blood pressure prevents intracranial hemorrhage in patients with CHS after CEA, there appears to be no relationship between blood pressure control and intracranial hemorrhage in those with CHS after CAS. Finally, the prognosis of CHS in patients with associated intracerebral hemorrhage is poor.