Hyperperfusion Syndrome After Stenting for Intracranial Artery Stenosis

Abstract

Hyperperfusion syndrome (HPS) is a rare but potentially devastating postoperative complication developing after endarterectomy and carotid stenting. Limited information is available about this complication. The aim of this study was to assess the incidence of HPS and risk factors leading to its development. We retrospectively reviewed 178 consecutive cases of patients who underwent stenting of intracranial artery revascularization. We analyzed the association between HPS and patient's age, collateral vascular supply of the lesion, the interval between operation and the last occurrence of ischemic symptom, adequacy of blood pressure control after the operation, and other risk factors such as diabetes, smoking, hypertension, and gender. Of 178 included patients, we found HPS in six cases (3.4%). Failure to strictly control postoperative blood pressure, a less than 3-week long interval between operation and the last occurrence of ischemic symptom, and poor collateral circulation were significantly associated with the development of HPS. The aforementioned factors are predictors for HPS. We argue that nitroprusside should not be used to control blood pressure after the operation because its use permits considerable blood pressure fluctuations.

Sentinel Angiographic Signs of Cerebral Hyperperfusion after Angioplasty and Stenting of Intracranial Atherosclerotic Stenosis: A Technical Note

“…1 CHS following intracranial angioplasty is less well-studied but is estimated in observational studies to occur in 3.4% of patients with nearly 80% mortality when complicated by intracerebral hemorrhage (ICH). [2][3][4] This likely contributed to the adverse outcomes in the intervention arm of the Stenting vs Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis (SAMMPRIS) trial. [4][5][6] While the exact pathophysiology of CHS is still not fully understood, impaired cerebral autoregulation and cerebral hemodynamic alterations following revascularization are considered the major mechanisms involved.…”

“…[2][3][4] This likely contributed to the adverse outcomes in the intervention arm of the Stenting vs Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis (SAMMPRIS) trial. [4][5][6] While the exact pathophysiology of CHS is still not fully understood, impaired cerebral autoregulation and cerebral hemodynamic alterations following revascularization are considered the major mechanisms involved. 4,5 In patients with intracranial atherosclerosis (ICAS), CHS development is associated with poor control of postoperative blood pressure (BP) and impaired collateral circulation.…”

“…[4][5][6] While the exact pathophysiology of CHS is still not fully understood, impaired cerebral autoregulation and cerebral hemodynamic alterations following revascularization are considered the major mechanisms involved. 4,5 In patients with intracranial atherosclerosis (ICAS), CHS development is associated with poor control of postoperative blood pressure (BP) and impaired collateral circulation. 4 For extracranial stenosis, other well-known risk factors include baseline hypertension, carotid stenosis of Ն90%, and impaired cerebrovascular reserve.…”

“…4,5 In patients with intracranial atherosclerosis (ICAS), CHS development is associated with poor control of postoperative blood pressure (BP) and impaired collateral circulation. 4 For extracranial stenosis, other well-known risk factors include baseline hypertension, carotid stenosis of Ն90%, and impaired cerebrovascular reserve. [4][5][6] These factors coupled with maximal arteriolar dilation, compromised cerebral autoregulation, and systemic hypertension translate to an increased cerebral perfusion pressure and cerebral hyperperfusion.…”

Correlation between high perfusion syndrome and stent restenosis after stent implantation

“…iii) Free radical toxicity (10): Free radicals can produce toxic effects on brain cells, which can be expressed as nucleic acid base changes, chromosome aberration or DNA fault. iv) Complement activation (11): The complement terminal complex affects the brain cell function through the membrane mechanism, which triggers the release of the macrophages, and produces a variety of inflammatory factors, which can cause damage to the neurons.…”