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2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia
Published on: June 22, 2013
Post-Carotid Artery Stenting Hyperperfusion Syndrome in a Hypotensive Patient: Case Report and Systematic Review of
Matija Zupan1, Matej Perovnik1, Janja Pretnar Oblak1,2
1Department of Vascular Neurology, University Medical Centre Ljubljana, Zaloška cesta 2, SI-1000 Ljubljana, Slovenia.
Insights
Cerebral hyperperfusion syndrome (CHS) can occur after carotid artery stenting (CAS), even without high blood pressure. This study highlights that hypotension, not just hypertension, may play a role in CHS development and recovery.
Area of Science:
- Neurology
- Vascular Surgery
- Neurosurgery
Background:
- Cerebral hyperperfusion syndrome (CHS) is a severe complication following carotid artery stenting (CAS).
- The exact mechanisms of CHS, particularly when arterial hypertension (AH) is absent, are not fully understood.
- Existing literature often links CHS to AH, but cases involving other hemodynamic states are less explored.
Abstract:
Cerebral hyperperfusion syndrome (CHS) is a serious post-procedural complication of carotid artery stenting (CAS). The pathophysiological mechanisms of CHS in the absence of arterial hypertension (AH) remain only partially understood. We performed a systematic literature search of the PubMed database using the terms »cerebral hyperperfusion syndrome«, »hypotension«, »hyperperfusion«, »stroke«, »intracranial hemorrhages«, »risk factors«, »carotid revascularization«, »carotid stenting«, »carotid endarterectomy«, »blood-brain barrier«, »endothelium«, »contrast encephalopathy«, and combinations. We present a case of a normotensive female patient who developed CHS post-CAS for symptomatic carotid stenosis while being hypotensive with complete recovery. We identified 393 papers, among which 65 were deemed relevant to the topic. The weighted average prevalence of CHS after CAS is 1.2% [0.0-37.7%] with that of intracranial hemorrhage (ICH) being 0.51% [0-9.3%]. Recently symptomatic carotid stenosis or contralateral carotid revascularization, urgent intervention, acute carotid occlusion, contralateral ≥70% stenosis, and the presence of leptomeningeal collaterals were associated with CHS. A prolonged hemodynamic instability after CAS conveys a higher risk for CHS. However, none of the articles mentioned isolated hypotension as a risk factor for CHS. Whereas mortality after ICH post-CAS ranges from 40 to 75%, in the absence of ICH, CHS generally carries a good prognosis. AH is not obligatory in CHS development. Even though impaired cerebral autoregulation and post-revascularization changes in cerebral hemodynamics seem to play a pivotal role in CHS pathophysiology, our case highlights the complexity of CHS, involving factors like endothelial dysfunction and sudden reperfusion. Further research is needed to refine diagnostic and management approaches for this condition.
