Artikel
Bilateral impaired cerebrovascular reactivity in unilateral carotid artery disease
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Autoren
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Jorn Fierstra
- Department of Neurosurgery, Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, Switzerland
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Bas van Niftrik
- Department of Neurosurgery, Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, Switzerland
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Marco Piccirelli
- Department of Neuroradiology, Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, Switzerland
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Jan Karl Burkhardt
- Department of Neurosurgery, Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, Switzerland
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Luca Regli
- Department of Neurosurgery, Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, Switzerland
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Oliver Bozinov
- Department of Neurosurgery, Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, Switzerland
| Veröffentlicht: | 8. Juni 2016 |
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Gliederung
Text
Objective: There is mounting evidence that unilateral carotid artery disease (CAD) has a bilateral hemodynamic effect on brain tissue and therefore on contralateral stroke risk. Impaired cerebrovascular reactivity (CVR) has been related to increased stroke risk. We therefore aim to quantify CVR impairment related to unilateral CAD ranging from subjects with unilateral internal carotid artery stenosis to occlusion and compare the findings to a healthy reference group.
Method: Thirty-four CAD subjects (18 subjects with unilateral carotid artery occlusion and 16 subjects with unilateral carotid artery high grade stenosis >70%) as well as 45 healthy subjects, were scanned on a 3T MRI system. Whole brain Blood Oxygenation-Level Dependent (BOLD) MRI volumes were obtained while applying standardized changes in carbon dioxide (CO2) to measure CVR. An independent two sample T-test was used to determine significant differences across groups, where the paired T-test was used to reveal differences between hemispheres of the same group.
Results: Whole brain CVR for healthy subjects was 0.27 ± 0.07, while subjects with unilateral stenosis had a CVR of 0.16 ± 0.05 and subjects with unilateral occlusion 0.11 ±0 .09. Significant differences were found between the contralateral hemisphere and ipsilateral hemisphere of carotid artery stenosis (0.17 ± 0.05 vs 0.15 ± 0.06, p<0.05) and occlusion (0.14 ± 0.09 vs 0.06 ± 0.11, p<0.01). Ipsilateral CVR values also differed significantly between healthy subjects versus stenosis (p<0.01) and occlusion (p<0.01). Interestingly, this was also the case for the contralateral hemisphere, where CVR was more impaired for stenosis and occlusion (p>0.01). In contrast, no significant CVR difference was found between the ‘’unaffected’’ contralateral hemisphere of subjects with stenosis and occlusion (p=0.27).
Conclusions: Unilateral carotid artery stenosis and occlusion results in CVR impairment of the contralateral hemisphere. Interestingly, the "unaffected" contralateral hemispheres of the two groups showed no significant difference, which might indicate that CVR as a compensatory hemodynamic mechanism may already be exhausted with >70% stenosis.
