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<meta name="DC.Title" content="Vasodilatory Capacity of the Cerebral Vasculature in Patients with Carotid Artery Stenosis" />
<meta name="DC.Identifier" content="10.3174/ajnr.A2438" />
<meta name="DC.Date" content="2011-06-01" />
<meta name="DC.Publisher" content="American Journal of Neuroradiology" />
<meta name="DC.Rights" content="Copyright © American Society of Neuroradiology" />
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<meta name="DC.Description" content="BACKGROUND AND PURPOSE: Impairment of the cerebral autoregulation is an important predictor of TIA and stroke in patients with an ICA stenosis. The autoregulative status can be assessed directly by measuring the vasodilatory capacity of the cerebral arteries. The aim of our study was to investigate the vasodilatory capacity of the proximal and distal cerebral vasculature in patients with an ICA stenosis and healthy control subjects by combining MRA with an acetazolamide provocation challenge.

MATERIALS AND METHODS: Fourteen functionally independent patients (mean age, 67.2 ± 8.7 years) with a symptomatic ICA stenosis and 19 healthy controls (mean age, 63.1 ± 7.2 years) were included. MRA was performed before and 20 minutes after intravenous administration of acetazolamide. The vasodilatory capacity of 11 proximal and distal cerebral vessels was assessed by measuring the increase in vessel diameter after acetazolamide.

RESULTS: In the hemisphere ipsilateral to the ICA stenosis, there was no increase in diameter after acetazolamide, whereas a significant increase was measured in the contralateral hemisphere for the A1 and A2 segments of the ACA, the pericallosal artery, and the BA. A significant diameter increase was measured in all except 1 vessel of the controls. The vasodilatory capacity was significantly lower ipsilateral to the ICA stenosis compared with the A1 segment of the ACA and the P2 segment of the PCA in the controls.

CONCLUSIONS: MRA combined with an acetazolamide provocation challenge can measure normal and impaired vasodilatory capacity of the cerebral vasculature.

ACA
:   anterior cerebral artery
AcomA
:   anterior communicating artery
BA
:   basilar artery
CO2
:   carbon dioxide
FWHM
:   full width at half maximum
ICA
:   internal carotid artery
MRA
:   MR angiography
PCA
:   posterior cerebral artery
PcomA
:   posterior communicating artery
TIA
:   transient ischemic attack
TOF
:   time of flight" />
<meta name="DC.Contributor" content="R.P.H. Bokkers" />
<meta name="DC.Contributor" content="F.J. Wessels" />
<meta name="DC.Contributor" content="H.B. van der Worp" />
<meta name="DC.Contributor" content="J.J.M. Zwanenburg" />
<meta name="DC.Contributor" content="W.P.Th.M. Mali" />
<meta name="DC.Contributor" content="J.  Hendrikse" />
<meta name="article:published_time" content="2011-06-01" />
<meta name="article:section" content="Brain" />
<meta name="citation_title" content="Vasodilatory Capacity of the Cerebral Vasculature in Patients with Carotid Artery Stenosis" />
<meta name="citation_abstract" lang="en" content="&lt;h3&gt;BACKGROUND AND PURPOSE:&lt;/h3&gt;
&lt;p&gt;Impairment of the cerebral autoregulation is an important predictor of TIA and stroke in patients with an ICA stenosis. The autoregulative status can be assessed directly by measuring the vasodilatory capacity of the cerebral arteries. The aim of our study was to investigate the vasodilatory capacity of the proximal and distal cerebral vasculature in patients with an ICA stenosis and healthy control subjects by combining MRA with an acetazolamide provocation challenge.&lt;/p&gt;&lt;h3&gt;MATERIALS AND METHODS:&lt;/h3&gt;
&lt;p&gt;Fourteen functionally independent patients (mean age, 67.2 ± 8.7 years) with a symptomatic ICA stenosis and 19 healthy controls (mean age, 63.1 ± 7.2 years) were included. MRA was performed before and 20 minutes after intravenous administration of acetazolamide. The vasodilatory capacity of 11 proximal and distal cerebral vessels was assessed by measuring the increase in vessel diameter after acetazolamide.&lt;/p&gt;&lt;h3&gt;RESULTS:&lt;/h3&gt;
&lt;p&gt;In the hemisphere ipsilateral to the ICA stenosis, there was no increase in diameter after acetazolamide, whereas a significant increase was measured in the contralateral hemisphere for the A1 and A2 segments of the ACA, the pericallosal artery, and the BA. A significant diameter increase was measured in all except 1 vessel of the controls. The vasodilatory capacity was significantly lower ipsilateral to the ICA stenosis compared with the A1 segment of the ACA and the P2 segment of the PCA in the controls.&lt;/p&gt;&lt;h3&gt;CONCLUSIONS:&lt;/h3&gt;
&lt;p&gt;MRA combined with an acetazolamide provocation challenge can measure normal and impaired vasodilatory capacity of the cerebral vasculature.&lt;/p&gt;" />
<meta name="citation_journal_title" content="American Journal of Neuroradiology" />
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<meta name="twitter:title" content="Vasodilatory Capacity of the Cerebral Vasculature in Patients with Carotid Artery Stenosis" />
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<meta name="twitter:description" content="BACKGROUND AND PURPOSE: Impairment of the cerebral autoregulation is an important predictor of TIA and stroke in patients with an ICA stenosis. The autoregulative status can be assessed directly by measuring the vasodilatory capacity of the cerebral arteries. The aim of our study was to investigate the vasodilatory capacity of the proximal and distal cerebral vasculature in patients with an ICA stenosis and healthy control subjects by combining MRA with an acetazolamide provocation challenge.

MATERIALS AND METHODS: Fourteen functionally independent patients (mean age, 67.2 ± 8.7 years) with a symptomatic ICA stenosis and 19 healthy controls (mean age, 63.1 ± 7.2 years) were included. MRA was performed before and 20 minutes after intravenous administration of acetazolamide. The vasodilatory capacity of 11 proximal and distal cerebral vessels was assessed by measuring the increase in vessel diameter after acetazolamide.

RESULTS: In the hemisphere ipsilateral to the ICA stenosis, there was no increase in diameter after acetazolamide, whereas a significant increase was measured in the contralateral hemisphere for the A1 and A2 segments of the ACA, the pericallosal artery, and the BA. A significant diameter increase was measured in all except 1 vessel of the controls. The vasodilatory capacity was significantly lower ipsilateral to the ICA stenosis compared with the A1 segment of the ACA and the P2 segment of the PCA in the controls.

CONCLUSIONS: MRA combined with an acetazolamide provocation challenge can measure normal and impaired vasodilatory capacity of the cerebral vasculature.

ACA
:   anterior cerebral artery
AcomA
:   anterior communicating artery
BA
:   basilar artery
CO2
:   carbon dioxide
FWHM
:   full width at half maximum
ICA
:   internal carotid artery
MRA
:   MR angiography
PCA
:   posterior cerebral artery
PcomA
:   posterior communicating artery
TIA
:   transient ischemic attack
TOF
:   time of flight" />
<meta name="og-title" property="og:title" content="Vasodilatory Capacity of the Cerebral Vasculature in Patients with Carotid Artery Stenosis" />
<meta name="og-url" property="og:url" content="http://ajnr-stage2.stage.highwire.org/content/32/6/1030" />
<meta name="og-site-name" property="og:site_name" content="American Journal of Neuroradiology" />
<meta name="og-description" property="og:description" content="BACKGROUND AND PURPOSE: Impairment of the cerebral autoregulation is an important predictor of TIA and stroke in patients with an ICA stenosis. The autoregulative status can be assessed directly by measuring the vasodilatory capacity of the cerebral arteries. The aim of our study was to investigate the vasodilatory capacity of the proximal and distal cerebral vasculature in patients with an ICA stenosis and healthy control subjects by combining MRA with an acetazolamide provocation challenge.

MATERIALS AND METHODS: Fourteen functionally independent patients (mean age, 67.2 ± 8.7 years) with a symptomatic ICA stenosis and 19 healthy controls (mean age, 63.1 ± 7.2 years) were included. MRA was performed before and 20 minutes after intravenous administration of acetazolamide. The vasodilatory capacity of 11 proximal and distal cerebral vessels was assessed by measuring the increase in vessel diameter after acetazolamide.

RESULTS: In the hemisphere ipsilateral to the ICA stenosis, there was no increase in diameter after acetazolamide, whereas a significant increase was measured in the contralateral hemisphere for the A1 and A2 segments of the ACA, the pericallosal artery, and the BA. A significant diameter increase was measured in all except 1 vessel of the controls. The vasodilatory capacity was significantly lower ipsilateral to the ICA stenosis compared with the A1 segment of the ACA and the P2 segment of the PCA in the controls.

CONCLUSIONS: MRA combined with an acetazolamide provocation challenge can measure normal and impaired vasodilatory capacity of the cerebral vasculature.

ACA
:   anterior cerebral artery
AcomA
:   anterior communicating artery
BA
:   basilar artery
CO2
:   carbon dioxide
FWHM
:   full width at half maximum
ICA
:   internal carotid artery
MRA
:   MR angiography
PCA
:   posterior cerebral artery
PcomA
:   posterior communicating artery
TIA
:   transient ischemic attack
TOF
:   time of flight" />
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      <h1 class="highwire-cite-title" id="page-title">Vasodilatory Capacity of the Cerebral Vasculature in Patients with Carotid Artery Stenosis</h1>  
    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0">R.P.H. Bokkers</span>, <span class="highwire-citation-author" data-delta="1">F.J. Wessels</span>, <span class="highwire-citation-author" data-delta="2">H.B. van der Worp</span>, <span class="highwire-citation-author" data-delta="3">J.J.M. Zwanenburg</span>, <span class="highwire-citation-author" data-delta="4">W.P.Th.M. Mali</span> and <span class="highwire-citation-author" data-delta="5">J.  Hendrikse</span></span></div>
  
    	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-journal highwire-cite-metadata">American Journal of Neuroradiology </span><span  class="highwire-cite-metadata-date highwire-cite-metadata">June 2011,  </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">32 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(6) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">1030-1033; </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata">DOI: https://doi.org/10.3174/ajnr.A2438 </span></div>
  
  
  
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<p id="p-1"><strong>BACKGROUND AND PURPOSE:</strong> Impairment of the cerebral autoregulation is an important predictor of TIA and stroke in patients with an ICA stenosis. The autoregulative status can be assessed directly by measuring the vasodilatory capacity of the cerebral arteries. The aim of our study was to investigate the vasodilatory capacity of the proximal and distal cerebral vasculature in patients with an ICA stenosis and healthy control subjects by combining MRA with an acetazolamide provocation challenge.</p>
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<p id="p-2"><strong>MATERIALS AND METHODS:</strong> Fourteen functionally independent patients (mean age, 67.2 ± 8.7 years) with a symptomatic ICA stenosis and 19 healthy controls (mean age, 63.1 ± 7.2 years) were included. MRA was performed before and 20 minutes after intravenous administration of acetazolamide. The vasodilatory capacity of 11 proximal and distal cerebral vessels was assessed by measuring the increase in vessel diameter after acetazolamide.</p>
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<p id="p-3"><strong>RESULTS:</strong> In the hemisphere ipsilateral to the ICA stenosis, there was no increase in diameter after acetazolamide, whereas a significant increase was measured in the contralateral hemisphere for the A1 and A2 segments of the ACA, the pericallosal artery, and the BA. A significant diameter increase was measured in all except 1 vessel of the controls. The vasodilatory capacity was significantly lower ipsilateral to the ICA stenosis compared with the A1 segment of the ACA and the P2 segment of the PCA in the controls.</p>
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<p id="p-4"><strong>CONCLUSIONS:</strong> MRA combined with an acetazolamide provocation challenge can measure normal and impaired vasodilatory capacity of the cerebral vasculature.</p>
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</div><div class="section glossary" id="glossary-1"><h2>Abbreviations</h2><dl id="def-list-1"><dt id="def-item-1">ACA<span class="def-item-dt-sep"></span></dt><dd>anterior cerebral artery<span class="def-item-dd-sep"></span></dd><dt id="def-item-2">AcomA<span class="def-item-dt-sep"></span></dt><dd>anterior communicating artery<span class="def-item-dd-sep"></span></dd><dt id="def-item-3">BA<span class="def-item-dt-sep"></span></dt><dd>basilar artery<span class="def-item-dd-sep"></span></dd><dt id="def-item-4">CO<sub>2</sub><span class="def-item-dt-sep"></span></dt><dd>carbon dioxide<span class="def-item-dd-sep"></span></dd><dt id="def-item-5">FWHM<span class="def-item-dt-sep"></span></dt><dd>full width at half maximum<span class="def-item-dd-sep"></span></dd><dt id="def-item-6">ICA<span class="def-item-dt-sep"></span></dt><dd>internal carotid artery<span class="def-item-dd-sep"></span></dd><dt id="def-item-7">MRA<span class="def-item-dt-sep"></span></dt><dd>MR angiography<span class="def-item-dd-sep"></span></dd><dt id="def-item-8">PCA<span class="def-item-dt-sep"></span></dt><dd>posterior cerebral artery<span class="def-item-dd-sep"></span></dd><dt id="def-item-9">PcomA<span class="def-item-dt-sep"></span></dt><dd>posterior communicating artery<span class="def-item-dd-sep"></span></dd><dt id="def-item-10">TIA<span class="def-item-dt-sep"></span></dt><dd>transient ischemic attack<span class="def-item-dd-sep"></span></dd><dt id="def-item-11">TOF<span class="def-item-dt-sep"></span></dt><dd>time of flight</dd></dl></div><ul class="copyright-statement"><li class="fn" id="copyright-statement-1">Copyright © American Society of Neuroradiology</li></ul><span class="highwire-journal-article-marker-end"></span></div><span class="related-urls"></span></div><a href="http://ajnr-stage2.stage.highwire.org/content/32/6/1030.full" class="hw-link hw-link-article-full-text" data-icon-position="" data-hide-link-title="0">View Full Text</a></div>  </div>

  
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      <div class="highwire-cite-title">Vasodilatory Capacity of the Cerebral Vasculature in Patients with Carotid Artery Stenosis</div>  
    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0"><span class="nlm-given-names">R.P.H.</span> <span class="nlm-surname">Bokkers</span></span>, <span class="highwire-citation-author" data-delta="1"><span class="nlm-given-names">F.J.</span> <span class="nlm-surname">Wessels</span></span>, <span class="highwire-citation-author" data-delta="2"><span class="nlm-given-names">H.B.</span> <span class="nlm-surname">van der Worp</span></span>, <span class="highwire-citation-author" data-delta="3"><span class="nlm-given-names">J.J.M.</span> <span class="nlm-surname">Zwanenburg</span></span>, <span class="highwire-citation-author" data-delta="4"><span class="nlm-given-names">W.P.Th.M.</span> <span class="nlm-surname">Mali</span></span>, <span class="highwire-citation-author" data-delta="5"><span class="nlm-given-names">J.</span> <span class="nlm-surname"> Hendrikse</span></span></span></div>
  
    	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-journal highwire-cite-metadata">American Journal of Neuroradiology </span><span  class="highwire-cite-metadata-date highwire-cite-metadata">Jun 2011, </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">32 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(6) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">1030-1033; </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata"><span class="label">DOI:</span> 10.3174/ajnr.A2438 </span></div>
  
  
  
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    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0"><span class="nlm-given-names">R.P.H.</span> <span class="nlm-surname">Bokkers</span></span>, <span class="highwire-citation-author" data-delta="1"><span class="nlm-given-names">F.J.</span> <span class="nlm-surname">Wessels</span></span>, <span class="highwire-citation-author" data-delta="2"><span class="nlm-given-names">H.B.</span> <span class="nlm-surname">van der Worp</span></span>, <span class="highwire-citation-author" data-delta="3"><span class="nlm-given-names">J.J.M.</span> <span class="nlm-surname">Zwanenburg</span></span>, <span class="highwire-citation-author" data-delta="4"><span class="nlm-given-names">W.P.Th.M.</span> <span class="nlm-surname">Mali</span></span>, <span class="highwire-citation-author" data-delta="5"><span class="nlm-given-names">J.</span> <span class="nlm-surname"> Hendrikse</span></span></span></div>
  
    	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-journal highwire-cite-metadata">American Journal of Neuroradiology </span><span  class="highwire-cite-metadata-date highwire-cite-metadata">Jun 2011, </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">32 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(6) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">1030-1033; </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata"><span class="label">DOI:</span> 10.3174/ajnr.A2438 </span></div>
  
  
  
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