Literature DB >> 21157476

Collateral circulation in symptomatic intracranial atherosclerosis.

David S Liebeskind1, George A Cotsonis, Jeffrey L Saver, Michael J Lynn, Harry J Cloft, Marc I Chimowitz.   

Abstract

Collateral circulation in intracranial atherosclerosis has never been systematically characterized. We investigated collaterals in a multicenter trial of symptomatic intracranial atherosclerotic disease. Baseline angiography was reviewed for information on collaterals in stenoses of the internal carotid, middle cerebral, vertebral, and basilar arteries. A battery of angiographic scales was utilized to evaluate lesion site, arterial patency, antegrade flow, downstream territorial perfusion, and collateral circulation, blinded to all other data. Collateral circulation was adequately available for analysis in 287/569 (50%) subjects with proximal arterial stenoses ranging from 50% to 99%. Extent of collaterals was absent or none in 69%, slow or minimal in 10%, more rapid, yet incomplete perfusion of territory in 7%, complete but delayed perfusion in 11%, and rapid, complete collateral perfusion in 4%. Extent of collateral flow correlated with percentage of stenosis (P<0.0001), with more severe stenoses exhibiting greater compensation via collaterals. Overall, collateral grade increased with diminished antegrade flow across the lesion (thrombolysis in myocardial ischemia) and resultant downstream perfusion (thrombolysis in cerebral infarction) (both P<0.001). Our findings provide the initial detailed description of collaterals across a variety of stenoses, suggesting that collateral perfusion is a pivotal component in pathophysiology of intracranial atherosclerosis and implicating the need for further evaluation in ongoing studies.

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Year:  2010        PMID: 21157476      PMCID: PMC3099635          DOI: 10.1038/jcbfm.2010.224

Source DB:  PubMed          Journal:  J Cereb Blood Flow Metab        ISSN: 0271-678X            Impact factor:   6.200


  22 in total

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  46 in total

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8.  The impact of native leptomeningeal collateralization on rapid blood flow recruitment following ischemic stroke.

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