Collateral Circulation in Symptomatic Intracranial Atherosclerosis

• Published in: Journal of cerebral blood flow and metabolism Vol. 31; no. 5; pp. 1293 - 1301
• Main Authors: Liebeskind, David S, Cotsonis, George A, Saver, Jeffrey L, Lynn, Michael J, Cloft, Harry J, Chimowitz, Marc I
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01.05.2011; Nature Publishing Group; Sage Publications Ltd
• Subjects: Atherosclerosis (general aspects, experimental research); Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Cerebral Angiography; Collateral Circulation - physiology; Humans; Intracranial Arteriosclerosis - diagnostic imaging; Intracranial Arteriosclerosis - physiopathology; Medical sciences; Multicenter Studies as Topic; Neurology; Original; Randomized Controlled Trials as Topic; Retrospective Studies; Vascular diseases and vascular malformations of the nervous system; intracranial atherosclerosis; stenosis; cerebral ischemia; collaterals; angiography; Intracranial; Nervous system diseases; Angiography; Stenosis; Cardiovascular disease; Cerebral disorder; Vascular disease; Collateral circulation; Central nervous system disease; Atherosclerosis; Brain ischemia; Cerebrovascular disease
• ISSN: 0271-678X; 1559-7016; 1559-7016
• DOI: 10.1038/jcbfm.2010.224

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.