Cerebral Hemodynamics Underlying Artery-to-Artery Embolism in Symptomatic Intracranial Atherosclerotic Disease
Artery-to-artery embolism (AAE) is a common stroke mechanism in intracranial atherosclerotic disease (ICAD), associated with a considerable risk of recurrent stroke. We aimed to investigate cerebral hemodynamic features associated with AAE in symptomatic ICAD. Patients with anterior-circulation, sym...
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Veröffentlicht in: | Translational stroke research 2024-06, Vol.15 (3), p.572-579 |
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creator | Feng, Xueyan Fang, Hui Ip, Bonaventure Y. M. Chan, Ka Lung Li, Shuang Tian, Xuan Zheng, Lina Liu, Yuying Lan, Linfang Liu, Haipeng Abrigo, Jill Ma, Sze Ho Fan, Florence S. Y. Ip, Vincent H. L. Soo, Yannie O. Y. Mok, Vincent C. T. Song, Bo Leung, Thomas W. Xu, Yuming Leng, Xinyi |
description | Artery-to-artery embolism (AAE) is a common stroke mechanism in intracranial atherosclerotic disease (ICAD), associated with a considerable risk of recurrent stroke. We aimed to investigate cerebral hemodynamic features associated with AAE in symptomatic ICAD. Patients with anterior-circulation, symptomatic ICAD confirmed in CT angiography (CTA) were recruited. We classified probable stroke mechanisms as isolated parent artery atherosclerosis occluding penetrating artery, AAE, hypoperfusion, and mixed mechanisms, largely based on infarct topography. CTA-based computational fluid dynamics (CFD) models were built to simulate blood flow across culprit ICAD lesions. Translesional pressure ratio (PR = Pressure
post-stenotic
/Pressure
pre-stenotic
) and wall shear stress ratio (WSSR = WSS
stenotic-throat
/WSS
pre-stenotic
) were calculated, to reflect the relative, translesional changes of the two hemodynamic metrics. Low PR (PR ≤ median) and high WSSR (WSSR ≥ 4th quartile) respectively indicated large translesional pressure and elevated WSS upon the lesion. Among 99 symptomatic ICAD patients, 44 had AAE as a probable stroke mechanism, 13 with AAE alone and 31 with coexisting hypoperfusion. High WSSR was independently associated with AAE (adjusted OR = 3.90;
P
= 0.022) in multivariate logistic regression. There was significant WSSR-PR interaction on the presence of AAE (
P
for interaction = 0.013): high WSSR was more likely to associate with AAE in those with low PR (
P
= 0.075), but not in those with normal PR (
P
= 0.959). Excessively elevated WSS in ICAD might increase the risk of AAE. Such association was more prominent in those with large translesional pressure gradient. Hypoperfusion, commonly coexisting with AAE, might be a therapeutic indicator for secondary stroke prevention in symptomatic ICAD with AAE. |
doi_str_mv | 10.1007/s12975-023-01146-4 |
format | Article |
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post-stenotic
/Pressure
pre-stenotic
) and wall shear stress ratio (WSSR = WSS
stenotic-throat
/WSS
pre-stenotic
) were calculated, to reflect the relative, translesional changes of the two hemodynamic metrics. Low PR (PR ≤ median) and high WSSR (WSSR ≥ 4th quartile) respectively indicated large translesional pressure and elevated WSS upon the lesion. Among 99 symptomatic ICAD patients, 44 had AAE as a probable stroke mechanism, 13 with AAE alone and 31 with coexisting hypoperfusion. High WSSR was independently associated with AAE (adjusted OR = 3.90;
P
= 0.022) in multivariate logistic regression. There was significant WSSR-PR interaction on the presence of AAE (
P
for interaction = 0.013): high WSSR was more likely to associate with AAE in those with low PR (
P
= 0.075), but not in those with normal PR (
P
= 0.959). Excessively elevated WSS in ICAD might increase the risk of AAE. Such association was more prominent in those with large translesional pressure gradient. Hypoperfusion, commonly coexisting with AAE, might be a therapeutic indicator for secondary stroke prevention in symptomatic ICAD with AAE.</description><identifier>ISSN: 1868-4483</identifier><identifier>EISSN: 1868-601X</identifier><identifier>DOI: 10.1007/s12975-023-01146-4</identifier><identifier>PMID: 36897543</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Aged ; Atherosclerosis ; Biomedical and Life Sciences ; Biomedicine ; Cardiology ; Carotid arteries ; Cerebral Angiography ; Cerebrovascular Circulation - physiology ; Computed Tomography Angiography ; Disease ; Embolisms ; Female ; Hemodynamics ; Hemodynamics - physiology ; Humans ; Intracranial Arteriosclerosis - complications ; Intracranial Arteriosclerosis - diagnostic imaging ; Intracranial Arteriosclerosis - physiopathology ; Intracranial Embolism - diagnostic imaging ; Intracranial Embolism - physiopathology ; Ischemia ; Male ; Medical imaging ; Middle Aged ; Neurology ; Neurosciences ; Neurosurgery ; Regression analysis ; Stroke ; Vascular Surgery</subject><ispartof>Translational stroke research, 2024-06, Vol.15 (3), p.572-579</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-df5be29ebe1af67af834c28d5eb19e3c1ef8542c39ac201c6111243835c43dee3</citedby><cites>FETCH-LOGICAL-c375t-df5be29ebe1af67af834c28d5eb19e3c1ef8542c39ac201c6111243835c43dee3</cites><orcidid>0000-0001-7300-6647 ; 0000-0001-5019-8893 ; 0000-0001-8193-0709</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12975-023-01146-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12975-023-01146-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27929,27930,41493,42562,51324</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36897543$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Feng, Xueyan</creatorcontrib><creatorcontrib>Fang, Hui</creatorcontrib><creatorcontrib>Ip, Bonaventure Y. M.</creatorcontrib><creatorcontrib>Chan, Ka Lung</creatorcontrib><creatorcontrib>Li, Shuang</creatorcontrib><creatorcontrib>Tian, Xuan</creatorcontrib><creatorcontrib>Zheng, Lina</creatorcontrib><creatorcontrib>Liu, Yuying</creatorcontrib><creatorcontrib>Lan, Linfang</creatorcontrib><creatorcontrib>Liu, Haipeng</creatorcontrib><creatorcontrib>Abrigo, Jill</creatorcontrib><creatorcontrib>Ma, Sze Ho</creatorcontrib><creatorcontrib>Fan, Florence S. Y.</creatorcontrib><creatorcontrib>Ip, Vincent H. L.</creatorcontrib><creatorcontrib>Soo, Yannie O. Y.</creatorcontrib><creatorcontrib>Mok, Vincent C. T.</creatorcontrib><creatorcontrib>Song, Bo</creatorcontrib><creatorcontrib>Leung, Thomas W.</creatorcontrib><creatorcontrib>Xu, Yuming</creatorcontrib><creatorcontrib>Leng, Xinyi</creatorcontrib><title>Cerebral Hemodynamics Underlying Artery-to-Artery Embolism in Symptomatic Intracranial Atherosclerotic Disease</title><title>Translational stroke research</title><addtitle>Transl. Stroke Res</addtitle><addtitle>Transl Stroke Res</addtitle><description>Artery-to-artery embolism (AAE) is a common stroke mechanism in intracranial atherosclerotic disease (ICAD), associated with a considerable risk of recurrent stroke. We aimed to investigate cerebral hemodynamic features associated with AAE in symptomatic ICAD. Patients with anterior-circulation, symptomatic ICAD confirmed in CT angiography (CTA) were recruited. We classified probable stroke mechanisms as isolated parent artery atherosclerosis occluding penetrating artery, AAE, hypoperfusion, and mixed mechanisms, largely based on infarct topography. CTA-based computational fluid dynamics (CFD) models were built to simulate blood flow across culprit ICAD lesions. Translesional pressure ratio (PR = Pressure
post-stenotic
/Pressure
pre-stenotic
) and wall shear stress ratio (WSSR = WSS
stenotic-throat
/WSS
pre-stenotic
) were calculated, to reflect the relative, translesional changes of the two hemodynamic metrics. Low PR (PR ≤ median) and high WSSR (WSSR ≥ 4th quartile) respectively indicated large translesional pressure and elevated WSS upon the lesion. Among 99 symptomatic ICAD patients, 44 had AAE as a probable stroke mechanism, 13 with AAE alone and 31 with coexisting hypoperfusion. High WSSR was independently associated with AAE (adjusted OR = 3.90;
P
= 0.022) in multivariate logistic regression. There was significant WSSR-PR interaction on the presence of AAE (
P
for interaction = 0.013): high WSSR was more likely to associate with AAE in those with low PR (
P
= 0.075), but not in those with normal PR (
P
= 0.959). Excessively elevated WSS in ICAD might increase the risk of AAE. Such association was more prominent in those with large translesional pressure gradient. Hypoperfusion, commonly coexisting with AAE, might be a therapeutic indicator for secondary stroke prevention in symptomatic ICAD with AAE.</description><subject>Aged</subject><subject>Atherosclerosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cardiology</subject><subject>Carotid arteries</subject><subject>Cerebral Angiography</subject><subject>Cerebrovascular Circulation - physiology</subject><subject>Computed Tomography Angiography</subject><subject>Disease</subject><subject>Embolisms</subject><subject>Female</subject><subject>Hemodynamics</subject><subject>Hemodynamics - physiology</subject><subject>Humans</subject><subject>Intracranial Arteriosclerosis - complications</subject><subject>Intracranial Arteriosclerosis - diagnostic imaging</subject><subject>Intracranial Arteriosclerosis - physiopathology</subject><subject>Intracranial Embolism - diagnostic imaging</subject><subject>Intracranial Embolism - physiopathology</subject><subject>Ischemia</subject><subject>Male</subject><subject>Medical imaging</subject><subject>Middle Aged</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Neurosurgery</subject><subject>Regression analysis</subject><subject>Stroke</subject><subject>Vascular Surgery</subject><issn>1868-4483</issn><issn>1868-601X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1P7CAUhonRqFH_gIubJm7coHyV0uVkrl-JiQs1cUcoPVVMoSN0Fv33Mna8JnchCzjJed73AC9Cp5RcUEKqy0RZXZWYMI4JpUJisYMOqZIKS0Jfdre1EIofoJOU3klePHOC76MDLlUWC36IwhIiNNH0xS34oZ2C8c6m4jm0EPvJhddiEUeIEx4HPFfFlW-G3iVfuFA8Tn41Dt6MzhZ3YYzGRhNcdluMbxCHZPu8b5p_XQKT4BjtdaZPcLI9j9Dz9dXT8hbfP9zcLRf32PKqHHHblQ2wGhqgppOV6RQXlqm2hIbWwC2FTpWCWV4bywi1klLKBFe8tIK3APwInc--qzh8rCGN2rtkoe9NgGGdNKuUJLUkjGb07D_0fVjHkG-nOSllLcuqEpliM2Xzq1KETq-i8yZOmhK9CUTPgegciP4KRG9Ef7bW68ZD-0_y_f0Z4DOQciu8QvyZ_YvtJ3GBl5M</recordid><startdate>20240601</startdate><enddate>20240601</enddate><creator>Feng, Xueyan</creator><creator>Fang, Hui</creator><creator>Ip, Bonaventure Y. M.</creator><creator>Chan, Ka Lung</creator><creator>Li, Shuang</creator><creator>Tian, Xuan</creator><creator>Zheng, Lina</creator><creator>Liu, Yuying</creator><creator>Lan, Linfang</creator><creator>Liu, Haipeng</creator><creator>Abrigo, Jill</creator><creator>Ma, Sze Ho</creator><creator>Fan, Florence S. Y.</creator><creator>Ip, Vincent H. L.</creator><creator>Soo, Yannie O. Y.</creator><creator>Mok, Vincent C. T.</creator><creator>Song, Bo</creator><creator>Leung, Thomas W.</creator><creator>Xu, Yuming</creator><creator>Leng, Xinyi</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7300-6647</orcidid><orcidid>https://orcid.org/0000-0001-5019-8893</orcidid><orcidid>https://orcid.org/0000-0001-8193-0709</orcidid></search><sort><creationdate>20240601</creationdate><title>Cerebral Hemodynamics Underlying Artery-to-Artery Embolism in Symptomatic Intracranial Atherosclerotic Disease</title><author>Feng, Xueyan ; Fang, Hui ; Ip, Bonaventure Y. M. ; Chan, Ka Lung ; Li, Shuang ; Tian, Xuan ; Zheng, Lina ; Liu, Yuying ; Lan, Linfang ; Liu, Haipeng ; Abrigo, Jill ; Ma, Sze Ho ; Fan, Florence S. Y. ; Ip, Vincent H. L. ; Soo, Yannie O. Y. ; Mok, Vincent C. T. ; Song, Bo ; Leung, Thomas W. ; Xu, Yuming ; Leng, Xinyi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-df5be29ebe1af67af834c28d5eb19e3c1ef8542c39ac201c6111243835c43dee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Aged</topic><topic>Atherosclerosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cardiology</topic><topic>Carotid arteries</topic><topic>Cerebral Angiography</topic><topic>Cerebrovascular Circulation - physiology</topic><topic>Computed Tomography Angiography</topic><topic>Disease</topic><topic>Embolisms</topic><topic>Female</topic><topic>Hemodynamics</topic><topic>Hemodynamics - physiology</topic><topic>Humans</topic><topic>Intracranial Arteriosclerosis - complications</topic><topic>Intracranial Arteriosclerosis - diagnostic imaging</topic><topic>Intracranial Arteriosclerosis - physiopathology</topic><topic>Intracranial Embolism - diagnostic imaging</topic><topic>Intracranial Embolism - physiopathology</topic><topic>Ischemia</topic><topic>Male</topic><topic>Medical imaging</topic><topic>Middle Aged</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Neurosurgery</topic><topic>Regression analysis</topic><topic>Stroke</topic><topic>Vascular Surgery</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Feng, Xueyan</creatorcontrib><creatorcontrib>Fang, Hui</creatorcontrib><creatorcontrib>Ip, Bonaventure Y. M.</creatorcontrib><creatorcontrib>Chan, Ka Lung</creatorcontrib><creatorcontrib>Li, Shuang</creatorcontrib><creatorcontrib>Tian, Xuan</creatorcontrib><creatorcontrib>Zheng, Lina</creatorcontrib><creatorcontrib>Liu, Yuying</creatorcontrib><creatorcontrib>Lan, Linfang</creatorcontrib><creatorcontrib>Liu, Haipeng</creatorcontrib><creatorcontrib>Abrigo, Jill</creatorcontrib><creatorcontrib>Ma, Sze Ho</creatorcontrib><creatorcontrib>Fan, Florence S. Y.</creatorcontrib><creatorcontrib>Ip, Vincent H. L.</creatorcontrib><creatorcontrib>Soo, Yannie O. Y.</creatorcontrib><creatorcontrib>Mok, Vincent C. T.</creatorcontrib><creatorcontrib>Song, Bo</creatorcontrib><creatorcontrib>Leung, Thomas W.</creatorcontrib><creatorcontrib>Xu, Yuming</creatorcontrib><creatorcontrib>Leng, Xinyi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Translational stroke research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Feng, Xueyan</au><au>Fang, Hui</au><au>Ip, Bonaventure Y. M.</au><au>Chan, Ka Lung</au><au>Li, Shuang</au><au>Tian, Xuan</au><au>Zheng, Lina</au><au>Liu, Yuying</au><au>Lan, Linfang</au><au>Liu, Haipeng</au><au>Abrigo, Jill</au><au>Ma, Sze Ho</au><au>Fan, Florence S. Y.</au><au>Ip, Vincent H. L.</au><au>Soo, Yannie O. Y.</au><au>Mok, Vincent C. T.</au><au>Song, Bo</au><au>Leung, Thomas W.</au><au>Xu, Yuming</au><au>Leng, Xinyi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cerebral Hemodynamics Underlying Artery-to-Artery Embolism in Symptomatic Intracranial Atherosclerotic Disease</atitle><jtitle>Translational stroke research</jtitle><stitle>Transl. Stroke Res</stitle><addtitle>Transl Stroke Res</addtitle><date>2024-06-01</date><risdate>2024</risdate><volume>15</volume><issue>3</issue><spage>572</spage><epage>579</epage><pages>572-579</pages><issn>1868-4483</issn><eissn>1868-601X</eissn><abstract>Artery-to-artery embolism (AAE) is a common stroke mechanism in intracranial atherosclerotic disease (ICAD), associated with a considerable risk of recurrent stroke. We aimed to investigate cerebral hemodynamic features associated with AAE in symptomatic ICAD. Patients with anterior-circulation, symptomatic ICAD confirmed in CT angiography (CTA) were recruited. We classified probable stroke mechanisms as isolated parent artery atherosclerosis occluding penetrating artery, AAE, hypoperfusion, and mixed mechanisms, largely based on infarct topography. CTA-based computational fluid dynamics (CFD) models were built to simulate blood flow across culprit ICAD lesions. Translesional pressure ratio (PR = Pressure
post-stenotic
/Pressure
pre-stenotic
) and wall shear stress ratio (WSSR = WSS
stenotic-throat
/WSS
pre-stenotic
) were calculated, to reflect the relative, translesional changes of the two hemodynamic metrics. Low PR (PR ≤ median) and high WSSR (WSSR ≥ 4th quartile) respectively indicated large translesional pressure and elevated WSS upon the lesion. Among 99 symptomatic ICAD patients, 44 had AAE as a probable stroke mechanism, 13 with AAE alone and 31 with coexisting hypoperfusion. High WSSR was independently associated with AAE (adjusted OR = 3.90;
P
= 0.022) in multivariate logistic regression. There was significant WSSR-PR interaction on the presence of AAE (
P
for interaction = 0.013): high WSSR was more likely to associate with AAE in those with low PR (
P
= 0.075), but not in those with normal PR (
P
= 0.959). Excessively elevated WSS in ICAD might increase the risk of AAE. Such association was more prominent in those with large translesional pressure gradient. Hypoperfusion, commonly coexisting with AAE, might be a therapeutic indicator for secondary stroke prevention in symptomatic ICAD with AAE.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>36897543</pmid><doi>10.1007/s12975-023-01146-4</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-7300-6647</orcidid><orcidid>https://orcid.org/0000-0001-5019-8893</orcidid><orcidid>https://orcid.org/0000-0001-8193-0709</orcidid></addata></record> |
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subjects | Aged Atherosclerosis Biomedical and Life Sciences Biomedicine Cardiology Carotid arteries Cerebral Angiography Cerebrovascular Circulation - physiology Computed Tomography Angiography Disease Embolisms Female Hemodynamics Hemodynamics - physiology Humans Intracranial Arteriosclerosis - complications Intracranial Arteriosclerosis - diagnostic imaging Intracranial Arteriosclerosis - physiopathology Intracranial Embolism - diagnostic imaging Intracranial Embolism - physiopathology Ischemia Male Medical imaging Middle Aged Neurology Neurosciences Neurosurgery Regression analysis Stroke Vascular Surgery |
title | Cerebral Hemodynamics Underlying Artery-to-Artery Embolism in Symptomatic Intracranial Atherosclerotic Disease |
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