{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T07:31:50Z","timestamp":1791099110336,"version":"4.1.0"},"reference-count":52,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[1996,6]]},"abstract":"<jats:p>\n            <jats:italic>Background and Purpose<\/jats:italic>\n            Increased resistance in the venous drainage of intracranial arteriovenous malformations (AVMs) may contribute to their increased risk of hemorrhage. Venous drainage impairment may result from naturally occurring stenoses\/occlusions, or if draining veins (DVs) undergo occlusion before feeding arteries during surgical removal, or after surgery in the presence of \u201cocclusive hyperemia.\u201d We employed a detailed biomathematical AVM model using electrical network analysis to investigate theoretically the hemodynamic consequences and the risk of AVM rupture due to venous drainage impairment.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods<\/jats:italic>\n            The AVM model consisted of a noncompartmentalized nidus with 28 vessels (24 plexiform components and 4 fistulous components), 4 arterial feeders, and 2 DVs. An expression for the risk of AVM nidus rupture was derived on the basis of functional distribution of the critical radii of component vessels. Risk was calculated from biomathematical simulations of volumetric flow rate with both DVs patent and for four stages of venous drainage obstruction: (1) 25%, (2) 50%, (3) 75%, and (4) 100%. Each stage of occlusion was applied to each DV while the other DV was patent and then to the patent DV while the other DV was totally occluded.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Results<\/jats:italic>\n            For flow through the AVM when both DVs were unobstructed, the baseline risk of AVM nidus rupture ranged from 4.4% to 91.2%. Theoretical rupture occurred in nidus components proximal to the DVs when the risk exceeded 100%, as was observed with the obstruction of DV1 and a patent DV2. The ranges for risk of rupture across the nidus for the four stages were (1) 4.7% to 90.5%, (2) 5.9% to 86.9%, (3) 0% to 98.4%, and (4) 0% to 106.3%, respectively. Rupture was observed for an 86% occlusion of DV1 (ie, the DV fed by the intranidal fistula) and DV2 patent, primarily because of the dramatic shift in the hemodynamic burden toward the weaker plexiform nidus vessels.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            On theoretical grounds, venous drainage impairment was predictive of AVM nidus rupture and was strongly dependent on AVM morphology (presence of intranidal fistulas and their spatial relation to DVs) and hemodynamics. Specifically, stenosis\/occlusion of a high-flow DV induces a rapid redistribution of blood into the weak plexiform vessels of the opposing region of the nidus, causing a hemodynamic overload and an increased risk of rupture. These findings should be carefully considered among all factors affecting the natural history of intracranial AVMs and the mechanisms implicated in their spontaneous rupture. They may also provide a theoretical rationale for some of the hemorrhagic complications that occur during and after surgical treatment.\n          <\/jats:p>","DOI":"10.1161\/01.str.27.6.1072","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T20:08:03Z","timestamp":1308341283000},"page":"1072-1083","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":99,"title":["Risk of Intracranial Arteriovenous Malformation Rupture Due to Venous Drainage Impairment"],"prefix":"10.1161","volume":"27","author":[{"given":"George J.","family":"Hademenos","sequence":"first","affiliation":[{"name":"From the Endovascular Therapy Service, Department of Radiological Sciences, University of California at Los Angeles School of Medicine."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tarik F.","family":"Massoud","sequence":"additional","affiliation":[{"name":"From the Endovascular Therapy Service, Department of Radiological Sciences, University of California at Los Angeles School of Medicine."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1001\/archneur.1980.00500510027003"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1227\/00006123-198503000-00026"},{"key":"e_1_3_2_3_2","first-page":"809","volume":"15","year":"1994","unstructured":"Norbash AM, Marks MP, Lane B. 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