Early Stroke Risk After Transient Ischemic Attack Among Individuals With Symptomatic Intracranial Artery Stenosis

Abstract

Background: Little is known about short-term vascular risk after transient ischemic attack (TIA) caused by intracranial atherosclerosis. Objectives: To quantify the early risk of ischemic stroke in the territory of a stenotic intracranial artery after TIA and to identify clinical and imaging features associated with increased risk of stroke in the territory among patients with TIA.

European Stroke Organisation guidelines on treatment of patients with intracranial atherosclerotic disease

“…In the WASID trial only 63% of the time patients randomized to receive VKA had an INR within the pre-specified target range (INR 2.0–3.0). 61 A dose-response effect was uncovered in a post-hoc analysis, suggesting that INRs of less than 2.0 were associated with a higher risk of ischemic stroke and major cardiac events than INRs of 2.0 or greater, whereas INRs greater than 3.0 were associated with a significantly higher risk of major hemorrhages than INRs of 3.0 or less. 61 It needs to be highlighted that the oral anticoagulation regimens evaluated in the aforementioned RCTs were VKAs (warfarin or coumadin, respectively), 59,60 with non-vitamin K oral anticoagulants (NOACs) have never been tested in a dedicated RCT of patients with ischemic stroke or TIA associated with ICAD to date.…”

European Stroke Organisation guidelines on treatment of patients with intracranial atherosclerotic disease

“…In the WASID trial only 63% of the time patients randomized to receive VKA had an INR within the pre-specified target range (INR 2.0–3.0). 61 A dose-response effect was uncovered in a post-hoc analysis, suggesting that INRs of less than 2.0 were associated with a higher risk of ischemic stroke and major cardiac events than INRs of 2.0 or greater, whereas INRs greater than 3.0 were associated with a significantly higher risk of major hemorrhages than INRs of 3.0 or less. 61 It needs to be highlighted that the oral anticoagulation regimens evaluated in the aforementioned RCTs were VKAs (warfarin or coumadin, respectively), 59,60 with non-vitamin K oral anticoagulants (NOACs) have never been tested in a dedicated RCT of patients with ischemic stroke or TIA associated with ICAD to date.…”

Collaterals dramatically alter stroke risk in intracranial atherosclerosis

“…Among patients with TIA alone, all ischemic strokes in the first 90 days were in the territory of the stenotic intracranial artery 22. In these cases with TIA alone, 140 subjects had moderate stenoses compared to 77 with severe arterial narrowing and the presence of infarcts on brain imaging portended a significantly higher risk of stroke 22. These findings have been previously ascribed to greater atherosclerotic plaque instability in the TIA versus stroke cohorts of WASID yet alternative explanations may invoke collateral flow 22.…”

Comparison of risk factors and work‐up in young and middle‐aged patients with TIA and ischaemic stroke

“…The TIA is generally accepted as a type of resolved ischaemic stroke. This conception is supported by the consistently high number of strokes temporally close to the index TIA [5–11], as well as by the results of neuroimaging [12–16], which are indistinguishable from stroke in many cases. In an attempt to determine the etiologic similarity or dissimilarity between the two conditions, many studies have been devoted to the search of factors predicting subsequent stroke in TIA patients [17–22].…”

European Stroke Organisation guidelines on treatment of patients with intracranial atherosclerotic disease

“…In the WASID trial only 63% of the time patients randomized to receive VKA had an INR within the pre-specified target range (INR 2.0–3.0). 61 A dose-response effect was uncovered in a post-hoc analysis, suggesting that INRs of less than 2.0 were associated with a higher risk of ischemic stroke and major cardiac events than INRs of 2.0 or greater, whereas INRs greater than 3.0 were associated with a significantly higher risk of major hemorrhages than INRs of 3.0 or less. 61 It needs to be highlighted that the oral anticoagulation regimens evaluated in the aforementioned RCTs were VKAs (warfarin or coumadin, respectively), 59,60 with non-vitamin K oral anticoagulants (NOACs) have never been tested in a dedicated RCT of patients with ischemic stroke or TIA associated with ICAD to date.…”

Collaterals dramatically alter stroke risk in intracranial atherosclerosis

“…Among patients with TIA alone, all ischemic strokes in the first 90 days were in the territory of the stenotic intracranial artery 22. In these cases with TIA alone, 140 subjects had moderate stenoses compared to 77 with severe arterial narrowing and the presence of infarcts on brain imaging portended a significantly higher risk of stroke 22. These findings have been previously ascribed to greater atherosclerotic plaque instability in the TIA versus stroke cohorts of WASID yet alternative explanations may invoke collateral flow 22.…”

Comparison of risk factors and work‐up in young and middle‐aged patients with TIA and ischaemic stroke

“…The TIA is generally accepted as a type of resolved ischaemic stroke. This conception is supported by the consistently high number of strokes temporally close to the index TIA [5–11], as well as by the results of neuroimaging [12–16], which are indistinguishable from stroke in many cases. In an attempt to determine the etiologic similarity or dissimilarity between the two conditions, many studies have been devoted to the search of factors predicting subsequent stroke in TIA patients [17–22].…”

European Stroke Organisation guidelines on treatment of patients with intracranial atherosclerotic disease

“…In the WASID trial only 63% of the time patients randomized to receive VKA had an INR within the pre-specified target range (INR 2.0–3.0). 61 A dose-response effect was uncovered in a post-hoc analysis, suggesting that INRs of less than 2.0 were associated with a higher risk of ischemic stroke and major cardiac events than INRs of 2.0 or greater, whereas INRs greater than 3.0 were associated with a significantly higher risk of major hemorrhages than INRs of 3.0 or less. 61 It needs to be highlighted that the oral anticoagulation regimens evaluated in the aforementioned RCTs were VKAs (warfarin or coumadin, respectively), 59,60 with non-vitamin K oral anticoagulants (NOACs) have never been tested in a dedicated RCT of patients with ischemic stroke or TIA associated with ICAD to date.…”

Collaterals dramatically alter stroke risk in intracranial atherosclerosis

“…Among patients with TIA alone, all ischemic strokes in the first 90 days were in the territory of the stenotic intracranial artery 22. In these cases with TIA alone, 140 subjects had moderate stenoses compared to 77 with severe arterial narrowing and the presence of infarcts on brain imaging portended a significantly higher risk of stroke 22. These findings have been previously ascribed to greater atherosclerotic plaque instability in the TIA versus stroke cohorts of WASID yet alternative explanations may invoke collateral flow 22.…”

Comparison of risk factors and work‐up in young and middle‐aged patients with TIA and ischaemic stroke

“…The TIA is generally accepted as a type of resolved ischaemic stroke. This conception is supported by the consistently high number of strokes temporally close to the index TIA [5–11], as well as by the results of neuroimaging [12–16], which are indistinguishable from stroke in many cases. In an attempt to determine the etiologic similarity or dissimilarity between the two conditions, many studies have been devoted to the search of factors predicting subsequent stroke in TIA patients [17–22].…”