Endarterectomy for symptomatic non-stenotic carotids: a systematic review and descriptive analysis

Larson, Anthony S.; Nardi, Valentina; Brinjikji, Waleed; Benson, John C.; Lanzino, Giuseppe; Savastano, Luis

doi:10.1136/svn-2021-001122

Cited by 13 publications

(13 citation statements)

References 35 publications

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“…Our proposed framework supports the hypothesis that a significant proportion of patients diagnosed with ‘embolic strokes of unknown source’ may actually suffer from thromboembolic phenomena from undiagnosed ulcers, fissures, excavations, IPH or erosions in non-stenotic (<50% narrowing) carotids. These patients could be classified as having a ‘symptomatic non-stenotic carotid’,33 and benefit from targeted interventions such as CEA 34…”

Section: Discussionmentioning

confidence: 99%

Unifying theory of carotid plaque disruption based on structural phenotypes and forces expressed at the lumen/wall interface

et al. 2022

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ObjectivesTo integrate morphological, haemodynamic and mechanical analysis of carotid atheroma driving plaque disruption.Materials and methodsFirst, we analysed the phenotypes of carotid endarterectomy specimens in a photographic dataset A, and matched them with the likelihood of preoperative stroke. Second, laser angioscopy was used to further define the phenotypes in intact specimens (dataset B) and benchmark with histology. Third, representative vascular geometries for each structural phenotype were analysed with Computational Fluid Dynamics (CFD), and the mechanical strength of the complicated atheroma to resist penetrating forces was quantified (n=14).ResultsIn dataset A (n=345), ulceration (fibrous cap disruption) was observed in 82% of all plaques, intraplaque haemorrhage in 68% (93% subjacent to an ulcer) and false luminal formation in 48%. At least one of these ‘rupture’ phenotypes was found in 97% of symptomatic patients (n=69) compared with 61% in asymptomatic patients. In dataset B (n=30), laser angioscopy redemonstrated the structural phenotypes with near-perfect agreement with histology. In CFD, haemodynamic stress showed a large pulse magnitude, highest upstream to the point of maximal stenosis and on ulceration the inflow stream excavates the necrotic core cranially and then recirculates into the true lumen. Based on mechanical testing (n=14), the necrotic core is mechanically weak and penetrated by the blood on fibrous cap disruption.ConclusionsFibrous cap ulceration, plaque haemorrhage and excavation are sequential phenotypes of plaque disruption resulting from the chiselling effect of haemodynamic forces over unmatched mechanical tissue strength. This chain of events may result in thromboembolic events independently of the degree of stenosis.

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Section: Discussionmentioning

confidence: 99%

Unifying theory of carotid plaque disruption based on structural phenotypes and forces expressed at the lumen/wall interface

et al. 2022

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“…Carotid plaque hemorrhage has repeatedly been shown to be associated with acute and future ipsilateral neurologic events ( Table ). 27 , 28 , 29 , 30 , 31 , 32 Saam et al, in a meta‐analysis of 689 patients who underwent MRI carotid plaque imaging, found that patients with carotid IPH had a 6‐fold higher risk for ipsilateral neurologic ischemic events, with a hazard ratio of 5.89. This equated to a 17% annual risk of cerebrovascular events in patients with IPH, compared with 2.4% in patients without IPH.…”

Section: Clinical Significance Of Iphmentioning

confidence: 99%

“…Rates of recurrent strokes among such patients undergoing CEA are exceptionally low, particularly in patients with <50% stenosis, suggesting that in appropriately selected patients this may be a feasible option. 28 Still, this is not without risk: a meta‐analysis by Brinjikji et al noted that the rate of postoperative strokes after carotid stenting was higher in patients with IPH, likely because such unstable plaques were more likely to seed emboli. 47 Our institution has begun treating some patients with nonstenotic carotid IPH with CEA or carotid stenting with anecdotal success.…”

Section: What Do We Do About Iph?mentioning

confidence: 99%

Change of Heart: The Underexplored Role of Plaque Hemorrhage in the Evaluation of Stroke of Undetermined Etiology

Holmes

Alkhouli

Klaas

et al. 2022

JAHA

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In the evaluation of embolic strokes of undetermined source, great emphasis is often placed on cardiovascular disease, namely on atrial fibrillation. Other pathophysiologic mechanisms, however, may also be involved. Carotid artery intraplaque hemorrhage (IPH)—the presence of blood components within an atheromatous plaque—has become increasingly recognized as a possible etiologic mechanism in some cryptogenic strokes. IPH is a marker of plaque instability and is associated with ipsilateral neurologic ischemic events, even in nonstenotic carotid plaques. As recognition of carotid IPH as an etiology of embolic strokes has grown, so too has the complexity with which such patients are evaluated and treated, particularly because overlaps exist in the risk factors for atrial fibrillation and IPH. In this article, we review what is currently known about carotid IPH and how this clinical entity should be approached in the context of the evaluation of embolic strokes of undetermined source.

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“…Some studies have even suggested that patients with ischemic stroke and ipsilateral IPH in minimal carotid stenosis may benefit from carotid endarterectomy. 11,12 Nevertheless, several questions remain regarding IPH. For example, IPH may persist within a plaque for years without any obvious progression or distal ischemic events.…”

Section: Mr Imagingmentioning

confidence: 99%

“…These patients may, therefore, benefit from a targeted therapeutic approach. 11,12 Although the SyNC criteria remain in their infancy and will likely evolve, an important feature of the SyNC criteria is the presence of carotid plaque with high-risk features. An understanding of which radiographic features have been associated with ipsilateral ischemic stroke in patients with ESUS is crucial to determine whether a patient likely meets the criteria for SyNC and may, therefore, benefit from targeted therapy.…”

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confidence: 99%

Nonstenotic Carotid Plaques and Embolic Stroke of Undetermined Source: A Multimodality Review

Larson¹,

Brinjikji²,

Lekah³

et al. 2022

AJNR Am J Neuroradiol

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Symptomatic nonstenotic carotid artery disease has been increasingly recognized as a thromboembolic source in patients who would otherwise be classified as having embolic stroke of undetermined source. Evidence suggests that certain plaque features seen on sonography, CT, and MR imaging in nonstenotic carotid artery disease may predispose to recurrent stroke in patients with embolic stroke of undetermined source. We performed a focused literature review to further study plaque features in the context of embolic stroke of undetermined source and to determine which plaque features may be associated with ipsilateral ischemic events in such patients. Plaque thickness as seen on both ultrasound and CT appears to have a consistent association with ipsilateral stroke in patients with embolic stroke of undetermined source across multiple studies. Intraplaque hemorrhage as seen on MR imaging is now understood to have a strong association with ipsilateral stroke in patients with embolic stroke of undetermined source. Continued study of various plaque features as seen on different modalities is warranted to uncover other potential associations.ABBREVIATIONS: ESUS ¼ embolic stroke of undetermined source; IPH ¼ intraplaque hemorrhage; LRNC ¼ lipid-rich necrotic core; SyNC ¼ symptomatic nonstenotic carotid artery disease; US ¼ ultrasound U p to one-third of strokes have no established mechanism and are considered to be cryptogenic. 1 In 2014, the term "embolic stroke of undetermined source" (ESUS) was established as a clinical entity in patients with nonlacunar cryptogenic stroke in which an embolic source was thought to be most likely, despite an appropriate diagnostic evaluation with negative findings (Fig 1). 2 This term (along with "cryptogenic stroke") has also been used to define patients who may have multiple, competing stroke etiologies in which a definitive source cannot be determined. Patients with ESUS have been estimated to have a .4% risk of recurrent stroke per annum despite being on antiplatelet medication. 1 Subsequent thought was directed to the idea that anticoagulation may be beneficial in such patients, given the likelihood that emboli originated from various nonevident atheroembolic sources. 3 This premise provided the impetus for 2 large clinical trials that compared anticoagulation with aspirin alone in patients with ESUS. 4,5 Despite this plausible theory, no benefit of anticoagulation was observed. These results spurred continued interest in additional

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Endarterectomy for symptomatic non-stenotic carotids: a systematic review and descriptive analysis

Cited by 13 publications

References 35 publications

Unifying theory of carotid plaque disruption based on structural phenotypes and forces expressed at the lumen/wall interface

Unifying theory of carotid plaque disruption based on structural phenotypes and forces expressed at the lumen/wall interface

Change of Heart: The Underexplored Role of Plaque Hemorrhage in the Evaluation of Stroke of Undetermined Etiology

Nonstenotic Carotid Plaques and Embolic Stroke of Undetermined Source: A Multimodality Review

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