Carotid artery stenosis

Carotid artery stenosis is a narrowing or constriction of the inner surface (lumen) of the carotid artery, usually caused by atherosclerosis.

Carotid artery stenosis (CS) is a major cause of ischemic stroke.

Classification

Asymptomatic carotid artery stenosis.

Symptomatic carotid artery stenosis

Clinical features

The mechanisms underlying acute cerebrovascular syndrome in patients with carotid artery stenosis remain unclear.

Carotid artery stenosis can present with no symptoms or with symptoms such as transient ischemic attacks (TIAs) or strokes, contributing to up to 10%-20% of strokes or transient ischemic attacks.

Cortical infarction occurs as a result of vulnerable plaque. Reduced cerebral perfusión induces border-zone infarction. Both factors are implicated in mixed-pattern infarction. Developments in noninvasive diagnostic modalities allow us to explore the mechanisms behind acute cerebrovascular syndrome in carotid artery stenosis and to determine the ideal therapies 1).

Diagnosis

Currently, MRI is the gold standard in carotid plaque imaging, with its high resolution and high sensitivity for identifying intraplaque hemorrhage (IPH), ulceration, lipid-rich necrotic core (LRNC), and inflammation. However, MRI is limited due to time constraints.

CT also allows for high-resolution imaging and can accurately detect ulceration and calcification, but cannot reliably differentiate LRNC from IPH.

PET/CT is an effective technique to identify active inflammation within the plaque, but it does not allow for assessment of anatomy, ulceration, IPH, or LRNC.

Ultrasonography, with the aid of contrast enhancement, is a cost-effective technique to assess plaque morphology and characteristics, but it is limited in sensitivity and specificity for detecting LRNC, plaque hemorrhage, and ulceration compared with MRI.

US can detect congenital variants, dissection, stenosis, and vasculopathy. In addition, correlation of US findings with both magnetic resonance imaging and computed tomography more comprehensively demonstrates the complementary nature of these imaging modalities 2).

Also summarized is how these advanced imaging techniques are being used in clinical practice to risk stratify patients with low- and high-grade carotid artery stenosis. For example, identification of IPH on MRI in patients with low-grade carotid artery stenosis is a risk factor for failure of medical therapy, and studies have shown that such patients may fair better with carotid endarterectomy (CEA). MR plaque imaging has also been found to be useful in identifying revascularization candidates who would be better candidates for CEA than carotid artery stenting (CAS), as high intraplaque signal on time of flight imaging is associated with vulnerable plaque and increased rates of adverse events in patients undergoing CAS but not CEA 3).

Treatment

Case series

Sixty-seven consecutive procedures were performed for internal carotid artery stenosis with CAS at the Ise Red Cross Hospital between November 2015 and February 2018. Procedures for emergency CAS for stroke in evolution or crescendo transient ischemic attack were excluded (n = 12). The embolic debris from remaining procedures (n = 55) was stained with hematoxylineosin and the red blood cells, white blood cells, and fibrinwere quantified by color-based segmentation. Cholesterol crystals and calcification were examined histopathologically. Diffusion-weighted imaging (DWI) was performed 1-3 days after CAS, and the images were used to classify procedures according to the presence of new lesions.

Of the 55 CAS procedures, new DWI lesions were identified after 32. One patient had symptomatic cerebral embolism. Higher proportions of patients with cholesterol crystals in embolic debris (17 vs. 78%, p < 0.001) and higher proportion of white blood cells (mean 2.3 [0-9.9] vs. 4.2% [0-29.9%], p < 0.01) were observed in the embolic debris of procedures with and without new DWI lesions.

Cholesterol crystals were common in the embolic debris from patients with postoperative ischemic lesions after CAS. These results suggest that inflammatory destabilization of the intraplaque lipid component is related to postprocedural DWI lesions 4).

References

1)

Kashiwazaki D, Akioka N, Kuwayama N, Noguchi K, Tanaka K, Kuroda S. Pathophysiology of acute cerebrovascular syndrome in patients with carotid artery stenosis: a magnetic resonance imaging/single-photon emission computed tomography study. Neurosurgery. 2015 Apr;76(4):427-34. doi: 10.1227/NEU.0000000000000655. PubMed PMID: 25621983.
2)

Deurdulian C, Emmanuel N, Tchelepi H, Grant EG, Malhi H. Beyond the Bifurcation: There Is More to Cerebrovascular Ultrasound Than Internal Carotid Artery Stenosis! Ultrasound Q. 2015 Nov 19. [Epub ahead of print] PubMed PMID: 26588099.
3)

Brinjikji W, Huston J 3rd, Rabinstein AA, Kim GM, Lerman A, Lanzino G. Contemporary carotid imaging: from degree of stenosis to plaque vulnerability. J Neurosurg. 2016 Jan;124(1):27-42. doi: 10.3171/2015.1.JNS142452. Epub 2015 Jul 31. PubMed PMID: 26230478.
4)

Maekawa K, Shibata M, Nakajima H, Kitano Y, Seguchi M, Kobayashi K, Sano T, Yabana T, Miya F. Cholesterol Crystals in Embolic Debris are Associated with Postoperative Cerebral Embolism after Carotid Artery Stenting. Cerebrovasc Dis. 2019 Jan 2;46(5-6):242-248. doi: 10.1159/000495795. [Epub ahead of print] PubMed PMID: 30602147.

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