Symptomatic non-stenotic carotid disease: current challenges and opportunities for diagnosis and treatment

Abstract

Symptomatic non-stenotic carotid plaques (SyNC) are an under-researched and under-recognized source of stroke. Various imaging markers of non-stenotic carotid plaques that are associated with stroke risk have been identified, but these causal relationships need to be confirmed in additional prospective studies. Currently, there exists neither a standardized SyNC definition nor a dedicated set of imaging protocols, although researchers have started to address these shortcomings. Moreover, many neuroradiologists are still unaware of the condition, and hence do not comment on high-risk plaque features other than stenosis in their reports. Regarding SyNC treatment, scant data exist as to whether and to what extent medical, interventional and surgical treatments could influence the course of the disease; the relative lack of data on the ‘natural’ history of untreated SyNC makes treatment comparisons difficult. In our opinion, endovascular SyNC treatment represents the most promising treatment option for SyNC, since it allows for targeted elimination of the embolic source, with few systemic side effects and without the need for general anesthesia. However, currently available carotid devices are designed to treat stenotic lesions, and thus are not optimally designed for SyNC. Developing a device specifically tailored to SyNC could be an important step towards establishing endovascular SyNC treatment in clinical practice. In this review, we provide an overview of the current state of evidence with regard to epidemiological, clinical and imaging features of SyNC, propose a SyNC definition based on imaging and clinical features, and outline a possible pathway towards evidence-based SyNC therapies, with a special focus on endovascular SyNC treatment.

Symptomatic Non-stenotic Carotid Disease in Embolic Stroke of Undetermined Source

“…Various potential thromboembolic sources, including cardiac valvular abnormalities, covert atrial fibrillation, paradoxical embolism or arterio-arterial emboli fall under the ESUS rubric [ 2 ]. Using the TOAST criteria, large artery atherosclerosis (LAA) as the cause of stroke only applies if there is more than 50% luminal narrowing of the ipsilateral internal carotid artery [ 3 ]; however, non-stenotic carotid disease, defined as < 50% luminal narrowing of the internal carotid artery, can be an underlying source of emboli and cause of ischemic stroke and yet these patients are still classified as cryptogenic stroke or ESUS [ 4 ]. A systematic review showed a prevalence of non-stenotic carotid disease of 51% in patients with ischemic stroke [ 5 ].…”