Non-Stenotic Carotid Disease is Common, Substantially Increases Risk After Ischemic Stroke

Non-stenotic carotid disease is not only common, but also associated with substantial risk after ischemic stroke, comparable to patients with ≥50% stenosis.1

Presented at the World Stroke Congress (WSC) 2026 in Seoul, South Korea, by Amy Yu, MD, MSc, associate professor of neurology at the University of Toronto and senior scientist at the Sunnybrook Research Institute, these data challenge the traditional understanding of “clinically insignificant” stenosis.1

“Carotid disease accounts for about 10% of all ischemic stroke, and we know that people with severe carotid stenosis should be treated with interventions for revascularization,” Yu told HCPLive in an exclusive interview. “The <50% carotid disease, the non-stenotic category, is really a mixed bag, and we’re now recognizing that some of these patients can go on to have high-risk stroke events or other kinds of major adverse cardiovascular events.”

Despite the clinical significance of non-stenotic carotid disease, it remains a relatively understudied pathology in stroke. Prior studies have identified imaging features of high-risk non-stenotic plaques, but as of July 2026, there is still no standardized definition of symptomatic non-stenotic carotid disease.2

To address this, Yu and colleagues conducted a population-based study in Ontario using the Ontario Stroke Registry, specifically sourcing data from 2019-2023. Patients who were hospitalized with ischemic stroke within 24 hours of onset and who had a documented carotid stenosis severity of <50% or ≥50% were enrolled in the study and categorized by the highest degree per patient. The team compared outcomes such as in-hospital mortality and major adverse cardiovascular events (MACE) until 2025 by stenosis severity, utilizing modified Poisson and Cox regression models adjusted for demographics, stroke severity, and comorbidities.1

A total of 15,796 patients were included in the study, among whom 78.5% had non-stenotic carotid disease (defined as stenosis severity <50%). Patients with <50% stenosis also had lower burdens of atherosclerotic risk factors like hypertension (81.7% vs 87.5%), diabetes (37.4% vs 43.7%), prior stroke (11.4% vs 14.7%), coronary artery disease (13.3% vs 22%), and smoking (13.5% vs 18.8%).1

However, despite these differences, Yu and colleagues noted that event rates for ischemic stroke (9.4% vs 9.5%; adjusted HR, 0.96; 95% CI, 0.84-1.11) and myocardial infarction (2% vs 3.2%; aHR, 0.76; 95% CI, 0.59-1) were similar in both groups. In-hospital mortality also remained substantial across both populations, although it was numerically lower in those with ≥50% stenosis (adjusted risk ratio [RR], 0.77; 95% CI, 0.7-0.86). Long-term mortality risk was only modestly lower in patients with <50% stenosis (aHR, 0.83; 95% CI, 0.77-0.89).1

Ultimately, Yu and colleagues concluded that these data, while relatively early and hypothesis-generating, still display the significant risk posed by non-stenotic carotid disease. Mortality and MACE risk in patients with <50% stenosis approached those seen in ≥50% stenosis, highlighting an underrepresented risk. The team determined that this population needs improved risk stratification and optimized disease management strategies.1

“If we’re able to quantify long-term risks on a population basis, it’s really helpful for other people who want to plan future clinical trials or cohort studies to be able to know the outcome numbers that we’re looking at, and the sample size calculations, and so on,” Yu said. “I’m hoping that this study can provide a bit of background information and be hypothesis-generating for future studies as well.”

Editors’ Note: Yu reports no relevant disclosures.

References

1. Yu A. Non-Stenotic Carotid Disease is Not Benign: Comparable Risk to ≥50% Stenosis After Stroke. Presented at the World Stroke Congress (WSC) 2026, Seoul, South Korea. October 21-23, 2026.

2. Chu T, Soufi K, Castillo J, Moskalik A, Gerndt C, Cord BJ. Non-stenotic Carotid Disease: Review of the Literature and Case Discussion of TCAR for Treatment. Semin Neurol. 2026;46(4):367-373. doi:10.1055/a-2893-7436