ESOC 2026 | Carotid atherosclerosis in patients with AF-related stroke: secondary analysis of RASUNOA-Prime

I’d like to share some findings from a secondary analysis of the RASUNOA-Prime cohort, which we recently published in Stroke, on the role of carotid atherosclerosis in patients with AF-related stroke, including breakthrough strokes. The motivation is a clinical problem we all recognize. Roughly one in five ischemic strokes in patients with atrial fibrillation occur while the patient is actually taking an anticoagulant. These breakthrough strokes carry an annual risk of recurrence of 5 to 9 percent. And so far, we don’t have an effective secondary prevention strategy. Switching anticoagulants or adding an antiplatelet has not been shown to improve patients’ outcome. Part of the problem is that we still don’t fully understand why these breakthrough strokes actually happen. We suspect that mechanisms other than cardioembolism contribute and large artery atherosclerosis is probably the dominant competing mechanism, but it has not been characterized in a prospective study, including patients with breakthrough strokes, yet.

So, we analyzed CT angiograms from the RASUNOA-Prime study, a prospective cohort across 46 German stroke centers, with central blinded core lab reading of the carotid arteries. The RASUNOA-Prime cohort included acute ischemic stroke patients on a DOAC, vitamin K antagonist, or without anticoagulation.

There are three key findings that I would like to highlight. First, the burden of carotid disease in patients with AF-related strokes. Any carotid atherosclerosis was overall present in 81% of patients and most of that was non-stenosing disease. A hemodynamically relevant stenosis or occlusion was present in about 17%. So, if you only look for hemodynamically relevant stenosis, you might miss the large majority of the atherosclerotic burden. Second key result is that we looked specifically at non-stenosing vulnerable plaques with features such as rim sign, soft plaque thickness greater than 3 mm, and plaque surface ulceration. In patients with a unilateral carotid territory stroke and no carotid stenosis greater than 50%, ipsilateral vulnerable plaques were present in about a third of patients, compared with only 5% on the contralateral side. And in DOAC-treated breakthrough stroke patients, the odds of an ipsilateral vulnerable plaque were fourfold higher compared to the contralateral side. Third, this association was particularly pronounced in women, although this exploratory finding is hypothesis-generating only.

So, to wrap it up, what does this mean? It suggests that in a meaningful proportion of breakthrough strokes, competing mechanisms such as stenosing and non-stenosing carotid atherosclerosis may be currently overlooked. That’s important because much of the current research effort focuses on cardiac sources, for instance, left atrial appendage occlusion. Our data argue that large artery atherosclerosis deserves more attention. The key message is to look beyond stenosis and beyond the heart when we think about why these patients have breakthrough strokes.

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