Background:

Inflammation within atherosclerosis promotes atheroma rupture and correlates with concentrations of circulating matrix metalloproteinases. Matrix metalloproteinases are implicated in blood-brain barrier disruption, contributing to the development of chronic cerebral small vessel disease and larger acute infarct volumes. 

Aims:

This study investigates the association between inflammation within carotid atherosclerosis and both acute and chronic cerebrovascular disease. 

Methods:

Individuals with ischaemic strokes with ipsilateral carotid artery stenosis of >50% underwent carotid 18Fluoride-fluorodeoxyglucose-positron emission tomography within 14 days of stroke. Small vessel disease severity (dichotomised using modified Fazekas scale) and infarct volumes were assessed using 3-Tesla MRI acutely and after 90 days. 

Results:

Of 26 participants, 15 had no/mild and 11 had moderate/severe small vessel disease. Adjusting for cardiovascular risk factors, average carotid artery fluorodeoxyglucose uptake (measured as maximum tissue-to-background ratio) was independently associated with more severe small vessel disease (OR 6.18, 95% CI 2.1-18.2, P<0.01). Average carotid artery fluorodeoxyglucose uptake was also independently associated with an increase in FLAIR lesion volume at 90 days (coefficient=0.81, P<0.01). 

Discussion:

We demonstrate that generalised inflammation within carotid atherosclerosis is independently associated with more severe chronic small vessel disease and adverse evolution of the acute infarct in the early post-stroke setting. These novel findings are important for understanding how vulnerable atherosclerosis may promote a “vulnerable brain” primed for injury, and have important implications for therapeutic exploitation in the management of systemic atherosclerosis, particularly non-stenotic disease previously considered asymptomatic, to reduce the burden of both acute and chronic cerebrovascular disease.

ESOC-2019