Plaque and Brain Inflammation in Symptomatic Carotid Stenosis: Role of the Ficolin-2
Status:
Not yet recruiting
Trial end date:
2025-01-30
Target enrollment:
Participant gender:
Summary
Carotid artery stenosis is observed in about 3% of ≥ 60 years subjects and accounts for
around 10-20% of all ischemic strokes. Beyond the degree of stenosis, plaque composition
affects the risk of ischemic stroke. Identification of patients with vulnerable plaques at
higher risk of stroke who might benefit from carotid revascularization is crucial.
A growing body of evidence suggests that the lectin pathway of the complement system, and
especially the ficolin-2, is involved in atherosclerosis. It has been hypothesized that
circulating levels of ficolin-2 increase during chronic inflammatory conditions (i.e. growing
atherosclerotic plaque) whereas they fall during sub-acute or acute inflammatory conditions
(i.e. plaque rupture and acute ischemic stroke) because of consumption (binding to targets).
Therefore, ficolin-2 has been proposed as a biomarker informing on the specific state of the
plaque. However, in acute ischemic stroke due to carotid stenosis, both plaque rupture and
stroke injury contribute to lectin pathway activation, thus affecting circulating levels of
ficolin-2. Until now, the relative contribution of plaque and brain inflammation on
circulating levels of ficolin-2 has not been documented.
In the present study we aim to assess the association between circulating levels of ficolin-2
and carotid and brain inflammation on [18F]DPA-714 positron emission tomography (PET)/MRI in
patients with transient ischemic attack or acute ischemic stroke due to carotid stenosis. For
that purpose, we intend to include 30 patients with transient ischemic attack or acute
ischemic stroke due to ≥ 50%. carotid stenosis. Each patient will have a measure of plasmatic
level of ficolin-2 as well a [18F]DPA-714 PET/MRI to quantify the fixation of the radiotracer
on carotid and brain.