Abstract
Arterial wall inflammation destabilizes atherosclerotic plaques and makes them prone to rupture (1) so detection of inflammatory activity may therefore assist discrimination between unstable and stable plaques. Inflammation of the vessel wall prompts transport of excess fluid into the interstitial space and results in the formation of edema (2). Hence, edema located within the vessel wall can be used as a marker for inflammatory activity.
Highlights
Arterial wall inflammation destabilizes atherosclerotic plaques and makes them prone to rupture (1) so detection of inflammatory activity may assist discrimination between unstable and stable plaques
We wished to determine whether edema could be detected in the carotid artery wall by cardiovascular magnetic resonance (CMR) using a T2-weighted shorttau inversion recovery sequence (T2-STIR)
The relative signal intensity and area of enhancement showed a linear correlation with the area of fibrinogen detected on the corresponding histopathology (r=0.80, p
Summary
Arterial wall inflammation destabilizes atherosclerotic plaques and makes them prone to rupture (1) so detection of inflammatory activity may assist discrimination between unstable and stable plaques. Inflammation of the vessel wall prompts transport of excess fluid into the interstitial space and results in the formation of edema (2). Edema located within the vessel wall can be used as a marker for inflammatory activity. Purpose We wished to determine whether edema could be detected in the carotid artery wall by cardiovascular magnetic resonance (CMR) using a T2-weighted shorttau inversion recovery sequence (T2-STIR). Agreement was detected between carotid artery wall enhancement (defined as SI four SD ≥ the sternocleidomastoid muscle) and the uptake of Evans blue (=0.83, p
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