Diabetes is associated with an increased risk of cardiovascular complications, as a reflection of the chronic inflammatory status. Monocytes-macrophages in diabetic subjects present impaired arachidonic acid metabolism. Moreover, atheromatous plaques in diabetic subjects seem to be significantly enriched in 2-AA-LPC (2-arachidonoyl-lysophosphatidylcholine) and are more inflammatory and more likely to rupture than are plaques in non-diabetic subjects. We therefore hypothesize that this vulnerability of atheromatous plaques in diabetic subjects could be explained by impaired 2-AA-LPC metabolism within the plaque.
Study Type
OBSERVATIONAL
Enrollment
204
3 tubes (5 ml volume) collected during surgery
a carotid sample collected during surgery
Chu Dijon Bourgogne
Dijon, France
Change in arachidonic acid metabolism of atheromatous plaques from diabetic versus non-diabetic subjects
Time frame: Baseline
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