Impact of glucose intolerance on the risk of carotid plaque instability assessed by MRI

Abstract

Atherosclerotic disease is a complex multifactorial and systemic condition that affects arteries, including carotid arteries. Atherosclerotic plaque instability can predict plaque rupture, the major cause of ischemic strokes. Intraplaque hemorrhage (IPH) is an important contributor of plaque instability caused by the pro-inflammatory and hypoxic environment of the atherosclerotic plaque promoting the development of intraplaque neo-vessels. Metabolic disturbances are known to promote atherosclerotic plaque formation. Ischemic stroke prevalence is increase in patients with obesity and/or type-2 diabetes. The objective of the present study is to evaluate whether glucose intolerance can increase IPH in patients with carotid atherosclerosis. This study involves 57 patients with carotid atherosclerotic plaque with more than 50% stenosis, asymptomatic for more than 6 months, with no surgical indication for endarterectomy and no recent inflammatory disease. IPH was evaluated by magnetic resonance imaging (MRI). A score was defined for IPH (from 0: non hemorrhage to 3: large hemorrhage). Fasting blood glucose level was measured and patients were allocated in glucose tolerant (< 5,6 mM) or glucose intolerant (> 5,6 mM) groups. We showed that the score of IPH quantified by MRI was increased in the glucose intolerant subgroup of patients (0.39 vs. 0.84, P = 0.04). This result was confirmed by a higher prevalence of hemorrhagic plaque in the glucose intolerant group (73 vs. 41%, P < 0.05). Interestingly, the fasting blood glucose level is higher in patients with a hemorrhagic plaque than non-hemorrhagic plaque (5.6 vs. 6.9 mM, P = 0.04). Moreover, neither other known pro-atherogenic markers (LDL, cholesterol, TG) nor obesity seem to increase the degree of IPH. In conclusion, we demonstrated a strong impact of blood glucose level on the risk of plaque instability reflected by IPH. Further experiments are needed to strengthen the relation between type-2 diabetes, blood glucose level and IPH to understand the underlying mechanisms.