Plasmatic biomarkers of inflammation correlate with 18FDG-PET-CT and microembolic signals in patients with carotid stenosis

Abstract

Methods:18 FDG-PET-CT and MES detection was performed in consecutive patients with 50% to 99% symptomatic or asymptomatic carotid stenosis. Uptake index was defined by a target to background ratio (TBR) between maximum standardized uptake value of the carotid plaque and the average uptake of the jugular veins. The analysis of biomarkers included adhesion molecules [intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule 1, P-selectin and E-selectin], interleukins (IL-1, IL-6), chemokines (RANTES, monocyte chemoattractant protein 1), cytokines (tumor necrosis factor α), matrix-metalloproteases (MMP), myeloperoxidase, and lipoprotein-associated phospholipase A2.Results: There were 54 symptomatic and 57 asymptomatic patients. TBR values were significantly higher in the symptomatic compared to the asymptomatic (median 2.1 vs . 1.8, P = 0.002) and in the MES positive (MES+) compared to the MES negative (MES-) group (MES+, n = 19, median 2.3 and MES-, n = 88, median 1.8, P = 0.01). The best threshold for TBR values was of 1.9. We found a significant correlation between higher 18 FDG uptake (TBR ≥ 1.9) and the plasmatic levels of chemokine RANTES (P = 0.03) and higher levels of ICAM-1 in MES+ patients (P = 0.03). Interestingly MMP-2 levels were more important in patients with lower TBR values (P = 0.02) and MMP-3 and P-selectin in those who were MES-(respectively P = 0.001 and P = 0.009). Conclusion:In the present study, ICAM-1 was associated with the presence of thrombotically active atherosclerotic plaques, while RANTES mainly correlated with the inflammatory process. MMP-2, MMP-3 and P-selectin levels were more important in patients with stable plaques.

Advancing the care of patients with cerebrovascular disease: editorial

“…As such, growing interest in radiographic and molecular biomarkers has sparked interest in multiple aspects of cerebrovascular disease. In their prospective analysis, Mueller et al [5] sought to characterize radiographic features and various potential serum biomarkers and their association with clinical presentation of atherosclerotic carotid disease. Transcranial ultrasound bubble studies and radiotracer computer tomography angiography were utilized to evaluate the stability of plaque formation in symptomatic and asymptomatic patients with clinically significant carotid stenosis [5] .…”

“…In their prospective analysis, Mueller et al [5] sought to characterize radiographic features and various potential serum biomarkers and their association with clinical presentation of atherosclerotic carotid disease. Transcranial ultrasound bubble studies and radiotracer computer tomography angiography were utilized to evaluate the stability of plaque formation in symptomatic and asymptomatic patients with clinically significant carotid stenosis [5] . Given the uncertain nature regarding the stability of atherosclerotic plaques and their tendency to rupture and produce atheroembolic events, the subject has seen significant interest in active studies involving the evaluation of prognostic factors and underlying biology in plaque formation [6] .…”

“…Given the uncertain nature regarding the stability of atherosclerotic plaques and their tendency to rupture and produce atheroembolic events, the subject has seen significant interest in active studies involving the evaluation of prognostic factors and underlying biology in plaque formation [6] . The authors chose to compare important clinical indicators, such as propensity of microemboli formation, with biomarkers under investigation, concluding that ICAM-1 was associated with thrombotic plaque formation [5] .…”

“…Candelaresi et al [7] presented a well written report of a patient who developed posterior reversible encephalopathy syndrome attributable to the administration of the myeloma protease inhibitor bortezomib. The case details the clinical course and association with drug and discusses potential mechanisms [5] . The patient in the case was ultimately successfully treated with systemic glucocorticoids [5] , a convenient option as such drugs are often a component of anti-myeloma drug regimens.…”

“…The case details the clinical course and association with drug and discusses potential mechanisms [5] . The patient in the case was ultimately successfully treated with systemic glucocorticoids [5] , a convenient option as such drugs are often a component of anti-myeloma drug regimens.…”