P6507ST2L and sST2: relationship in the carotid plaque - a study on 76 cases underwent endarterectomy

Background ST2 receptor (suppression of tumorigenity) has been described as receptor for the interleukin 33 (IL-33), a member of the IL-1 family of cytokines. This receptor is associated in various way to coronary artery disease, all-causes mortality and cardiovascular mortality. It's role in the pathogenesis of atherosclerosis is not well-defined yet. Purpose The present study was designed to assess the relationship between serum level of sST2, a decoy receptor, and immunohistochemicalespression of ST2L in atherosclerotic plaques of formalin fixed paraffin-embedded internal carotid arteries of patients underwent endarterectomy, accepted the predictive value of ST2 in atherosclerosis. Methods The study involved 76 cases (31 symptomatic= 41%, 45 asymptomatic= 59%), age range from 47 to 86 years old, underwent endarterectomy for the treatment of internal carotid stenosis in our vascular surgery of polyclinic, all procedures performed by the same physician. Patients were divided into three groups, depending on the presence of ST2Ltransmembrane receptor on the carotid plaque after immunoistochemical evaluation (group low presence of ST2L= 0–1+; moderate presence of ST2= 2+; high presence of ST2= 3+). Serum level of sST2 were defined through the use of an ELISA-kit, specific for ST2 and ready-to-use. Results There was a relationship between ST2L and sST2 values: if considering sST2 mean and median value referring to specific subgroup (low, moderate and high), this is lower if the group (i.e. ST2L presence on the atherosclerotic plaque) is higher, and vice-versa. This shows an inverse relationship between this two parameters. Moreover, using Pearson correlation coefficient, all the three sub-group show a strong correlation to the leukocytes value (low=0.658, moderate= 0.434, high= 0.358). Conclusions The ST2L immunohistochemical expression was for the first time investigated in a large number of human carotid atherosclerotic plaques. The inverse relationship between ST2L and sST2 supports the pathogenetic hypothesis that ST2L/IL33 axis could drive the mechanism of plaque development and eventually rupture. Correlation with leukocytes provides a further strong evidence confirming inflammatory pathogenesis of atherosclerosis, but most of all leukocytes' high value could be associated to a greater plaque instability. Acknowledgement/Funding None