Abstract TP120: IL-17a Correlates With Coated-Platelet Levels Among Patients With Carotid Atherosclerosis
Introduction: Coated-platelets are a subset of platelets with high procoagulant potential observed on dual agonist stimulation with collagen and thrombin. Elevated coated-platelets identify asymptomatic carotid stenosis patients at high risk for stroke or TIA and are associated with stenosis progression.
Hypothesis: Specific inflammatory markers correlate with coated-platelet levels among patients with carotid atherosclerosis.
Methods: Patients referred for carotid Doppler evaluation with at least one additional follow-up scan were analyzed. Coated-platelet levels were determined at baseline and reported as percent of cells converted to coated-platelets. Serum was obtained simultaneously for measurement of inflammatory markers using the Bio-Plex Pro Human Cytokine 27-plex Assay kit (Bio-Rad Laboratories). Rank order correlation between inflammatory marker concentrations and coated-platelet levels was determined using the Spearman correlation coefficient.
Results: Among 28 subjects followed for a mean of 28.6 ± 5.7 months, 9 developed progression of carotid stenosis severity. IL-17a concentration significantly correlated with coated-platelet levels (r = 0.68, p = 0.005). There was a trend toward a significant correlation between IL-17a and progression of carotid stenosis severity (r = 0.46, p = 0.08), which was no longer apparent after controlling for baseline coated-platelet level (r = 0.26, p = 0.37).
Conclusions: Coated-platelet levels correlate with IL-17a concentration among patients with carotid atherosclerosis. Produced by a subclass of T helper cells, IL-17a has been associated with plaque instability in previous human studies demonstrating increased expression of IL-17a mRNA in patients with symptomatic carotid plaques. These results, in combination with previous findings showing an association between coated-platelets and carotid stenosis progression, support a role for inflammation and coated-platelets in modulation of atherosclerotic plaque.
Author Disclosures: A.C. Kirkpatrick: Research Grant; Modest; AHA grant. A.S. Vincent: None. L. Guthery: None. N. Nguyen: None. C.I. Prodan: Research Grant; Modest; VA Merit grant. G.L. Dale: None.
This research has received full or partial funding support from the American Heart Association, SouthWest - Arkansas, Colorado, New Mexico, Oklahoma, Texas, Wyoming.
- © 2016 by American Heart Association, Inc.