Platelet FcγRIIa Expression in Ischemic Stroke: A Marker of Increased Platelet Reactivity

Author:

Schneider David J.1ORCID,Honda Tristan2,Feldmann Edward3,de Havenon Adam4,Romano Jose G.5,Nogueira Raul G.6,Prabhakaran Shyam7,Mishra Nishant K.8,Beaman Charles B.2,Hinman Jason2,Commichau Christopher S.1,Callas Peter1,Kaneko Naoki2,Morales Jose M.2,Patel Smit D.2,Sharma Latisha K.2,Kim Song Julia2,Taatjes‐Sommer Heidi S.1,Liebeskind David S.2

Affiliation:

1. Departments of Medicine Neurology, and Mathematics and Statistics The University of Vermont Burlington VT

2. Departments of Neurology and Radiology UCLA Los Angeles CA

3. Department of Neurology University of Massachusetts Springfield MA

4. Department of Neurology University of Utah Salt Lake UT

5. Department of Neurology University of Miami Miami FL

6. Department of Neurology Emory University Atlanta GA

7. Department of Neurology University of Chicago Chicago IL

8. Department of Neurology Yale University New Haven CT

Abstract

Background Platelet FcγRIIa amplifies platelet activation and, thus, increased expression identifies patients with increased platelet reactivity. Previous work has demonstrated that platelet FcγRIIa can identify patients at high and low risk of subsequent cardiovascular events after myocardial infarction (MI). This study was designed to compare platelet expression of FcγRIIa in patients with stroke and transient ischemic attack (TIA) with that in patients with a recent MI. Methods Patients were enrolled based on an admitting diagnosis of stroke/TIA, and the discharge diagnosis was used to categorize patients into stroke/TIA (n=99) and other causes of neurologic dysfunction (hemorrhagic, trauma, toxic, and seizure; n=14). Patients with stroke/TIA were divided into embolic (both cardioembolic and thromboembolic; n=32) and not embolic causes (n=67). Results were compared with platelet FcγRIIa expression in patients with recent MI from a previous study (n=197). Platelet expression of FcγRIIa (molecules of FcγRIIa/platelet) was quantified with the use of flow cytometry. Results are mean±SD. Results Platelet expression of FcγRIIa was similar in patients with ischemic (both embolic and nonembolic) stroke/TIA (11 332±4127), embolic (11 204±3889) and nonembolic (11 393±4263) causes, and MI (11 479±2405). Patients with other causes of neurologic dysfunction had modestly but not significantly lower platelet expression of FcγRIIa (9389±2883; P =0.13). Conclusions Platelet expression of FcγRIIa was similar in patients with stroke/TIA and recent MI. These results support future studies designed to determine whether platelet FcγRIIa expression can discriminate risk of subsequent stroke/TIA and its potential use as a precision tool capable of guiding individualized treatment decisions.

Publisher

Ovid Technologies (Wolters Kluwer Health)

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