Key result
Platelet expression of FcγRIIa was similar in patients with ischemic stroke or TIA (11,332 molecules/platelet) compared to those with recent myocardial infarction (11,479 molecules/platelet).
Why the study?
Platelet FcgRIIa expression stratifies cardiovascular risk after MI, but its expression in patients with stroke and TIA compared with recent MI was unknown.
Observational (n=310)
Platelet FcγRIIa expression is similarly elevated in patients with ischemic stroke/TIA and recent MI, suggesting its potential utility as a biomarker for platelet reactivity across different ischemic cardiovascular events.
Answers are grounded in this paper and cite their sources.
Similar FcγRIIa expression supports risk stratification after stroke/TIA; extends prior post-MI findings to cerebrovascular events.
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.
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Schneider et al. (2022) conducted an observational in Ischemic stroke, TIA, and recent myocardial infarction (n=310). Ischemic stroke or TIA vs. Recent myocardial infarction was evaluated on Platelet expression of FcγRIIa (molecules of FcγRIIa/platelet). Platelet expression of FcγRIIa was similar in patients with ischemic stroke or TIA (11,332 molecules/platelet) compared to those with recent myocardial infarction (11,479 molecules/platelet).
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