Foam Cells Analysis from Retrieved Stroke Clot for the Identification of Atherothrombotic Etiology

Author:

Giammello Fabrizio123ORCID,Ciacciarelli Antonio1ORCID,Cosenza Domenico4,Galletta Santi5,Barresi Valeria6ORCID,La Spina Paolino1,Fazio Maria Carolina1,De Caro Jolanda4,Cotroneo Masina1,Dell’Aera Cristina1,Grillo Francesco1,Ammendola Serena6,Tessitore Agostino7ORCID,Vinci Sergio Lucio7,Musolino Rosa Fortunata1,Casella Carmela1ORCID,Toscano Antonio1

Affiliation:

1. Stroke Unit, Department of Clinical and Experimental Medicine, University of Messina, 98124 Messina, Italy

2. Translational Molecular Medicine and Surgery, Department of Biomedical, Dental Science and Morphological and Functional Images, University of Messina, 98124 Messina, Italy

3. Neurology and Stroke Unit, Neuchâtel Hospital Network, 2000 Neuchâtel, Switzerland

4. Neurology Division, IRCCS Centro Neurolesi Bonino Pulejo, 98124 Messina, Italy

5. Service of Neurology and Neurorehabilitation, Neuchatel Hospital Network, 2000 Neuchâtel, Switzerland

6. Department of Diagnostics and Public Health, University of Verona, 37124 Verona, Italy

7. Neuroradiology Unit, Department of Biomedical Sciences and of Morphologic and Functional Images, University of Messina, 98124 Messina, Italy

Abstract

Background: In atherothrombotic acute ischemic stroke (AIS), when the atheroma breaks down, the clot can incorporate foam cells (FCs). The identification of the correct etiology is paramount for secondary stroke prevention. This study aims to evaluate the presence of the FC in the arterial clot, and to determine whether patients with FCs and patients without FCs (NFCs) had different cerebrovascular risk factors, haemato-chemical parameters, and atherosclerotic disease incidence, in order to predict the etiological diagnosis. Methods: We collected 100 clots retrieved by mechanical thrombectomy from 495 consecutive AIS patients with large vessel occlusion. An expert pathologist evaluated the FC presence by histological examination stained with hematoxylin and eosin. Results: We observed FCs in 29/100 (29%) of retrieved clots and divided the patients into two groups, with/without FCs. The two groups had similar clinical and laboratory features, with a discrepancy between the FC presence in the clot and the clinical etiological diagnosis, even if not statistically significant. Conclusions: Our study showed the presence of FCs in approximately one-third of the retrieved clots, but the identification of the clot that presumably comes from the atheromatous plaque rupture tended to disagree with the clinical diagnosis. Future studies may reveal their potential to disclose clot origin or specific patient characteristics, guiding treatment options.

Publisher

MDPI AG

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