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. 2023 Sep;123(9):892-903.
doi: 10.1055/s-0043-57017. Epub 2023 Apr 19.

Platelet-Released Extracellular Vesicle Characteristics Differ in Chronic and in Acute Heart Disease

Affiliations

Platelet-Released Extracellular Vesicle Characteristics Differ in Chronic and in Acute Heart Disease

Alba Vilella-Figuerola et al. Thromb Haemost. 2023 Sep.

Abstract

Background: Extracellular vesicles (EVs), shed in response to cell activation, stress, or injury, are increased in the blood of patients with cardiovascular disease. EVs are characterized by expressing parental-cell antigens, allowing the determination of their cellular origin. Platelet-derived EVs (pEVs) are the most abundant in blood. Although not universally given, EVs generally express phosphatidylserine (PS) in their membrane.

Objectives: To investigate pEVs in chronic and acute conditions, such as chronic heart failure (CHF) and first-onset acute coronary syndrome (ACS), in patients treated as per guidelines.

Methods: EVs in CHF patients (n = 119), ACS patients (n = 58), their respective controls (non-CHF [n = 21] and non-ACS [n = 24], respectively), and a reference control group (n = 31) were characterized and quantified by flow cytometry, using monoclonal antibodies against platelet antigens, and annexin V (AV) to determine PS exposure.

Results: CHF patients had higher EVs-PS- numbers, while ACS had predominantly EVs-PS+. In contrast to ACS, CHF patients had significantly reduced numbers of pEVs carrying PECAM and αIIb-integrin epitopes (CD31+/AV+, CD41a+/AV+, and CD31+/CD41a+/AV+), while no differences were observed in P-selectin-rich pEVs (CD62P+/AV+) compared with controls. Additionally, background etiology of CHF (ischemic vs. nonischemic) or ACS type (ST-elevation myocardial infarction [STEMI] vs. non-STEMI [NSTEMI]) did not affect pEV levels.

Conclusion: PS exposure in EV and pEV-release differ between CHF and ACS patients, with tentatively different functional capacities beyond coagulation to inflammation and cross-talk with other cell types.

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Conflict of interest statement

L.B. declares to have acted as a SAB member of Sanofi, Novartis, Ionnis, and Pfizer, to have a Research Grant of AstraZeneca, to have received speaker fees of Sanofi, Novartis, and Bayer, and to have founded the Spin-offs Glycardial Diagnostics SL and Ivastatin Therapeutics S (all unrelated to this work). T.P. declares to be a co-founder of the Spin-offs Glycardial Diagnostics SL and Ivastatin Therapeutics S (all unrelated to this work). A.C. reports honoraria for lectures from AstraZeneca, Bristol-Myers Squibb, Ferrer, Boehringer Ingelheim, MSD, Novartis, Bristol-Myers Squibb, and AMGEN and to have received consulting fees from Novartis, AstraZeneca, Ferrer, and AMGEN. The remaining authors have nothing to disclose.

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