Platelet microvesicles are associated with the severity of coronary artery disease: comparison between peripheral and co
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Platelet microvesicles are associated with the severity of coronary artery disease: comparison between peripheral and coronary circulation E. Gkaliagkousi1 · E. Gavriilaki1 · E. Yiannaki2 · I. Vasileiadis3 · B. Nikolaidou1 · A. Lazaridis1 · P. Dolgyras1 · S. Grigoriadis4 · A. Triantafyllou1 · P. Anyfanti1 · D. Markala2 · I. Zarifis3 · S. Douma1 Accepted: 28 September 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Microvesicles (MVs) have recently emerged as markers of thrombosis. Furthermore, there is an unexplained residual thrombotic risk is observed in patients with acute coronary syndrome (ACS) and/or stable coronary artery disease (CAD), despite treatment. We measured platelet (PMVs) and erythrocyte (ErMVs) in patients with ACS and stable CAD, both in the peripheral and coronary circulation. We studied consecutive eligible patients during a coronary angiography. Blood samples were collected from the stem of the left coronary artery and femoral artery. PMVs were significantly increased in CAD patients compared to controls. ACS patients had also increased PMVs in coronary and peripheral circulation, compared to controls. Furthermore, ACS patients exhibited increased PMVs in coronary compared to peripheral circulation. Lastly, coronary PMVs were associated with the severity of CAD based on the SYNTAX score. No significant differences were observed in the levels of ErMVs among groups. Therefore, PMVs emerge as novel markers of thrombosis in CAD, further augmenting the vicious cycle of inflammation and thrombosis during ACS. Importantly, coronary PMVs may reflect the severity of CAD in this population. Keywords Microvesicles · Erythrocyte · Platelet · Coronary artery disease · Acute coronary syndrome
Introduction Circulating microvesicles (MVs) stem from the membrane of activated or apoptotic cells and are characterized by a diameter of 100–1000 nm and the type of cells they originate Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11239-020-02302-5) contains supplementary material, which is available to authorized users. * E. Gkaliagkousi [email protected] 1
3rd Department of Internal Medicine, Papageorgiou Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece
2
Hematology Laboratory, Theagenion Cancer Center, Thessaloniki, Greece
3
Cardiology Department, G Papanicolaou Hospital, Thessaloniki, Greece
4
Cardiology Department, General Hospital of Veria, Veria, Greece
from [1]. In cardiovascular health, MVs are produced in low numbers and contribute significantly to physiological homeostasis. By contrast, increased circulating MVs have been documented in hypertension, diabetes mellitus, dyslipidemia, heart failure and coronary artery disease (CAD) [2]. Platelet MVs (PMVs) promote expression of P-selectin, leucocyte-leucocyte interactions and monocyte infiltration in vulnerable sites of endothelial damage [3]. We have also recently shown that erythrocyte MVs (ErMVs) are significantly increased i
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