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Updated: May 6, 2026

Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model
Published on: September 3, 2020
Dynamic release and clearance of circulating microparticles during cardiac stress
Daniel Augustine1, Lisa V Ayers, Eduardo Lima
1From the Oxford Cardiovascular Clinical Research Facility, University of Oxford, Oxford, United Kingdom (D.A., E.L., L.N., A.J.L., E.F.D., P.L.); and Department of Clinical Immunology, Oxford University Hospitals NHS Trust, Oxford, United Kingdom (L.V.A., B.F.).
Rationale:
Microparticles are cell-derived membrane vesicles, relevant to a range of biological responses and known to be elevated in cardiovascular disease.
Objective:
To investigate microparticle release during cardiac stress and how this response differs in those with vascular disease.
Methods And Results:
We measured a comprehensive panel of circulating cell-derived microparticles by a standardized flow cytometric protocol in 119 patients referred for stress echocardiography. Procoagulant, platelet, erythrocyte, and endothelial but not leukocyte, granulocyte, or monocyte-derived microparticles were elevated immediately after a standardized dobutamine stress echocardiogram and decreased after 1 hour. Twenty-five patients developed stress-induced wall motion abnormalities suggestive of myocardial ischemia. They had similar baseline microparticle levels to those who did not develop ischemia, but, interestingly, their microparticle levels did not change during stress. Furthermore, no stress-induced increase was observed in those without inducible ischemia but with a history of vascular disease. Fourteen patients subsequently underwent coronary angiography. A microparticle rise during stress echocardiography had occurred only in those with normal coronary arteries.
Conclusions:
Procoagulant, platelet, erythrocyte, and endothelial microparticles are released during cardiac stress and then clear from the circulation during the next hour. This stress-induced rise seems to be a normal physiological response that is diminished in those with vascular disease.
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