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Microparticles in atrial fibrillation: a link between cell activation or apoptosis, tissue remodelling and

L Jesel¹, M Abbas, F Toti

¹Pôle d'activité médico-chirurgicale Cardiovasculaire, Nouvel Hôpital Civil, Université de Strasbourg, France; EA 7293, stress vasculaire et tissulaire en transplantation, Université de Strasbourg, France.

International Journal of Cardiology

|April 30, 2013

Abstract:

Microparticles (MPs) are small membrane vesicles that are shed from virtually all cells in response to stress. Widely described in atherothrombotic diseases, recent data suggest a role for circulating MPs in the hypercoagulable state associated with supraventricular tachyarrhythmia. During atrial fibrillation, several mechanisms, such as high ventricular heart rate, low or oscillatory shear stress, stretch, hypoxia, inflammation and oxidative stress, are potent inducers of apoptotic cell death, which leads to the shedding of procoagulant MPs within the vasculature. As key regulators of cell-cell cross-talk and important mediators of inflammatory, thrombogenic and proteolytic pathways, MPs directly or indirectly contribute to the amplification loops involved in atrial fibrillation. Because high levels of platelets and endothelial-derived MPs are identified during stroke and are associated with infarct size and clinical outcome, they are proposed to be a potent marker of ischaemic risk. During pulmonary vein isolation, the additional increases of platelet and leukocyte MP levels suggest the extent of tissue damage and reflect a transient activation of the coagulation cascade that could favour ischaemic stroke. Conversely, the observed decreases of several apoptotic markers some months after the restoration of sinus rhythm suggest that the extent of apoptotic processes is reversible and might enable restoration of haemostasis. In this review, we will summarise the current evidence supporting the roles of apoptosis and cell activation in the development of the prothrombotic state observed in atrial fibrillation, with a particular focus on procoagulant MPs.

Insights

Circulating microparticles (MPs) are shed during atrial fibrillation, contributing to a prothrombotic state and potentially indicating ischemic stroke risk. Reducing these apoptotic markers may restore normal blood clotting.

Area of Science:

Cardiovascular Medicine
Hematology
Cell Biology

Background:

Microparticles (MPs) are vesicles released by cells under stress, implicated in atherothrombotic diseases.
Circulating MPs are increasingly recognized for their role in the hypercoagulable state of supraventricular tachyarrhythmias like atrial fibrillation.

Purpose of the Study:

To review the evidence linking apoptosis and cell activation to the prothrombotic state in atrial fibrillation.
To focus on the role of procoagulant MPs in atrial fibrillation and their association with ischemic stroke risk.

Main Methods:

Literature review of studies investigating microparticle shedding and apoptosis in atrial fibrillation.
Analysis of mechanisms inducing MP release during atrial fibrillation, including shear stress, hypoxia, and inflammation.
Examination of the association between MP levels, stroke, and outcomes following pulmonary vein isolation.

Main Results:

Atrial fibrillation induces apoptotic cell death, leading to the release of procoagulant MPs that mediate inflammatory and thrombotic pathways.
Elevated platelet and endothelial MPs correlate with stroke severity and outcome, serving as potential markers of ischemic risk.
Pulmonary vein isolation transiently increases MP levels, indicating tissue damage and coagulation activation, while decreases post-procedure suggest reversibility.

Conclusions:

Apoptosis and cell activation, particularly through procoagulant MPs, are key drivers of the prothrombotic state in atrial fibrillation.
Circulating MPs represent a significant marker for assessing ischemic risk and monitoring treatment outcomes in atrial fibrillation patients.
The reversibility of apoptotic processes post-rhythm restoration highlights potential therapeutic targets for improving hemostasis.

Read full analysis

Keywords:

Endothelium Leukocytes Platelet Pulmonary vein isolation Stroke Thrombosis

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