Abstract

Lysophosphatidic acid (LPA), which is proposed to play an important role in normal physiological situations such as wound healing, vascular tone, vascular integrity and reproduction, may be involved in the etiology of some diseases such as atherosclerosis, cancer, obesity or myocardial infarction. Abnormal findings, including silent brain infarction (SBI), are frequently observed by magnetic resonance imaging (MRI) in patients with nonvalvular atrial fibrillation (NVAF). However, whether there is a relationship between LPA level and the prevalence of SBI has not been extensively studied. In the present study, the association between them was investigated. 235 patients with NVAF, 116 cases of SBI without NVAF and 120 cases of healthy volunteers (control group), who did not receive any antithrombotic therapy, were enrolled in this study. Plasma LPA levels in the NVAF with SBI group were significantly higher than that in the control group (p < 0.01), NVAF without SBI group (p < 0.01) and SBI without NVAF group (p < 0.01). The LPA levels are lower in the control group than in the NVAF without SBI and SBI without NVAF groups (p < 0.01), however, the latter two groups did not significantly differ from each other for LPA levels (p > 0.05) There were significant differences in the positive rate of platelet activation between each of the groups (p < 0.01). The positive rate of platelet activation was significantly higher in the NVAF with SBI group. We suggest that LPA might be a novel marker for estimation of the status of platelet activation and the risk factor for SBI onset in NVAF patients. We expected that plasma LPA levels could predict the occurrence of SBI in NVAF patients.

Highlights

  • Atrial fibrillation (AF) is the most common sustained arrhythmia and its incidence increases with age [1,2]

  • Our data indicate that the plasma lysophosphatidic acid (LPA) levels significantly increased in non-valvular atrial fibrillation (NVAF) or NVAF patients with silent brain infarction (SBI), which was accompanied by the high incidence of SBI

  • Based on the results presented here, we suggest that LPA might be a novel marker for estimation of the status of platelet activation and the risk factor for SBI onset in NVAF patients

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Summary

Introduction

Atrial fibrillation (AF) is the most common sustained arrhythmia and its incidence increases with age [1,2]. It seems important to explore the mechanism of emboli formation in non-valvular atrial fibrillation (NVAF) patients. Few studies have addressed the platelet activation state in patients with NVAF in vivo since there are few molecular markers which can effectively reflect the platelet activation in vivo [5]. Studies have found that lysophosphatidic acid (LPA), as a multifunctional “phospholipid messenger”, is mainly produced by activated platelets and may be an ideal molecular marker [6,7] reflecting platelet activation state in vivo. Platelets contribute to the production of LPA [8], which has been proposed to be a primary lipid in atherosclerotic plaque that is responsible for platelet activation [9]. Platelet depletion or treatment with anti-platelet agents reduces circulating LPA levels in animals [11,12]

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