Why the study?
Do patients with mitral valve disease with or without atrial fibrillation have increased levels of circulating endothelial cells and platelet microparticles compared to healthy controls?
Do patients with mitral valve disease with or without atrial fibrillation have increased levels of circulating endothelial cells and platelet microparticles compared to healthy controls?
Mitral valve disease is associated with excess platelet activation regardless of atrial fibrillation, while endothelial damage is further exacerbated by the presence of atrial fibrillation.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for endothelial and platelet roles in MVD ± AF; leaves open prognostic value and therapeutic implications.
Hypercoagulability in mitral valve disease (MVD), a cause of atrial fibrillation (AF) and stroke, is potentially due to endothelial damage/dysfunction (marked by circulating endothelial cells [CECs]), platelet activation (soluble P-selectin [sPsel], platelet microparticles [PMPs], and soluble CD40 [sCD40]), and oxidized low-density lipoprotein (oxLDL) cholesterol. We measured these variables in 24 patients with MVD as well as in 21 with MVD + AF and compared them with 20 healthy controls (HCs). The CECs and PMPs were measured by flow cytometry; sPsel, oxLDL, and CD40 by enzyme-linked immunosorbent assay. Compared with HCs, sPsel and PMPs were equally higher in MVD and MVD + AF; sCD40 and oxLDL were higher in MVD + AF than in HCs and MVD; and CECs were higher in MVD than in the HCs, with further increases in MVD + AF (all P < .001). We conclude that excess platelet activation is present in MVD regardless of AF, and that increased endothelial damage in MVD is greater when compounded by AF.
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Idriss et al. (2014) studied this question.
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