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Reveals elevated circulating endothelial cells and platelet microparticles in rheumatic mitral disease with atrial fibrillation, indicating endothelial injury and hypercoagulability.
Background: Atrial fibrillation (AF) is a continued cardiac arrhythmia, which islinked to a high risk thromboembolism. The association of AF and valvular heartdisease results in a substantial stroke and thromboembolic risk. AF is interrelatedwith a hypercoagulable state and abnormalities of plasma indices of endothelialdamage/dysfunction such as circulating endothelial cells (CECs) and plateletmicroparticles (PMPs), the levels of which are elevated in patients with coronaryartery disease (CAD), diabetes mellitus `and stroke, all of which are conditions thatlead to (AF). Thus, we hypothesized that the levels of CECs and PMPs would beraised in rheumatic atrial fibrillation diseases. Methods: 60 patients with rheumaticvalvular diseases [(30 patients (35±12 years; 10 male and 20 females)] withrheumatic mitral valve disease [(Mitral stenosis MS and Mitral regurgitation MR)]and with normal sinus (RNAF) compared to [(30 patients (31±11 years; 11 male and19 females)] with rheumatic valvular diseases with AF (RAF) and 20 healthy controlsHC (31±10 years; 17 male and 3 females). CECs were calculated using flowcytometry after staining with mouse anti-human CD45 antibody (pan-leukocytemarker), mouse anti-human CD 146 antibody (endothelial cell marker). PMPs weredistinguished from non-platelet events by their fluorescence from Fluorescein 6-isothiocyanate (FITC) conjugated anti-CD41a bound to the particle surfaces.Results: RAF patients had significantly elevated numbers of CECs and PMPscompared to healthy controls HC (P<0.0001). CECs levels were significantly higherin RAF diseases compared to patients with RNAF (P<0.05). RAF patients hadsignificantly higher levels of PMPs (p <0.001) compared to HC. Conclusion: Severeendothelial damage, as assessed by increased numbers of CECs, not to be aprominent trait of rheumatic valvular lesions in sinus rhythm patients, however levelsare definitely high in rheumatic valvular diseases with AF. There is evidence ofplatelet activation in rheumatic AF patients, owing to original cardiovasculardiseases rather than the arrhythmia as such.
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Idriss et al. (2012) studied this question.
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