Background: Atrial fibrillation (AF) is a continued cardiac arrhythmia, which is
linked to a high risk thromboembolism. The association of AF and valvular heart
disease results in a substantial stroke and thromboembolic risk. AF is interrelated
with a hypercoagulable state and abnormalities of plasma indices of endothelial
damage/dysfunction such as circulating endothelial cells (CECs) and platelet
microparticles (PMPs), the levels of which are elevated in patients with coronary
artery disease (CAD), diabetes mellitus `and stroke, all of which are conditions that
lead to (AF). Thus, we hypothesized that the levels of CECs and PMPs would be
raised in rheumatic atrial fibrillation diseases. Methods: 60 patients with rheumatic
valvular diseases [(30 patients (35±12 years; 10 male and 20 females)] with
rheumatic mitral valve disease [(Mitral stenosis MS and Mitral regurgitation MR)]
and with normal sinus (RNAF) compared to [(30 patients (31±11 years; 11 male and
19 females)] with rheumatic valvular diseases with AF (RAF) and 20 healthy controls
HC (31±10 years; 17 male and 3 females). CECs were calculated using flow
cytometry after staining with mouse anti-human CD45 antibody (pan-leukocyte
marker), mouse anti-human CD 146 antibody (endothelial cell marker). PMPs were
distinguished 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 PMPs
compared to healthy controls HC (P<0.0001). CECs levels were significantly higher
in RAF diseases compared to patients with RNAF (P<0.05). RAF patients had
significantly higher levels of PMPs (p <0.001) compared to HC. Conclusion: Severe
endothelial damage, as assessed by increased numbers of CECs, not to be a
prominent trait of rheumatic valvular lesions in sinus rhythm patients, however levels
are definitely high in rheumatic valvular diseases with AF. There is evidence of
platelet activation in rheumatic AF patients, owing to original cardiovascular
diseases rather than the arrhythmia as such.