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Atrial fibrillation (AF) is the most common arrhythmia in clinical, but the pathophysiological mechanism of AF remains largely unknown. Recently, an accumulating body of evidence suggests a link between inflammation and AF. CD 11b is an important marker of leukocytes activation and also plays a critical role in the inflammation by promoting the adhesion and infiltration of leukocytes. But to our knowledge, there is little information available about the expression of CD 11b on peripheral monocytes and granulocytes in patients with AF and the affection of ACE inhibitors/ARBs therapy on the activation of leukocytes.
Eighty-five AF patients (43 paroxysmal AF patients and 42 persistent AF patients), age ranging from 34 to 80 years old, who planned to catheter ablation from February 2014 to September 2015 were enrolled in this study. Another 57 age- and gender-matched control subjects were also recruited from outpatients attending cardiology clinics. Flow-cytometric quantification analysis was done to determine the expression of CD11b on peripheral monocytes (MC-DC11b) and granulocytes (GC-DC11b).
Compared with that in the control sinus group, the expression of CD 11b on monocytes in the AF patients was increased almost two-fold (37.1±1.0 vs. 24.1±5.3 MFI, p<0.001). For another leukocyte activation marker, there were also significant increase in the expression of CD 11b on granulocytes in AF patients compared with control sinus group (35.6±3.2 vs. 27.1±5.5 MFI, p<0.001). Plasma hs-CRP were significantly up-regulated in AF patients compared with control sinus individuals [2.45 (1.19-3.71) vs. 1.31 (0.75-2.49) mg/L, p<0.001]. In subgroup analysis of AF patients, CD11b on peripheral monocytes were decreased significantly in ACEI/ARBs therapy group than no-ACEI/ARBs therapy group (26.9±2.3 vs. 40.3±8.1 MFI, p<0.001). CD 11b on granulocytes were also significantly decreased following ACEI/ARB therapy when compared with that in AF patients without ACEI/ARB therapy (27.6±2.3 vs. 43.1±8.3 MFI, p=0.001). The plasma hs-CRP were significantly down-regulated in AF patients in ACEI/ARB therapy group compared with AF patients with non-ACEI/ARB therapy group [1.91 (1.08-3.39) vs. 3.23 (1.12-4.26) mg/L, p=0.034]. For correlation analysis in AF patients, MC-CD11b, GC-CD11b and hs-CRP levels were all correlated with left atrial diameter (r=0.649, r=0.646 and r=0.680, respectively, all p < 0.01).
Peripheral leukocytes are activated with upregulation of CD11b expression in AF patients and ACEI/ARBs therapy may play an anti-inflammation role by decrease the expression of CD11b on peripheral leukocytes.