Abstract
Purpose: Studies have shown that Atrial fibrillation (AF) associated with rheumatic mitral stenosis (MS) is not invariably linked to severity of stenosis. We hypothesized that continuing low-grade inflammation may be the causative factor for AF in rheumatic MS. Methods: 65 patients of severe rheumatic MS (Mitral Valve area of less than 1.0 cm2) were studied. Patients with acute rheumatic activity, an active infective process and more than mild involvement of other valves were excluded. Patients in normal sinus rhythm (NSR) were subjected to 24 hour holter analysis to detect paroxysmal AF. The patients were studied in three groups; NSR (group A), paroxysmal AF (group B), and permanent AF (group C). Level of inflammatory biomarkers hs-CRP, IL-6 and sCD-40L were measured in the three groups. Results: Mean age was 33.83±8.03 years. There were 24, 12 and 29 patients respectively in Groups A, B and C. 10 healthy volunteers served as controls. Levels of hs-CRP were elevated ≥6mg/dl in 2 patients (8.33%), 1 patient (8.33%) and 11 patients (37.93%) in groups A, B and C respectively and in none of the controls. CRP levels were significantly higher in group C as compared to group A (p=0.013). sCD-40 level was 2.23±1.732 ng/dl in normal population, while it was 3.90±2.64, 3.46±3.24 and 4.84±3.80ng/dl in group A, B and C respectively.(p=NS). IL-6 levels showed graded increase across the groups. Level in controls was 1.36±1.25 mg/dl, while group A, B and C had levels at 1.40±1.69, 2.97±5.76 and 5.41±7.48 mg/dl respectively. The difference was statistically significant between group A and C (p=0.005). Conclusion: Levels of hs-CRP and IL-6 were selectively elevated in patients of Rheumatic severe MS with AF as compared with those in NSR. This suggests that inflammation may play a role in the pathogenesis of AF in RHD independent of valve severity.
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