Left atrial inflammation and platelet reactivity: a comparison of atrial arrhythmia and underlying substrate (#368)
Introduction: Atrial fibrillation (AF) is associated with increased risk of thromboembolic events, which occur as a consequence of left atrial thrombus formation. Rheumatic mitral disease is a potent substrate for AF. Inflammation and platelet hyperactivity are a key process involved in thrombus formation. This study investigated the left atrial specific inflammatory and platelet response in patients with AF and in a chronically remodelled substrate for AF (rheumatic mitral stenosis [MS])
Methods: This study involved 12 patients with AF (CHADS ≤ 1)undergoing catheter ablation, 19 patients with severe MS (no AF) undergoing balloon mitral valvuloplasty and 6 reference patients with supraventricular tachycardia (SVT) undergoing a electrophysiology study. Blood samples were collected from the left atria (LA) in all patients groups (start of procedure). Plasma levels of vascular cell (VCAM-1) and intracellular (I CAM-1) adhesion molecule were measured as markers of inflammation, with soluble CD40 Ligand (CD40L) measured as a marker for platelet reactivity. All were analysed by ELISA technique.
Results: Patients with AF had a significant increase in VCAM-1 and CD40L levels within the LA compared to SVT (p=0.005, 0.03). Furthermore, AF patients demonstrated a 2-fold increase in V CAM-1 from patients with rheumatic mitral stenosis ( p<0.001). There was no significant difference between rheumatic mitral stenosis and reference patients. A Similar pattern of results were obtained for ICAM-1, although there were not significant .
Conclusion: This data sugests that AF is associated with significant LA inflammation and platelet reactivity. This was significantly greater in the AF population than the underlying substrate.