Transseptal Puncture and Thrombotic Risk

Introduction: Left atrial (LA) procedures are associated with a short term increase in thromboembolic events. The mechanisms underlying this phenomenon are unclear. It is plausible that transseptal puncture acts as a precipitating event inducing thrombus formation. Therefore this study investigated whether transseptal puncture acutely increases markers of thrombogenesis, endothelial function and inflammation. Methods: Patients undergoing radiofrequency ablation (n = 16, 41 ± 14 years) for left sided accessory pathway disease were studies. Blood samples were taken from the right atrium (RA) prior to transseptal puncture and the LA 10 minute after transseptal puncture, and before the administration of heparin. Platelet activation was assessed using whole blood flow cytometry (P-selectin [CD62P]) and ADP (5 μm) induced impedance aggregometry. Markers of thrombin generation (thrombin/anti-thrombin [TAT]), endothelial function (asymmetric dimethylarginine [ADMA]) and inflammation (intracellular adhesion molecule [ICAM-1] and vascular adhesion molecule [VCAM-1]), were measured by ELISA. Results: Following transseptal puncture there was no difference between the RA and LA for any measured variables (see table). Conclusion: This study shows that atrial platelet reactivity, thrombin generation, endothelial function and inflammation are not altered acutely by transseptal puncture alone. This data suggests that transseptal puncture its self does not contribute to the increased thrombotic risk. Further evaluation of primary disease process and theatre management need to be considered in the risk of thrombus formation.Tabled 1Right atriaLeft atriaP valueCD62P (%)20.2 ± 1027.5 ± 130.19Aggregation (Ohms)5.3 ± 2.05.1 ± 0.50.88TAT (μg/L)22.5 ± 10.723 ± 10.50.79ADMA (μmol/L)0.4 ± 0.90.4 ± 0.050.56I CAM-1 (mg/mL130 ± 80121 ± 760.79VCAM1 (mg/mL)389 ± 150386 ± 1900.96 Open table in a new tab