Abstract 4511: Left Ventricular Diastolic Dysfunction Occurs Following Percutaneous ASD Closure: An Effect of Ventricular-Arterial Compliance Mismatch?

Abstract

Percutaneous ASD closure can result in hemodynamic compromise and pulmonary edema immediately after closure, particularly in older adults. We hypothesized that the percutaneous Amplatzer® septal occluder (ASO) device would influence LV diastolic function. Eighteen adult patients (6 male, 41±20 years) undergoing elective ASO device implantation for secundum ASD closure (Qp:Qs >1.5) under general anaesthetic had LV (18 patients) and RV (11 patients) conductance catheter assessment. Load dependent (time constant of diastolic relaxation (Tau)) and independent (end-diastolic pressure volume relationship (EDPVR), effective arterial elastance (Ea) and ventricular-arterial (V-A) coupling (Ees/Ea)) indices were measured before and after closure. Following closure of the ASD with an ASO device (8 –34mm), LV Tau increased (msec: 47.7(8.2) vs. 51.4(9.6), p<0.05) and there was a trend to increased LV EDPVR (1.1 (0.7) vs. 1.4 (1.1), p=0.19). The Ea increased significantly (mmHg/ml: 8.6 (5.8) vs. 10.8 (6.3), p=0.01) and V-A coupling deteriorated (Ees/Ea 0.61 (0.59) vs. 0.37 (0.18), p=0.09). RV hemodynamics remained constant. Percutaneous ASD closure causes an immediate deterioration in LV diastolic function, as a result of altered V-A coupling due to an increase in Ea. This could explain why patients develop pulmonary edema after ASD closure. Correcting Ea offers a potential therapeutic target to prevent diastolic dysfunction following ASO implantation.