Intrinsic Diastolic Function Determines Left Ventricular Volume Increment after Transcatheter Atrial Septal Defect Occlusion

Abstract

Background: Transcatheter atrial septal defect occlusion (ASO) results in increased end-diastolic and stroke volume of left ventricle (LV), thereby improving exercise capacity in the chronic phase. However, not all patients demonstrate LV volume dilation after ASO. The aim of this study is to assess the change of LV volume after ASO and the relationship between the diastolic LV function and the grade of LV volume expansion after ASO. Methods: Thirty-five patients (median, 19.2 years; range, 6.9–67.5) who underwent successful ASO and sequential LV volume analyses using real-time three-dimensional echocardiography were included in this study. LV volume and LV diastolic function were assessed at baseline, at 48 hours, and at 3 months after ASO. Serum concentrations of natriuretic peptides were measured simultaneously. Results: LV end-diastolic volume index was 40.8 (25.6–62.9) ml/m2 at baseline, 45.5 (26.1–72.5) (p<0.05) at 48 hours and 53.4 (36.9–70.9) at 3 months (p<0.001). Group#1 (n=18) included those with significant increase of LV volume after ASO at 48 hours, while Group#2 (n=17) included those without LV volume change. LV inflow-E/A was significantly lower and pulmonary venous-S/D was significantly higher in Group#2 (E/A: 1.9 (0.8-3.6); S/D: 1.2 (0.9-1.8)) than in Group#1 (E/A: 2.9 (1.4–4.3); S/D: 0.9 (0.7–1.3)), and this difference persisted in the chronic phase after ASO. Serum atrial natriuretic peptide at 48 hours was significantly higher in Group#2 (25.6 (12.0–54.0) pg/ml) than in Group#1 (18.1 (7.1–33.1)). These results suggest the acute response of LV volume is significantly influenced by the intrinsic LV diastolic function, and the significantly high serum atrial natriuretic peptide concentration in Group#2 at acute phase might be caused by the increased left atrial pressure after ASO due to relatively reduced diastolic function of LV in this group. Conclusion: Nearly half patients after ASO showed no LV expansion in the acute phase, and the intrinsic diastolic LV function determines the acute response in LV volume after ASO.