Invasive filling pressures, not defect size, predict heart failure after asd closure

Background Transcatheter atrial septal defect (ASD) closure improves right heart remodeling and symptoms. However, a clinically relevant subset of patients develops heart failure–related symptoms after closure. The mechanisms underlying this heterogeneous response remain poorly defined. Purpose To determine whether pre-closure invasive hemodynamic load, rather than anatomical defect characteristics, predicts heart failure–related clinical response after ASD closure. Methods We retrospectively analyzed 220 consecutive patients undergoing transcatheter ASD closure between 2014 and 2025 at a tertiary referral center. Heart failure–related adverse response (HF adverse) was defined as post-procedural dyspnea and/or initiation of diuretic therapy. Baseline evaluation included invasive right heart catheterization parameters (mean pulmonary artery pressure [mPAP], pulmonary capillary wedge pressure [PCWP], pulmonary vascular resistance, Qp/Qs), NT-proBNP, and clinical variables. Clinical response was categorized as neutral, improved, or HF adverse. Multivariable logistic regression included age, PCWP, mPAP, and ln(NT-proBNP), with sensitivity adjustment for chronic kidney disease. Results Among 220 patients (median age 56 years [IQR 38–71]; 60% female), HF adverse occurred in 28 patients (12.7%). Anatomical parameters including ASD diameter, device size, and shunt ratio (Qp/Qs) showed no association with HF adverse. In contrast, pre-closure filling pressures demonstrated a clear stepwise gradient across response groups. Median PCWP was 8 mmHg in the neutral group, 9 mmHg in the improved group, and 12 mmHg in the HF adverse group (p<0.001). Median mPAP was 16, 18, and 24 mmHg, respectively (p<0.001). In multivariable analysis, age (OR 1.05 per year, 95% CI 1.01–1.10, p=0.021), PCWP (OR 1.19 per mmHg, 95% CI 1.01–1.41, p=0.040), and mPAP (OR 1.11 per mmHg, 95% CI 1.02–1.21, p=0.020) independently predicted HF adverse, whereas baseline NT-proBNP was not significant. Results remained consistent after adjustment for chronic kidney disease. The discriminative ability of PCWP for HF adverse was moderate (AUC 0.73), and risk increased progressively with combined elevation of PCWP and mPAP. Notably, pulmonary vascular resistance was not independently associated with HF adverse, underscoring the predominant role of filling pressures. Conclusion Clinical response after ASD closure appears to be pressure-driven rather than anatomy-driven. Pre-closure invasive filling pressure assessment may refine patient selection and identify individuals at increased risk of post-closure heart failure–related intolerance. These findings support consideration of pre-closure invasive hemodynamic assessment in selected patients.