Percutaneous atrial septal defect closure in patients with pulmonary arterial hypertension

IF 2.2 3区医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

Archives of Cardiovascular Diseases Pub Date : 2025-09-01 DOI:10.1016/j.acvd.2025.06.018

Annabel Sudaka , Estíbaliz Valdeolmillos , Grégoire Albenque , clement Batteux , Olivier Sitbon , Laurent Savale , David Montani , Sébastien Hascoët

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引用次数: 0

Abstract

Introduction

Transcatheter atrial septal defect (ASD) closure may be feasible in selected patients with pulmonary arterial hypertension (PAH) and elevated pulmonary vascular resistance (PVR > 5 Wood units, WU), particularly following PAH-specific therapy (PAHST) within a treat-and-repair strategy. This study aimed to evaluate clinical and hemodynamic outcomes of patients with PAH and persistent left-to-right shunting who underwent transcatheter ASD closure.

Method

We retrospectively analyzed 30 patients (77% female) with PAH—defined by mean pulmonary arterial pressure (mPAP) > 20 mmHg, PVR > 2 WU, and pulmonary arterial wedge pressure (PAWP) ≤ 15 mmHg—who underwent percutaneous ASD closure between 2008 and 2024.

Results

Median age at PAH diagnosis was 42 [30–54] years and 49 [36–58] years at ASD closure. At baseline, 60% of patients were in NYHA functional class III–IV. Eleven patients (37%) received pre-closure PAHST (monotherapy: n = 4; dual therapy: n = 6). All patients had left-to-right shunting without evidence of right-to-left flow. Median Qp/Qs was 2.0 [1.5–2.3] (range 1.2–3.0), median PVR 5.8 [4.1–6.3] WU (max 9.1), and median mPAP 39.0 [33.0–46.0] mmHg (max 56). Median ASD diameter was 28.0 [22.5–34.0] mm. No major adverse events were reported. Five patients initiated PAHST post-closure due to PAH risk factors (portal hypertension, BMPR2 mutation, family history of idiopathic PAH, or HIV).

Median follow-up was 6.0 [2.6–9.7] years. Right heart catheterization (RHC) was performed post-closure in 21 patients (70%). In this subgroup, mPAP and PVR significantly decreased (ΔmPAP–13.5 [–7.5 to–18.5] mmHg; ΔPVR–2.0 [–0.9 to–3.4] WU). PVR moderately increased in 4/21 patients (19%), including one aged over 50 at closure. Three patients without post-closure RHC died from unrelated causes.

Conclusion

This study supports transcatheter ASD closure as a safe and effective intervention in selected patients with moderate-to-severe PAH and persistent left-to-right shunting, offering durable hemodynamic and clinical improvement.

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肺动脉高压患者房间隔缺损的经皮闭合术

经导管房间隔缺损（ASD）关闭对于肺动脉高压（PAH）和肺血管阻力升高（PVR > 5 Wood units， WU）的特定患者可能是可行的，特别是在治疗和修复策略中进行PAH特异性治疗（PAHST）后。本研究旨在评估PAH和持续性左向右分流接受经导管ASD关闭的患者的临床和血流动力学结果。方法回顾性分析2008年至2024年间30例经皮ASD闭合术的pah患者（77%为女性），诊断标准为平均肺动脉压(mPAP)≤20mmhg, PVR≤2wu，肺动脉楔压(PAWP)≤15mmhg。结果PAH诊断时的中位年龄为42[30-54]岁，ASD闭合时的中位年龄为49[36-58]岁。基线时，60%的患者处于NYHA功能III-IV级。11例（37%）患者接受了闭合前PAHST治疗（单药治疗：n = 4；双药治疗：n = 6）。所有患者均有左至右分流，无右至左血流迹象。中位Qp/Qs为2.0[1.5-2.3]（范围1.2-3.0），中位PVR为5.8 [4.1-6.3]WU（最大9.1），中位mPAP为39.0 [33.0-46.0]mmHg（最大56）。中位ASD直径为28.0 [22.5-34.0]mm，无重大不良事件报道。5例患者由于PAH危险因素（门脉高压、BMPR2突变、特发性PAH家族史或HIV）而在闭锁后开始PAH。中位随访时间为6.0年[2.6-9.7]年。21例（70%）患者在闭锁后行右心导管（RHC）。在该亚组中，mPAP和PVR显著降低（ΔmPAP-13.5[-7.5至18.5]mmHg； ΔPVR-2.0[-0.9至3.4]WU）。4/21例（19%）患者PVR中度升高，包括1例闭合时年龄超过50岁。无关闭后RHC的3例患者死于无关原因。结论：本研究支持经导管ASD关闭作为一种安全有效的干预措施，用于中重度PAH和持续左向右分流的患者，提供持久的血流动力学和临床改善。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Archives of Cardiovascular Diseases 医学-心血管系统

CiteScore

4.40

自引率

6.70%

发文量

审稿时长

34 days

期刊介绍： The Journal publishes original peer-reviewed clinical and research articles, epidemiological studies, new methodological clinical approaches, review articles and editorials. Topics covered include coronary artery and valve diseases, interventional and pediatric cardiology, cardiovascular surgery, cardiomyopathy and heart failure, arrhythmias and stimulation, cardiovascular imaging, vascular medicine and hypertension, epidemiology and risk factors, and large multicenter studies. Archives of Cardiovascular Diseases also publishes abstracts of papers presented at the annual sessions of the Journées Européennes de la Société Française de Cardiologie and the guidelines edited by the French Society of Cardiology.