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Mechanism of valve failure and efficacy of reintervention through catheterization in patients with bioprosthetic valves in the pulmonary position

机译:肺位置生物人工瓣膜患者的瓣膜衰竭机制和通过导管再介入的有效性

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Background: Surgical and transcatheter bioprosthetic valves (BPVs) in the pulmonary position in patients with congenital heart disease may ultimately fail and undergo transcatheter reintervention. Angiographic assessment of the mechanism of BPV failure has not been previously described. Aims: The aim of this study was to determine the mode of BPV failure (stenosis/regurgitation) requiring transcatheter reintervention and to describe the angiographic characteristics of the failed BPVs and report the types and efficacy of reinterventions. Materials and Methods: This is a retrospective single-center review of consecutive patients who previously underwent pulmonary BPV placement (surgical or transcatheter) and subsequently underwent percutaneous reintervention from 2005 to 2014. Results: Fifty-five patients with surgical (41) and transcutaneous pulmonary valve (TPV) (14) implantation of BPVs underwent 66 catheter reinterventions. The surgically implanted valves underwent fifty reinterventions for indications including 16 for stenosis, seven for regurgitation, and 27 for both, predominantly associated with leaflet immobility, calcification, and thickening. Among TPVs, pulmonary stenosis (PS) was the exclusive failure mode, mainly due to loss of stent integrity (10) and endocarditis (4). Following reintervention, there was a reduction of right ventricular outflow tract gradient from 43 ± 16 mmHg to 16 ± 10 mmHg ( P < 0.001) and RVp/AO ratio from 0.8 ± 0.2 to 0.5 ± 0.2 ( P < 0.001). Reintervention with TPV placement was performed in 45 (82%) patients (34 surgical, 11 transcatheter) with no significant postintervention regurgitation or paravalvular leak. Conclusion: Failing surgically implanted BPVs demonstrate leaflet calcification, thickness, and immobility leading to PS and/or regurgitation while the mechanism of TPV failure in the short- to mid-term is stenosis, mainly from loss of stent integrity. This can be effectively treated with a catheter-based approach, predominantly with the valve-in-valve technique.
机译:背景:先天性心脏病患者在肺部位置的手术和经导管生物人工瓣膜(BPV)最终可能会失败并进行经导管再干预。先前没有描述BPV失败机制的血管造影评估。目的:本研究的目的是确定需要经导管再介入的BPV失败(狭窄/反流)的模式,并描述失败的BPV的血管造影特征,并报告再介入的类型和疗效。材料和方法:这是一项回顾性单中心回顾性研究,对先前曾接受过肺BPV放置(手术或经导管)并随后于2005年至2014年进行经皮再次介入治疗的连续患者进行了回顾性研究。结果:55例接受手术(41)和经皮肺部治疗的患者对BPV的瓣膜(TPV)(14)植入进行了66次导管再干预。手术植入的瓣膜进行了五十次再手术以适应症,其中包括16例狭窄,7例反流和27例两者,主要与小叶固定,钙化和增厚有关。在TPV中,肺动脉狭窄(PS)是唯一的失败模式,主要是由于支架完整性的丧失(10)和心内膜炎(4)。再次干预后,右心室流出道梯度从43±16 mmHg降低到16±10 mmHg(P <0.001),RVp / AO比从0.8±0.2降低到0.5±0.2(P <0.001)。 45例(82%)患者(34例外科手术,11例经导管)无冠状动脉介入术后返流或瓣膜旁渗漏,进行了TPV植入再干预。结论:未通过手术植入的BPV表现出小叶钙化,厚度和固定性不足,导致PS和/或反流,而中短期内TPV失败的机制是狭窄,主要是由于支架完整性的丧失。这可以通过基于导管的方法(主要是瓣膜瓣技术)有效地进行治疗。

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