Pawelec-Wojtalik Małgorzata, Nozyński Jerzy, Wojtalik Michał, Piaszczyński Maciej, Surmacz Rafał, Bukowska Dorota, Mrówczyński Wojciech
Department of Pediatric Radiology, University of Medical Sciences, Poznań, Poland.
Eur J Cardiothorac Surg. 2006 Jul;30(1):4-9. doi: 10.1016/j.ejcts.2006.03.065. Epub 2006 May 24.
Despite the progress made in the development of valved stents for trans-apical valve replacement, a reliable closure of the access orifice remains a major issue. The present study was designed to evaluate if device closure of the ventricular wall is safe.
Transventricular access for pulmonary valve replacement was simulated with a 26F sheath and the resulting orifice was closed with an Amplatzer Muscular VSD Occluder (AMuscVSDO) in chronic sheep experiments (body weight 45-48 kg). Mean procedure time, blood loss, and standard hemo-dynamics were recorded. The animals were sacrificed electively and the histopathological changes in and around AMuscVSDO in the right ventricular wall were systematically studied by semi-quantitative analysis of collagenisation, inflammatory response and 'resorptive' process.
Mean procedure time was 31+/-10.7 min, blood loss was 22.5+/-8.7 ml, heart rate was 123+/-22.6 bits/min before and 128+/-28.7 bits/min after, mean arterial blood pressure was 88+/-16.7 mm Hg before and 82.6+/-18.3 mm Hg after the procedure. Mean survival was 5.3 weeks. The collagen and scar formation studies revealed three different periods: (1) initial fibrosis (0-3 weeks); (2) so-called 'capsulation' (3-9 weeks after the implantation of the Occluder); and (3) final remodelling and differentiation (9 weeks). The fabric inside the Occluder played the role of a collagenisation promoter, active from the 3rd week till it vanishes. Inflammation plays a role as a temporary reaction (0-3 weeks) during the healing process, with no signs of any active, focal or circumscribed, myocardial damage.
(1) The closure of the free ventricular wall perforation with AMuscVSDO is safe due to the scar tissue resulting from the healing process around and in the device. (2) The myocardial healing around and inside an implanted AMuscVSDO represents two processes: extensive fibrosis ensues around metallic wires with the progression towards the inside of the myocardium, whereas inside AMuscVSDO the loose connective tissue fills the myocardial lesion. During cicatrisation, the fabric elements of AMuscVSDO act as the ground for collagen formation and fibroblast proliferation. (3) The cicatrisation processes after ventricular AMuscVSDO implantation show remodelling, with rearrangement of collagen fibres architecture and distribution.
尽管经心尖瓣膜置换的带瓣支架研发取得了进展，但可靠地封闭穿刺孔仍是一个主要问题。本研究旨在评估心室壁的器械封闭是否安全。
在慢性绵羊实验（体重45 - 48千克）中，用26F鞘模拟经心室途径进行肺动脉瓣置换，并用Amplatzer肌部室间隔缺损封堵器（AMuscVSDO）封闭由此产生的穿刺孔。记录平均手术时间、失血量和标准血流动力学参数。选择性处死动物，通过对胶原化、炎症反应和“吸收”过程的半定量分析，系统研究右心室壁中及周围AMuscVSDO的组织病理学变化。
平均手术时间为31±10.7分钟，失血量为22.5±8.7毫升，术前心率为123±22.6次/分钟，术后为128±28.7次/分钟，术前平均动脉血压为88±16.7毫米汞柱，术后为82.6±18.3毫米汞柱。平均生存期为5.3周。胶原和瘢痕形成研究显示出三个不同阶段：（1）初始纤维化（0 - 3周）；（2）所谓的“包囊形成”（封堵器植入后3 - 9周）；（3）最终重塑和分化（9周）。封堵器内部的织物起到胶原化促进剂的作用，从第3周起直至消失一直发挥作用。炎症在愈合过程中作为一种暂时反应（0 - 3周）起作用，没有任何活动性、局灶性或局限性心肌损伤的迹象。
（1）用AMuscVSDO封闭心室游离壁穿孔是安全的，这归因于器械周围及内部愈合过程产生的瘢痕组织。（2）植入的AMuscVSDO周围及内部的心肌愈合代表两个过程：金属丝周围会发生广泛纤维化，并向心肌内部发展，而在AMuscVSDO内部，疏松结缔组织填充心肌病变处。在瘢痕形成过程中，AMuscVSDO的织物成分充当胶原形成和成纤维细胞增殖的基础。（3）心室植入AMuscVSDO后的瘢痕形成过程显示出重塑，胶原纤维结构和分布重新排列。
