自体组织重建心脏瓣膜。

C P Bailey, J Zimmerman, T T Hirose, F S Folk, A A Bakst
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引用次数: 1

摘要

对二尖瓣疾病患者进行组织重建的长期和广泛的经验,以及对耳廓病变的不那么广泛的经验,使我们确信所提出的重建技术的优越性,以及阔筋膜比迄今为止尝试的所有其他组织更可取。尽管每次线性测量的早期收缩幅度约为30%,但对几年后(超过5年)从重建瓣膜中移除的阔筋膜的后期研究表明,没有细胞的损失,也没有可测量的组织强度或柔韧性的损失。在我们的狒狒中没有观察到晚期钙化,尽管它在狗身上似乎是一致的发展。到目前为止,只有一位患者(四年后)出现了这种情况。现在相信,我们可以为许多年轻患者提供接近真正“治愈”的长期临床益处,否则他们将别无选择,只能求助于假肢姑息治疗。最近,Willen, Dubiel和Johansson (50,51), Gersbach和Wegmann (52), Senning和Rothlin(53)证明,植入心血管腔内的筋膜表面纤维蛋白的重复沉积会导致结缔组织(瘢痕)的进行性包裹。在手术后的一段时间内,大约10年而不是5年,筋膜变性发生,可能是由于有组织的渗出物“扼杀”,从而中断了基于流动血液扩散的“正常”营养机制。Sullivan, Harken和Gorlin (54), Weily和Genton(55),以及Harker和Slicter(56)最近对血小板在启动这种纤维沉积中的作用的理解,为我们提供了一种预防阔筋膜瓣膜晚期变性的方法。常规治疗剂量的血小板分散剂(阿司匹林、泊桑丁或吲哚酚)似乎具有完全的保护作用。毫无疑问,抗凝治疗同样有效。然而,在植入人工心脏瓣膜后,永久维持适当的“抗凝”水平通常被认为是必要的,这对患者来说是一种沉重的心理和生理负担。许多这样的人生活在血栓栓塞的危险和出血的危险之间。血栓栓塞实际上只代表了在初始血小板聚集和沉积后纤维蛋白蓄积准备程度谱上的一个更远的点。由于明显的血栓栓塞似乎“永远不会”在心内阔筋膜植入后发生,因此在这种情况下,血小板分散治疗似乎就足够了。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Reconstruction of the cardiac valves with autologous tissue.

A rather long and extensive experience with tissue reconstruction in patients with mitral valve disease, and a much less extensive one with oartic lesions, has convinced us of the superiority of the presented techniques of reconstruction, and of the preferability of fascia lata over all other tissues so far tried for this purpose. Despite an early increment of shrinkage of the order of about 30% of each linear measurement, late studies of fascia lata removed from reconstructed valves after several years (over five) indicate no loss of cellularity and no measurable loss of tissue strength or flexibility. Late calcification was not observed in any of our baboons, although it appears to be a consistent development in dogs. It has been seen in only one patient (after four years) to date. It is now believed that we can offer prolonged clinical benefit approaching actural "cure" to many of the younger patients who otherwise would have no recourse but to prosthetic palliation. It is true that recently Willen, Dubiel and Johansson (50, 51), Gersbach and Wegmann (52), and Senning and Rothlin (53) have demonstrated that repetitive deposits of fibrin upon the surfaces of fascia lata implanted within the cardiovascular chambers lead to progressive encapsulation with organizing connective tissue (scar). At some time period following surgery, closer to 10 years than to 5, degeneration of the fascia takes place, presumably due to "strangulation" by the organized exudate which interrupts the "normal" mechanism of its nutrition which is based upon diffusion from the flowing blood. The recent contributions of Sullivan, Harken and Gorlin (54), Weily and Genton (55), and Harker and Slicter (56) to our understanding of the role of the platelets in initiating such fibrinous deposition now provide us with a way to prevent such late degeneration of valves made of fascia lata. The regular administration of platelet dispersing agents (aspirin, Persantin, or inderol) in ordinary therapeutic dosage would seem to be completely protective. Undoubtedly, anticoagulant therapy would be equally effective. However, the permanent maintenance of a proper level of "anti-coagulation" such as is usually deemed necessary following implantation of a prosthetic heart valve is a heavy psychological and biological burden for a patient to bear. Many such individuals live precariously between the risks of thromboembolism and the risks of hemorrhage. Thromboembolism really only represents a farther point along the spectrum of the readiness of fibrin accumulation following initial platelet aggregation and deposition. Since frank thromboembolism appears "never" to follow intracardiac implantation of fascia lata, it would seem that platelet dispersive therapy sould suffice in such cases.

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