三尖瓣小叶历来被认为是“被动瓣”。然而,我们最近表明,三尖瓣小叶在功能性三尖瓣反流的绵羊中活跃地重塑。我们假设这些重塑诱导的变化减少了小叶接合,因此,导致瓣膜功能障碍。为了测试这个,我们在人三尖瓣的逆向工程计算机模型中模拟了重塑引起的变化对瓣膜力学的影响。为此,我们结合了离体跳动心脏中记录的右心压和三尖瓣环动力学,与受试者匹配的瓣膜几何形状和材料特性的体外测量,建立特定主题的有限元模型。接下来,我们修改了环形几何形状和边界条件,以模拟肺动脉高压患者的变化.在这个模型中,然后,我们增加了小叶的厚度和刚度,并减少了小叶变硬的拉伸,我们称之为“过渡-λ”。“随后,我们量化了平均小叶应力,小叶收缩角,和接合面积作为阀门功能的量度。我们发现传单强调,小叶收缩角,接合面积对刚度的独立变化敏感,厚度,和过渡λ。当结合增厚时,加劲,以及转换λ的变化,我们发现前后小叶应力分别下降了26%和28%,分别。此外,收缩角增加了43%,接合面积减少了66%;从而阻碍了瓣膜的功能。虽然只是一项计算研究,我们提供了首次证据,证明重塑诱导的小叶增厚和硬化可能导致瓣膜功能障碍.有针对性地抑制患病瓣膜的这种变化可以恢复正常的瓣膜力学并促进小叶接合。
Tricuspid valve leaflets have historically been considered \"passive flaps\". However, we have recently shown that tricuspid leaflets actively remodel in sheep with functional tricuspid regurgitation. We hypothesize that these remodeling-induced changes reduce leaflet coaptation and, therefore, contribute to valvular dysfunction. To test this, we simulated the impact of remodeling-induced changes on valve mechanics in a reverse-engineered computer model of the human tricuspid valve. To this end, we combined right-heart pressures and tricuspid annular dynamics recorded in an ex vivo beating heart, with subject-matched in vitro measurements of valve geometry and material properties, to build a subject-specific finite element model. Next, we modified the annular geometry and boundary conditions to mimic changes seen in patients with pulmonary hypertension. In this model, we then increased leaflet thickness and stiffness and reduced the stretch at which leaflets stiffen, which we call \"transition-λ.\" Subsequently, we quantified mean leaflet stresses, leaflet systolic angles, and coaptation area as measures of valve function. We found that leaflet stresses, leaflet systolic angle, and coaptation area are sensitive to independent changes in stiffness, thickness, and transition-λ. When combining thickening, stiffening, and changes in transition-λ, we found that anterior and posterior leaflet stresses decreased by 26% and 28%, respectively. Furthermore, systolic angles increased by 43%, and coaptation area decreased by 66%; thereby impeding valve function. While only a computational study, we provide the first evidence that remodeling-induced leaflet thickening and stiffening may contribute to valvular dysfunction. Targeted suppression of such changes in diseased valves could restore normal valve mechanics and promote leaflet coaptation.