Garcia M J, Vandervoort P, Stewart W J, Lytle B W, Cosgrove D M, Thomas J D, Griffin B P
Department of Cardiology, Cleveland Clinic Foundation, Ohio 44195, USA.
J Am Coll Cardiol. 1996 Feb;27(2):399-406. doi: 10.1016/0735-1097(95)00403-3.
The aims of this study were to define the hydrodynamic mechanisms involved in the occurrence of hemolysis in prosthetic mitral valve regurgitation and to reproduce them in a numeric simulation model in order to estimate peak shear stress.
Although in vitro studies have demonstrated that shear stresses > 3,000 dynes/cm2 are associated with significant erythrocyte destruction, it is not known whether these values can occur in vivo in conditions of abnormal prosthetic regurgitant flow.
We studied 27 patients undergoing reoperation for significant mitral prosthetic regurgitation, 16 with and 11 without hemolysis. We classified the origin and geometry of the regurgitant jets by using transesophageal echocardiography. By using the physical and morphologic characteristics defined, several hydrodynamic patterns were simulated numerically to determine shear rates.
Eight (50%) of the 16 patients with hemolysis had paravalvular leaks and the other 8 had a jet with central origin, in contrast to 2 (18%) and 9 (82%), respectively, of the 11 patients without hemolysis (p = 0.12, power 0.38). Patients with hemolysis had patterns of flow fragmentation (n = 2), collision (n = 11) or rapid acceleration (n = 3), whereas those without hemolysis had either free jets (n = 7) or slow deceleration (n = 4) (p < 0.001, power 0.99). Numeric simulation demonstrated peak shear rates of 6,000, 4,500, 4,500, 925 and 950 dynes/cm2 in these five models, respectively.
The distinct patterns of regurgitant flow seen in these patients with mitral prosthetic hemolysis were associated with rapid acceleration and deceleration or high peak shear rates, or both. The nature of the flow disturbance produced by the prosthetic regurgitant lesion and the resultant increase in shear stress are more important than the site of origin of the flow disturbance in producing clinical hemolysis.
本研究旨在确定人工二尖瓣反流时溶血发生所涉及的流体动力学机制，并在数值模拟模型中再现这些机制，以估计峰值剪切应力。
尽管体外研究表明，剪切应力>3000达因/平方厘米与显著的红细胞破坏有关，但尚不清楚在人工瓣膜反流异常的情况下，这些值是否会在体内出现。
我们研究了27例因严重人工二尖瓣反流而接受再次手术的患者，其中16例有溶血，11例无溶血。我们使用经食管超声心动图对反流束的起源和几何形状进行分类。根据所定义的物理和形态学特征，对几种流体动力学模式进行数值模拟以确定剪切速率。
16例有溶血的患者中，8例（50%）存在瓣周漏，另外8例反流束起源于中心，而11例无溶血的患者中分别为2例（18%）和9例（82%）（p = 0.12，检验效能0.38）。有溶血的患者存在血流破碎模式（n = 2）、碰撞模式（n = 11）或快速加速模式（n = 3），而无溶血的患者则为自由射流（n = 7）或缓慢减速（n = 4）（p < 0.001，检验效能0.99）。数值模拟显示，这五个模型中的峰值剪切速率分别为6000、4500、4500、925和950达因/平方厘米。
这些人工二尖瓣溶血患者中观察到的不同反流模式与快速加速和减速或高峰值剪切速率，或两者均有关。人工瓣膜反流病变产生的血流紊乱的性质以及由此导致的剪切应力增加，在产生临床溶血方面比血流紊乱的起源部位更为重要。
