Myofiber organization in the failing systemic right ventricle
Myofiber organization in the failing systemic right ventricle
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DOI：
10.1186/s12968-020-00637-9
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发表时间：
2020-06-29
影响因子：
6.4
通讯作者：
Sanders, Stephen P.
中科院分区：
文献类型：
--
作者：
Campanale, Cosimo M.;Scherrer, Benoit;Sanders, Stephen P.
背景：右室(RV)在作为体脑室功能时经常发生故障，但其原因尚不清楚。我们验证了肌纤维组织在衰竭的全身性右心室中异常的假设。方法应用弥散加权心血管磁共振成像技术，对3例年轻系统性RV患者的衰竭心脏和1例结构正常的后天获得性RV肥厚患者进行对比研究。扩散室成像被计算来分离代表自由水的自由扩散分量和表征肌纤维取向和扩散特性的各向异性分量。各向异性隔室的方位以字形格式显示，并用于肌纤维的定性描述和肌束图的构建。计算5个位置的室壁螺旋角度，并以图形方式显示。比较了不同样品的标量参数(分数各向异性和平均扩散系数)。结果肥厚的全身性RV有一内层，约2/3的壁由肥厚的小梁和一层心外膜环周肌纤维组成。较小的小梁内的肌纤维以平行的纤维排列和组织，而较大的复合束表现出明显的无序，主要是在成分小梁之间。我们观察到外壁致密部分的螺旋角范围很小，与排列的、大致为周向的纤维一致。但内侧骨小梁部螺旋角度有明显变化，与纤维取向的明显变化一致。心尖的旋涡被破坏或不完整，我们在其他位置观察到心肌旋涡或旋涡。与结构正常的心脏相比，异常心脏的各向异性分数较低，而平均弥散率的变化更大，有2颗心脏的各向异性分数高于正常心脏，但有1颗心脏的平均弥散系数较低。结论在衰竭的全身性RV中，肌纤维结构异常，可能是心力衰竭和心律失常的重要底物。目前尚不清楚肌纤维紊乱是由于血流动力学因素、发育问题，还是两者兼而有之。
Background The right ventricle (RV) often fails when functioning as the systemic ventricle, but the cause is not understood. We tested the hypothesis that myofiber organization is abnormal in the failing systemic right ventricle. Methods We used diffusion-weighted cardiovascular magnetic resonance imaging to examine 3 failing hearts explanted from young patients with a systemic RV and one structurally normal heart with postnatally acquired RV hypertrophy for comparison. Diffusion compartment imaging was computed to separate the free diffusive component representing free water from an anisotropic component characterizing the orientation and diffusion characteristics of myofibers. The orientation of each anisotropic compartment was displayed in glyph format and used for qualitative description of myofibers and for construction of tractograms. The helix angle was calculated across the ventricular walls in 5 locations and displayed graphically. Scalar parameters (fractional anisotropy and mean diffusivity) were compared among specimens. Results The hypertrophied systemic RV has an inner layer, comprising about 2/3 of the wall, composed of hypertrophied trabeculae and an epicardial layer of circumferential myofibers. Myofibers within smaller trabeculae are aligned and organized with parallel fibers while larger, composite bundles show marked disarray, largely between component trabeculae. We observed a narrow range of helix angles in the outer, compact part of the wall consistent with aligned, approximately circumferential fibers. However, there was marked variation of helix angle in the inner, trabecular part of the wall consistent with marked variation in fiber orientation. The apical whorl was disrupted or incomplete and we observed myocardial whorls or vortices at other locations. Fractional anisotropy was lower in abnormal hearts while mean diffusivity was more variable, being higher in 2 but lower in 1 heart, compared to the structurally normal heart. Conclusions Myofiber organization is abnormal in the failing systemic RV and might be an important substrate for heart failure and arrhythmia. It is unclear if myofiber disorganization is due to hemodynamic factors, developmental problems, or both.