Distinguishing shear and tensile myocardial wall stiffness using ex vivo anisotropic Magnetic Resonance Elastography.

Cyril Tous, Guillaume Flé, Stanislas Rapacchi, Matthew McGarry, Philip Bayly, Keith Paulsen, Curtis L Johnson, Elijah Van Houten
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Abstract

The organized myofiber structure within the myocardium indicates its mechanical anisotropy. By projecting the MR Elastography (MRE) stiffness matrix along either the myocardial fiber or sheet orientations determined by Diffusion Tensor Imaging (DTI), anisotropic MRE (aMRE) maps axial and transverse shear and Young's moduli into three tensile and six shear deformation modes. Ten healthy ex vivo swine hearts were imaged three times at 3T using MRE and DTI sequences. aMRE results showed a within-subject coefficient of variation at 19% for the fiber model and 28% for the sheet model across specimens and metrics, with coefficients lower than 15% for seven of the ten specimens across models. Repeatability coefficient of ±0.5 kPa for Young's moduli and ±0.17 kPa for shear's moduli, demonstrating repeatability within the 95% agreement limit. Isotropic MRE underestimated stiffnesses by 31% compared to aMRE, where anisotropic moduli aligned more closely with prior finite element studies and some mechanical loading tests. The myocardium's anisotropic elasticity reflects with its helicoidal myofiber microstructure, with mid-wall circumferential fibers requiring twice the force to deform as longitudinal fibers at the epicardium or endocardium. At the mid-wall, fiber model values were μax = 1.9 ± 0.1 kPa, μtra = 1.3 ± 0.1 kPa, Eax = 5.6 ± 0.4 kPa, and Etra = 3.8 ± 0.3 kPa. Identified deformation modes included: (FF), (NN), (FF or SS), (NN or SS), (SN or NS), (FN or FS), (SF or FS), and (SN or NF), where N is normal to both fiber (F) and sheet (S) orientations. By aligning elasticity matrices more accurately with myocardial architecture than isotropic MRE, aMRE was able to reliably measure shear and Young's moduli in ex vivo swine hearts. These mappings of deformation modes may bring myocardial stiffness assessment closer to clinical application, providing a foundation for a non-invasive methodology capable of true mechanical characterization of the cardiac wall using MR imaging. STATEMENT OF SIGNIFICANCE: The myocardium's anisotropic elasticity, due to its helicoidal myofiber structure, is revealed through anisotropic MR elastography, using fiber and sheet elastic models. Mid-wall circumferential fibers require twice the force to deform equally compared to epicardial or endocardial fibers. Characterizing shear and Young's moduli across cardiac modes offers noninvasive measures of ventricular compliance, comparable to pressure-volume relationships. This could enhance early diagnosis of "stiff heart syndrome" and clarify its underlying mechanisms. Additionally, it aids understanding of myocardial pathologies, including amyloidosis, hypertrophic and dilated cardiomyopathies, and ischemic damage. By characterizing tensile and shear interactions, it may inform diagnosis and treatment of conduction issues and arrhythmia, where tissue has lost its normal mechanical behavior, while patient-specific models could optimize surgical and therapeutic outcomes.

利用离体各向异性磁共振弹性成像技术区分心肌壁剪切和拉伸刚度。
心肌内有组织的肌纤维结构表明其力学各向异性。通过沿扩散张量成像(DTI)确定的心肌纤维或薄片方向投影MR弹性成像(MRE)刚度矩阵,各向异性MRE (aMRE)将轴向和横向剪切和杨氏模量映射为三种拉伸和六种剪切变形模式。10个健康的离体猪心脏在3T时使用MRE和DTI序列进行三次成像。aMRE结果显示,纤维模型的受试者内变异系数为19%,薄片模型的受试者内变异系数为28%,10个模型中有7个试件的系数低于15%。杨氏模量的重复性系数为±0.5 kPa,剪切模量的重复性系数为±0.17 kPa,重复性在95%以内。与aMRE相比,各向异性MRE低估了31%的刚度,在aMRE中,各向异性模量与先前的有限元研究和一些机械加载测试更为接近。心肌的各向异性弹性反映在其螺旋肌纤维微观结构上,在心外膜或心内膜处,中壁的周向纤维需要的变形力是纵向纤维的两倍。中壁纤维模型值为μax = 1.9±0.1 kPa, μtra = 1.3±0.1 kPa, Eax = 5.6±0.4 kPa, Etra = 3.8±0.3 kPa。确定的变形模式包括:(FF), (NN), (FF或SS), (NN或SS), (NN或SS), (SN或NS), (FN或FS), (SF或FS)和(SN或NF),其中N与纤维(F)和片材(S)方向都是垂直的。通过比各向同性MRE更准确地将弹性矩阵与心肌结构对齐,aMRE能够可靠地测量离体猪心脏的剪切和杨氏模量。这些变形模式的映射可能使心肌刚度评估更接近临床应用,为能够使用MR成像对心壁进行真正力学表征的非侵入性方法提供基础。意义声明:心肌的各向异性弹性,由于其螺旋肌纤维结构,通过各向异性磁共振弹性成像显示,使用纤维和片弹性模型。与心外膜或心内膜纤维相比,中壁纤维需要两倍的力来变形。跨心脏模式的剪切模量和杨氏模量的特征提供了无创的心室顺应性测量,可与压力-容量关系相媲美。这可以提高“心脏僵硬综合征”的早期诊断,并阐明其潜在的机制。此外,它有助于了解心肌病理,包括淀粉样变性、肥厚和扩张性心肌病和缺血性损伤。通过表征拉伸和剪切相互作用,它可以为组织失去正常力学行为的传导问题和心律失常的诊断和治疗提供信息,而患者特异性模型可以优化手术和治疗结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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