A Novel Method for Quantifying Smooth Regional Variations in Myocardial Contractility Within an Infarcted Human Left Ventricle Based on Delay-Enhanced Magnetic Resonance Imaging
A Novel Method for Quantifying Smooth Regional Variations in Myocardial Contractility Within an Infarcted Human Left Ventricle Based on Delay-Enhanced Magnetic Resonance Imaging
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DOI：
10.1115/1.4030667
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发表时间：
2015-08-01
影响因子：
1.7
通讯作者：
Guccione, Julius M.
中科院分区：
文献类型：
--
作者：
Genet, Martin;Lee, Lik Chuan;Guccione, Julius M.
心力衰竭正在以惊人的速度增加，使其成为全球流行的疾病。随着人口老龄化和预期寿命的增加，这一趋势不太可能改变。近70%的心力衰竭患者是由心肌梗死(MI)引起的不良左心室(LV)重构引起的。不利的重构过程涉及心肌梗死附近的边缘地带(BZ)的延伸，通常是灌流的，但表现为肌纤维收缩功能障碍。为了改进特定患者的心脏力学建模，我们试图创建一个有限元模型，直接从延迟增强磁共振(DE-MR)图像中集成BZ和MI形态的人左室。我们没有将LV分成不同的区域(例如MI、BZ和偏远区域)，每个区域都具有相同的心肌材料属性，而是假设了DE-MR图像像素强度与心肌硬度和收缩能力之间的函数关系-我们将材料属性的线性变化视为DE-MR图像像素强度的函数，这已知可以提高模型响应的准确性。然后，使用从同一患者获得的测量-即3D应变测量-使用磁化磁共振(CSPAMM-MR)图像的互补空间调制来校准有限元模型。这导致美国心脏协会(AHA)所有节段的平均周向应变误差为8.9%。我们使用心脏DE-MR和CSPAMM-MR图像证明了我们的方法用于量化心肌收缩能力的平滑区域变化，这些图像来自一名78岁的女性，她在大约一年前经历了心肌梗死。我们发现远端心肌舒张期硬度(C-0)超过bar(0)=0.102 kpa，远端心肌收缩能力(T-max)超过bar 146：9kpa，两者都在先前公布的正常人范围内。此外，我们发现BZ的归一化像素强度范围为30%，这与文献中的结果是一致的。基于这些局部心肌材料的特性，我们使用我们的有限元模型来计算患者特定的舒张期和收缩期左室肌纤维的应力分布，这是无法直接测量的。异常高水平的室壁应力被认为是不良左室壁重构的主要驱动力之一，许多现有的和新的治疗心力衰竭的方法试图从根本上使左室壁应力正常化。因此，我们的无创方法估计心肌收缩能力的平滑区域变异对于优化新的外科或医学策略以限制从梗死到心力衰竭的慢性演变应该是有价值的。
Heart failure is increasing at an alarming rate, making it a worldwide epidemic. As the population ages and life expectancy increases, this trend is not likely to change. Myocardial infarction (MI)-induced adverse left ventricular (LV) remodeling is responsible for nearly 70% of heart failure cases. The adverse remodeling process involves an extension of the border zone (BZ) adjacent to an MI, which is normally perfused but shows myofiber contractile dysfunction. To improve patient-specific modeling of cardiac mechanics, we sought to create a finite element model of the human LV with BZ and MI morphologies integrated directly from delayed-enhancement magnetic resonance (DE-MR) images. Instead of separating the LV into discrete regions (e.g., the MI, BZ, and remote regions) with each having a homogeneous myocardial material property, we assumed a functional relation between the DE-MR image pixel intensity and myocardial stiffness and contractility-we considered a linear variation of material properties as a function of DE-MR image pixel intensity, which is known to improve the accuracy of the model's response. The finite element model was then calibrated using measurements obtained from the same patient-namely, 3D strain measurements-using complementary spatial modulation of magnetization magnetic resonance (CSPAMM-MR) images. This led to an average circumferential strain error of 8.9% across all American Heart Association (AHA) segments. We demonstrate the utility of our method for quantifying smooth regional variations in myocardial contractility using cardiac DE-MR and CSPAMM-MR images acquired from a 78-yr-old woman who experienced an MI approximately 1 yr prior. We found a remote myocardial diastolic stiffness of (C-0) over bar (0) = 0.102 kPa, and a remote myocardial contractility of (T-max) over bar 146: 9 kPa, which are both in the range of previously published normal human values. Moreover, we found a normalized pixel intensity range of 30% for the BZ, which is consistent with the literature. Based on these regional myocardial material properties, we used our finite element model to compute patient-specific diastolic and systolic LV myofiber stress distributions, which cannot be measured directly. One of the main driving forces for adverse LV remodeling is assumed to be an abnormally high level of ventricular wall stress, and many existing and new treatments for heart failure fundamentally attempt to normalize LV wall stress. Thus, our noninvasive method for estimating smooth regional variations in myocardial contractility should be valuable for optimizing new surgical or medical strategies to limit the chronic evolution from infarction to heart failure.