Quantitative analysis of hypertrophic myocardium using diffusion tensor magnetic resonance imaging.

Quantitative analysis of hypertrophic myocardium using diffusion tensor magnetic resonance imaging.
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使用扩散张量磁共振成像对肥厚心肌进行定量分析。

DOI:
10.1117/1.jmi.3.4.046001
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发表时间:
2016
期刊:
Journal of medical imaging (Bellingham, Wash.)
影响因子:
--
通讯作者:
Seo,Youngho
Seo,Youngho
中科院分区:
--
文献类型:
--
作者:
Tran,Nicholas;Giannakidis,Archontis;Gullberg,GrantT;Seo,Youngho

文献摘要

相似文献

系统性高血压是左心室肥厚(LVH)的致病因素。这项研究的动机是有可能逆转或处理与这种病理中的心肌结构重构相关的功能障碍。应用弥散张量磁共振成像技术,利用弥散张量的协方差分析了活体肥厚(6SHR)和正常(5WKY)大鼠心脏的心肌纤维和板层取向。首先,使用WKY b0图像形成正常心脏微结构图谱。然后,SHR和WKY b0心脏在图谱上注册。将获得的形变场应用于SHR和WKY心脏张量场,然后采用保留主方向(PPD)重定向策略。然后由配准的WKY张量图像形成平均张量场。计算每个心脏的配准张量图像的协方差,肥厚心肌显示出显著增加的心肌纤维排列紊乱(),平均离散度为38.7度,与正常心脏的34.8度和51.8度相比,正常心肌层的离散度()增加了54.8度。结果表明,高血压左室肥厚大鼠心肌纤维和板层结构明显改变。
Systemic hypertension is a causative factor in left ventricular hypertrophy (LVH). This study is motivated by the potential to reverse or manage the dysfunction associated with structural remodeling of the myocardium in this pathology. Using diffusion tensor magnetic resonance imaging, we present an analysis of myocardial fiber and laminar sheet orientation inex vivohypertrophic (6 SHR) and normal (5 WKY) rat hearts using the covariance of the diffusion tensor. First, an atlas of normal cardiac microstructure was formed using the WKY b0 images. Then, the SHR and WKY b0 hearts were registered to the atlas. The acquired deformation fields were applied to the SHR and WKY heart tensor fields followed by the preservation of principal direction (PPD) reorientation strategy. A mean tensor field was then formed from the registered WKY tensor images. Calculating the covariance of the registered tensor images about this mean for each heart, the hypertrophic myocardium exhibited significantly increased myocardial fiber derangement () with a mean dispersion of 38.7 deg, and an increased dispersion of the laminar sheet normal () of 54.8 deg compared with 34.8 deg and 51.8 deg, respectively, in the normal hearts. Results demonstrate significantly altered myocardial fiber and laminar sheet structure in rats with hypertensive LVH.