介入超声印压系统研制及心肌硬度检测
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摘要
活体组织病变可引起硬度改变,且硬度与病变程度有一定关系,通过检测活体组织硬度,有助于临床诊断及判断病变程度。应用超声印压(Ultrasound indention,US indention)方法,已成功检测了糖尿病人足底、残肢、放射治疗前后颈部、脊柱、关节软骨等组织的硬度变化,表明用该法可定量检测因组织病变而引起力学特性改变。与传统触诊方法相比,超声印压法所得的硬度值或杨氏模量可反映病变部位硬度变化,使病变程度得到更为准确的定量描述。事实上组织硬度改变多发生在深部体腔,缺乏有效的检测方法,尤其在心血管系统,由于硬度变化可影响心脏收缩和舒张功能,特别是心室肌被动僵硬度增加将导致舒张功能不全,进一步可发展为舒张性心力衰竭(Diastolic Heart Failure,DHF),因此,检测心肌硬度可为部分心脏疾病提供重要的诊断信息。
目前,虽可采用超声印压法对体表组织进行硬度检测,但所用仪器体积大,印压头质硬,不适于深部腔道组织,特别是处于高压、搏动状态的心血管内腔。目前尚无直接、可靠检测活体心肌硬度的方法和仪器,故本研究设计研制一种可直接检测活体心肌硬度的仪器,并对其可行性、可信性、准确性及安全性进行验证。
第一部分介入超声印压系统的研制-介入式超声硬度检测仪的研制2
目的:研制用于检测心肌硬度的介入超声印压系统系统设计:该系统包括介入超声硬度检测导管(简称超声导管)、心电前置放大器和主机。超声导管头端安装印压球囊和微型超声换能器,其尾部连接压力传感器,导管体直径为7F,通过外周动脉血管进入心腔以印压心室壁。印压球囊提供直接印压力,微型超声换能器检测印压过程心室壁厚度的变化,压力传感器检测球囊印压力变化,心电前置放大器提供心电信号,为印压及数据分析提供时间参考点。主机为应力、应变和心电信号显示提供平台,并能进行图形储存、分析和测量。采用心肌拟弹性理论和应力-应变关系原理得到反映组织力学属性的硬度值。并采用该系统对心肌体模进行检测。
结果:超声导管能检测到心肌体模厚度和压力的变化,心电放大器能提供体表心电信号。主机能以M型模式显示超声信号,以曲线方式显示压力波形,以常规的体表心电图方式显示心电信号,并具备对图形进行储存、分析和测量的功能。
结论:介入超声印压系统将印压球囊、微型超声换能器和压力传感器结合并实现导管化,能提供应力-应变数据和心电信号,并能显示、储存、分析应力、形变和心电图形,满足设计要求,为活体心肌硬度检测提供了成套原型仪器。
5第二部分介入超声印压系统检测弹性超声仿体的实验研究
目的:采用介入超声印压系统检测弹性超声仿体的硬度,评价系统检测硬度的可行性和准确性。
方法:制作三种不同硬度超声仿体,分成两组,一组寄往香港理工大学生物力学超声研究室行单轴压缩实验,测定杨氏模量,作为本研究检测弹性超声仿体硬度的参照标准,另一组用本实验研制的系统对仿体硬度进行检测。在球囊内注入不同量的脱气水,使其充盈形成4.72mm、5.3mm、7.0mm三种直径,在对实际印压压强与检测压强进行标定后,分别用上述三种直径球囊印压相同硬度的超声仿体,以了解球囊直径是否影响硬度值的检测;再用同一直径球囊(4.72mm)印压不同硬度的超声仿体,以了解该系统对不同硬度仿体的检测能力;最后用4.72mm球囊印压安有不同硬度超声仿体的模型心室壁,以评价超声导管对心室壁进行印压可行性和导管操控性;所得硬度值与杨氏模量进行相关分析和Bland-Altman曲线分析,以判断系统检测仿体硬度的准确性和是否能满足生物组织硬度检测。
结果:(1)不同直径球囊实际印压压强与检测压强标定,二者有线性关系(P<0.05),回归系数分别为0.62、0.78、0.98,通过换算,可得到实际印压压强。(2)不同直径球囊印压同一硬度仿体,其值分别为(86.1±15.0) kPa、(87.2±18.0) kPa、(82.9±14.9) kPa,差别无显著性(P>0.05)。(3)同一直径球囊印压不同硬度超声仿体,其值分别为(45.5±5.7) kPa、(86.1±15.0 )kPa、(117.9±10.9) kPa ,差别有显著性(P<0.05)。(4)单轴压缩试验测定不同硬度超声仿体,杨氏模量分别为(21.8±5.1)kPa、(44.8±7.1) kPa、(85.2±7.7) kPa,本系统检测的硬度值与杨氏模量值呈强相关(r=0.94,P<0.05),同时,检测硬度值也满足Bland-Altman曲线。(5)模型心脏仿体壁检测的硬度值分别为(47.7±7.9) kPa、(89.3±17.3) kPa、(121.7±13.9)kPa ,与直接印压检测值相比,差别无显著性(P>0.05),三组值之间比较,差别有显著性(P<0.05)。
结论:介入超声印压系统能够检测出超声仿体的不同硬度,检出硬度与仿体杨氏模量值呈强相关性,且球囊直径对检测仿体硬度值无影响。球囊印压检测的硬度值与杨氏模量具有强相关,表明球囊印压能够准确检测仿体硬度。Bland-Altman曲线分析显示,该检测方法可作为一种检测生物组织硬度的新手段。且超声导管具有印压模型心室壁检测硬度的可行性和可操作性。
第三部分介入超声印压检测活体心肌硬度的实验研究
目的:探索介入超声印压系统检测活体心肌硬度的可行性和安全性。
方法: 18只健康成年杂种犬,随机分为心肌梗死组(n=9)和假手术组(n=9),结扎冠状动脉建立心肌梗死模型,建模6周后对两组动物进行检测。在X线引导下,将超声导管经外周动脉进入左心室,分别印压左室前壁和心尖部,超声测量其厚度形变值,压力传感器获得印压压强值,根据应力-应变关系,得到前壁和心尖部心肌组织硬度值,并进行应力-相关形变曲线拟合。活体心肌硬度检测完成后,取心肌行HE和天狼猩红染色,同时取假手术组印压部位心内膜行扫描电镜。
结果:(1)梗死组舒张晚期左室前壁和心尖部心肌硬度值分别为(140.7±30.7)kPa、(49.1±6.2)kPa,假手术组为(19.3±4.6) kPa、(34.2±6.5)kPa,梗死组前壁及心尖部硬度值均高于假手术组,差异有显著性(P<0.05)。(2)梗死组和假手术组前壁应力-相关形变均呈线性,相关系数分别为r= 0.90、0.84,P<0.05。(3)HE染色可见梗死区大量纤维增生;天狼猩红染色可见梗死区大量胶原增生,梗死组前壁和心尖部CVF、IOD、CVFⅠ/CVFⅢ分别为33.0±11.9、10.23±0.79、17.01±4.2和6.6±1.3、7.22±0.7、9.0±3.1 ;假手术组分别为3.0±0.9、0.69±0.1、7.7±1.9和3.4±1.1、0.79±0.09、7.0±2.01,梗死组前壁及心尖部CVF、IOD、CVFⅠ/CVFⅢ均高于假手术组,差异有显著性(P<0.05)。(4)假手术组心内膜扫描电镜观察未见内皮细胞损伤。
结论:该仪器可以直接、定量检测活体局部心肌硬度,并可区别正常和梗死心肌的硬度差异,且硬度值增加与局部胶原含量增加和胶原表型的改变有关。印压过程安全。应用该方法检测的硬度值,可为心脏局部舒张功能异常提供有用的信息。
Tissue stiffness usually changed with different pathologic situations. Detection of tissue stiffness in vivo could be contributed to clinical diagnosis and assessment of pathologic state. Up to now, ultrasound indentation technique has been widely used for assessing for the stiffness of tissue including residual limbs, diabetic feet, fibrotic neck induced by radiotherapy, spinae , and articular cartilage, which indicated that the technique can provide a quantitative measurement of tissue stiffness. Compared with palpation method , ultrasound indentation technique could determine the material property of pathologic tissue in vivo or in situ and then more precise quantitative data about pathologic state can be acquired. Actually, stiffness change in most of pathologic tissue occured at deep coelom. However, tissue stiffness instruments invented were not suitable for detecting stiffness of coelom-tissue, especially the cardiovascular system. The change of myocardium stiffness could influenced systolic and/or diastolic function, especially increased ventricular passive stiffness would result into diastolic dysfunction and then deteriorate to diastolic heart failure. Consequently it was vital to assess for local myocardium stiffness. So far, there was no direct and reliable way of detecting myocardium stiffness. So the study was engaged to design an apparatus for detecting myocardium stiffness in vivo and explore its feasibility further more.
PART I DEVELOPMENT OF INTERVENTIONAL ULTRASOUND INDENTATION SYSTEM
Objective: To develop an intervention ultrasound indentation system for quantitative measurement of myocardium stiffness.
Idea: The system was composed of an intervention ultrasound stiffness detection catheter(ultrasound catheter) ,ECG preamplifier and mainframe. Ultrasound catheter (Diameter :7F) with balloon and ultrasound mini-transducer fixed on its head and pressure transducer linked to its tail passed through peripheral artery into chambers heart and indented ventricle wall. Balloon offered direct pressure, ultrasound mini-transducer detected ventricle wall thickness during indentation , and pressure transducer measured balloon pressure . ECG preamplifier provided electrocardiogram and at same time offered time reference point for indentation and data analysis. Mainframe can show, saved, analyze and measure the images of stress , strain, and electrocardiogram .According to strain-stress relation ,stiffness value reflecting mechanical properties of myocardium tissue was gained.
Results: The ultrasound catheter had been successfully used for the measurement of thickness and pressure of phantom. ECG amplifier was able to provide surface electrocardiogram, with myocardium thickness displayed by M-type ultrasound, pressure wave showed by curves, and electrocardio-signals demonstrated by surface electrocardiogram.
Conclusion: Interventional ultrasound indentation system was able to provide strain-stress data and electrocardio-signals ,meanwhile it was also able to display,save,and analyze strain,deformation and electrocardiogram,which satisfied expecting design requirement .This system made it possible to assess the myocardium tissue stiffness in vivo .
PARTⅡAN EXPERIMENTAL STUDY ON ASSESSMENT OF ELASTICITY PHANTOMS STIFFNESS BY INTERVENTION ULTRASOUND INDENTION SYSTEM
Objective : To explore the feasibility and accurate of interventional ultrasound indention system detecting phantoms stiffness.
Methods: The different stiffness phantoms were made and Young’s modulus measured by a uniaxial compression trial was regarded as a standard. Calibration was conducted between actual indentation pressure of three kinds of balloons (Diameter: 4.72mm、5.3mm、7.0mm) and tested indentation pressure. These balloons were applied for detecting the same stiffness phantom respectively and then the different stiffness phantoms were tested by a balloon (Diameter: 4.72mm) and at last the different stiffness phantoms inserted cardiac model were also assessed by a balloon (Diameter: 4.72mm)
Results: These phantoms Young’s module measured by uniaxial compression trial were (21.8±5.1) kPa, (44.8±7.1) kPa, (85.2±7.7) kPa respectively and calibrating regression coefficient were 0.62, 0.78, 0.98, respectively. Stiffness value of the same stiffness phantom measured by different diameter balloons were (86.1±15.0) kPa, (87.2±18.0)kPa and (82.9±14.9)kPa respectively, there were no strikingly difference (P>0.05).Stiffness value of the phantom with different stiffness assessed by balloon with same diameter were (45.5±5.7 )kPa, (86.1±15.0)kPa and (117.9±10.9) kPa respectively, there was significant difference (P<0.05)and correlation coefficient between these value and Young’s modulus was 0.94( r=0.94,P<0.05) and at the same time these value were also consistent with Bland-Altman curve。Stiffness values of phantom fixed heart model indented were (47.7±7.9) kPa, (89.3±17.3)kPa and (121.7±13.9) kPa respectively, and compared with those of phantom directly indented, there was no apparent difference (P>0.05).
Conclusion: These results demonstrated that the intervention ultrasound indention system may be applied for detecting stiffness of different phantoms and there was apparent relationship of tested values with Young’s modulus. The result of Bland-Altman plot demonstrated that the results were acceptable for clinical applications.
PARTⅢINTERVENTION ULTRASOUND INDENTION ASSESSMENT OF MYOCARDIAL STIFFNESS: IN VIVO EXPERIMENTAL STUDY
Objective: To explore the feasibility of interventional ultrasound indention for detecting myocardial stiffness in vivo and to offer a direct measurement method of myocardial stiffness in vivo.
Methods : Adult dogs were assigned randomly to myocardial infarct group(n=9)and sham operation group (n=9). Myocardial infarct model was established by coronary artery ligation. Six weeks post operation, using self-made interventional ultrasound stiffness detection meter and under X-ray guidance,Ultrasound catheter passed through peripheral artery into left ventricle and indented left ventricle wall. Myocardium deformation value was acquired by ultrasound and indentation pressure was also obtained. According to Strain-stress relation, myocardium stiffness parameter of left ventricle was gained through calculation and curve fitting. After assessment of myocardium stiffness, HE staining and Sirius red staining of myocardium were conducted and endocardium indented by balloon was observed by scan electron microscope in sham group.
Results: Stiffness values of left ventricular anterior and apex wall myocardium during diastasis in heart infarction group were (140.7±30.7) kPa and (49.1±6.2) kPa; those of sham operation group were (34.2±6.5) kPa and (19.3±4.6) kPa. Myocardium strain-stress relation in infarct region was linearity and its correlation coefficient was 0.90 (r= 0.90, P<0.05) and that of sham operation was also linearity and its correlation coefficient was 0.84 (r= 0.84, P<0.05). By HE staining, it showed a large quantity of fibrotic hyperplasia within infarct zone. By Sirius red staining, it showed an amount of collagen hyperplasia. To the anterior wall and the apex of infarction group, the values of CVF, IOD and CVFⅠ/CVFⅢwere 33.0±11.9,10.23±0.79, 17.01±4.2 and 6.6±1.3, 7.22±0.7, 9.0±3.1 separately, while to the sham group, the values of CVF, IOD and CVFⅠ/CVFⅢwere 3.0±0.9, 0.69±0.1, 7.7±1.9 and 3.4±1.1, 0.79±0.09, 7.0±2.01 separately. Content of collagen and the value of CVFⅠ/CVFⅢwere higher in the anterior wall and the apex of infarction group than in the sham group(P<0.05). There wasn’t any damage of endothelial cells detected under electron microscope in the endocardium of the sham group.
Conclusions: The interventional ultrasound indention meter for stiffness detection was able to detect and measure the stiffness of regional myocardium directly in vivo through a safe and reliable method and steps. With the help of detection meter, local diastolic dysfunction of myocardium would be assessed conveniently, while deep tissue stiffness would be assessed easily.
目前,虽可采用超声印压法对体表组织进行硬度检测,但所用仪器体积大,印压头质硬,不适于深部腔道组织,特别是处于高压、搏动状态的心血管内腔。目前尚无直接、可靠检测活体心肌硬度的方法和仪器,故本研究设计研制一种可直接检测活体心肌硬度的仪器,并对其可行性、可信性、准确性及安全性进行验证。
第一部分介入超声印压系统的研制-介入式超声硬度检测仪的研制2
目的:研制用于检测心肌硬度的介入超声印压系统系统设计:该系统包括介入超声硬度检测导管(简称超声导管)、心电前置放大器和主机。超声导管头端安装印压球囊和微型超声换能器,其尾部连接压力传感器,导管体直径为7F,通过外周动脉血管进入心腔以印压心室壁。印压球囊提供直接印压力,微型超声换能器检测印压过程心室壁厚度的变化,压力传感器检测球囊印压力变化,心电前置放大器提供心电信号,为印压及数据分析提供时间参考点。主机为应力、应变和心电信号显示提供平台,并能进行图形储存、分析和测量。采用心肌拟弹性理论和应力-应变关系原理得到反映组织力学属性的硬度值。并采用该系统对心肌体模进行检测。
结果:超声导管能检测到心肌体模厚度和压力的变化,心电放大器能提供体表心电信号。主机能以M型模式显示超声信号,以曲线方式显示压力波形,以常规的体表心电图方式显示心电信号,并具备对图形进行储存、分析和测量的功能。
结论:介入超声印压系统将印压球囊、微型超声换能器和压力传感器结合并实现导管化,能提供应力-应变数据和心电信号,并能显示、储存、分析应力、形变和心电图形,满足设计要求,为活体心肌硬度检测提供了成套原型仪器。
5第二部分介入超声印压系统检测弹性超声仿体的实验研究
目的:采用介入超声印压系统检测弹性超声仿体的硬度,评价系统检测硬度的可行性和准确性。
方法:制作三种不同硬度超声仿体,分成两组,一组寄往香港理工大学生物力学超声研究室行单轴压缩实验,测定杨氏模量,作为本研究检测弹性超声仿体硬度的参照标准,另一组用本实验研制的系统对仿体硬度进行检测。在球囊内注入不同量的脱气水,使其充盈形成4.72mm、5.3mm、7.0mm三种直径,在对实际印压压强与检测压强进行标定后,分别用上述三种直径球囊印压相同硬度的超声仿体,以了解球囊直径是否影响硬度值的检测;再用同一直径球囊(4.72mm)印压不同硬度的超声仿体,以了解该系统对不同硬度仿体的检测能力;最后用4.72mm球囊印压安有不同硬度超声仿体的模型心室壁,以评价超声导管对心室壁进行印压可行性和导管操控性;所得硬度值与杨氏模量进行相关分析和Bland-Altman曲线分析,以判断系统检测仿体硬度的准确性和是否能满足生物组织硬度检测。
结果:(1)不同直径球囊实际印压压强与检测压强标定,二者有线性关系(P<0.05),回归系数分别为0.62、0.78、0.98,通过换算,可得到实际印压压强。(2)不同直径球囊印压同一硬度仿体,其值分别为(86.1±15.0) kPa、(87.2±18.0) kPa、(82.9±14.9) kPa,差别无显著性(P>0.05)。(3)同一直径球囊印压不同硬度超声仿体,其值分别为(45.5±5.7) kPa、(86.1±15.0 )kPa、(117.9±10.9) kPa ,差别有显著性(P<0.05)。(4)单轴压缩试验测定不同硬度超声仿体,杨氏模量分别为(21.8±5.1)kPa、(44.8±7.1) kPa、(85.2±7.7) kPa,本系统检测的硬度值与杨氏模量值呈强相关(r=0.94,P<0.05),同时,检测硬度值也满足Bland-Altman曲线。(5)模型心脏仿体壁检测的硬度值分别为(47.7±7.9) kPa、(89.3±17.3) kPa、(121.7±13.9)kPa ,与直接印压检测值相比,差别无显著性(P>0.05),三组值之间比较,差别有显著性(P<0.05)。
结论:介入超声印压系统能够检测出超声仿体的不同硬度,检出硬度与仿体杨氏模量值呈强相关性,且球囊直径对检测仿体硬度值无影响。球囊印压检测的硬度值与杨氏模量具有强相关,表明球囊印压能够准确检测仿体硬度。Bland-Altman曲线分析显示,该检测方法可作为一种检测生物组织硬度的新手段。且超声导管具有印压模型心室壁检测硬度的可行性和可操作性。
第三部分介入超声印压检测活体心肌硬度的实验研究
目的:探索介入超声印压系统检测活体心肌硬度的可行性和安全性。
方法: 18只健康成年杂种犬,随机分为心肌梗死组(n=9)和假手术组(n=9),结扎冠状动脉建立心肌梗死模型,建模6周后对两组动物进行检测。在X线引导下,将超声导管经外周动脉进入左心室,分别印压左室前壁和心尖部,超声测量其厚度形变值,压力传感器获得印压压强值,根据应力-应变关系,得到前壁和心尖部心肌组织硬度值,并进行应力-相关形变曲线拟合。活体心肌硬度检测完成后,取心肌行HE和天狼猩红染色,同时取假手术组印压部位心内膜行扫描电镜。
结果:(1)梗死组舒张晚期左室前壁和心尖部心肌硬度值分别为(140.7±30.7)kPa、(49.1±6.2)kPa,假手术组为(19.3±4.6) kPa、(34.2±6.5)kPa,梗死组前壁及心尖部硬度值均高于假手术组,差异有显著性(P<0.05)。(2)梗死组和假手术组前壁应力-相关形变均呈线性,相关系数分别为r= 0.90、0.84,P<0.05。(3)HE染色可见梗死区大量纤维增生;天狼猩红染色可见梗死区大量胶原增生,梗死组前壁和心尖部CVF、IOD、CVFⅠ/CVFⅢ分别为33.0±11.9、10.23±0.79、17.01±4.2和6.6±1.3、7.22±0.7、9.0±3.1 ;假手术组分别为3.0±0.9、0.69±0.1、7.7±1.9和3.4±1.1、0.79±0.09、7.0±2.01,梗死组前壁及心尖部CVF、IOD、CVFⅠ/CVFⅢ均高于假手术组,差异有显著性(P<0.05)。(4)假手术组心内膜扫描电镜观察未见内皮细胞损伤。
结论:该仪器可以直接、定量检测活体局部心肌硬度,并可区别正常和梗死心肌的硬度差异,且硬度值增加与局部胶原含量增加和胶原表型的改变有关。印压过程安全。应用该方法检测的硬度值,可为心脏局部舒张功能异常提供有用的信息。
Tissue stiffness usually changed with different pathologic situations. Detection of tissue stiffness in vivo could be contributed to clinical diagnosis and assessment of pathologic state. Up to now, ultrasound indentation technique has been widely used for assessing for the stiffness of tissue including residual limbs, diabetic feet, fibrotic neck induced by radiotherapy, spinae , and articular cartilage, which indicated that the technique can provide a quantitative measurement of tissue stiffness. Compared with palpation method , ultrasound indentation technique could determine the material property of pathologic tissue in vivo or in situ and then more precise quantitative data about pathologic state can be acquired. Actually, stiffness change in most of pathologic tissue occured at deep coelom. However, tissue stiffness instruments invented were not suitable for detecting stiffness of coelom-tissue, especially the cardiovascular system. The change of myocardium stiffness could influenced systolic and/or diastolic function, especially increased ventricular passive stiffness would result into diastolic dysfunction and then deteriorate to diastolic heart failure. Consequently it was vital to assess for local myocardium stiffness. So far, there was no direct and reliable way of detecting myocardium stiffness. So the study was engaged to design an apparatus for detecting myocardium stiffness in vivo and explore its feasibility further more.
PART I DEVELOPMENT OF INTERVENTIONAL ULTRASOUND INDENTATION SYSTEM
Objective: To develop an intervention ultrasound indentation system for quantitative measurement of myocardium stiffness.
Idea: The system was composed of an intervention ultrasound stiffness detection catheter(ultrasound catheter) ,ECG preamplifier and mainframe. Ultrasound catheter (Diameter :7F) with balloon and ultrasound mini-transducer fixed on its head and pressure transducer linked to its tail passed through peripheral artery into chambers heart and indented ventricle wall. Balloon offered direct pressure, ultrasound mini-transducer detected ventricle wall thickness during indentation , and pressure transducer measured balloon pressure . ECG preamplifier provided electrocardiogram and at same time offered time reference point for indentation and data analysis. Mainframe can show, saved, analyze and measure the images of stress , strain, and electrocardiogram .According to strain-stress relation ,stiffness value reflecting mechanical properties of myocardium tissue was gained.
Results: The ultrasound catheter had been successfully used for the measurement of thickness and pressure of phantom. ECG amplifier was able to provide surface electrocardiogram, with myocardium thickness displayed by M-type ultrasound, pressure wave showed by curves, and electrocardio-signals demonstrated by surface electrocardiogram.
Conclusion: Interventional ultrasound indentation system was able to provide strain-stress data and electrocardio-signals ,meanwhile it was also able to display,save,and analyze strain,deformation and electrocardiogram,which satisfied expecting design requirement .This system made it possible to assess the myocardium tissue stiffness in vivo .
PARTⅡAN EXPERIMENTAL STUDY ON ASSESSMENT OF ELASTICITY PHANTOMS STIFFNESS BY INTERVENTION ULTRASOUND INDENTION SYSTEM
Objective : To explore the feasibility and accurate of interventional ultrasound indention system detecting phantoms stiffness.
Methods: The different stiffness phantoms were made and Young’s modulus measured by a uniaxial compression trial was regarded as a standard. Calibration was conducted between actual indentation pressure of three kinds of balloons (Diameter: 4.72mm、5.3mm、7.0mm) and tested indentation pressure. These balloons were applied for detecting the same stiffness phantom respectively and then the different stiffness phantoms were tested by a balloon (Diameter: 4.72mm) and at last the different stiffness phantoms inserted cardiac model were also assessed by a balloon (Diameter: 4.72mm)
Results: These phantoms Young’s module measured by uniaxial compression trial were (21.8±5.1) kPa, (44.8±7.1) kPa, (85.2±7.7) kPa respectively and calibrating regression coefficient were 0.62, 0.78, 0.98, respectively. Stiffness value of the same stiffness phantom measured by different diameter balloons were (86.1±15.0) kPa, (87.2±18.0)kPa and (82.9±14.9)kPa respectively, there were no strikingly difference (P>0.05).Stiffness value of the phantom with different stiffness assessed by balloon with same diameter were (45.5±5.7 )kPa, (86.1±15.0)kPa and (117.9±10.9) kPa respectively, there was significant difference (P<0.05)and correlation coefficient between these value and Young’s modulus was 0.94( r=0.94,P<0.05) and at the same time these value were also consistent with Bland-Altman curve。Stiffness values of phantom fixed heart model indented were (47.7±7.9) kPa, (89.3±17.3)kPa and (121.7±13.9) kPa respectively, and compared with those of phantom directly indented, there was no apparent difference (P>0.05).
Conclusion: These results demonstrated that the intervention ultrasound indention system may be applied for detecting stiffness of different phantoms and there was apparent relationship of tested values with Young’s modulus. The result of Bland-Altman plot demonstrated that the results were acceptable for clinical applications.
PARTⅢINTERVENTION ULTRASOUND INDENTION ASSESSMENT OF MYOCARDIAL STIFFNESS: IN VIVO EXPERIMENTAL STUDY
Objective: To explore the feasibility of interventional ultrasound indention for detecting myocardial stiffness in vivo and to offer a direct measurement method of myocardial stiffness in vivo.
Methods : Adult dogs were assigned randomly to myocardial infarct group(n=9)and sham operation group (n=9). Myocardial infarct model was established by coronary artery ligation. Six weeks post operation, using self-made interventional ultrasound stiffness detection meter and under X-ray guidance,Ultrasound catheter passed through peripheral artery into left ventricle and indented left ventricle wall. Myocardium deformation value was acquired by ultrasound and indentation pressure was also obtained. According to Strain-stress relation, myocardium stiffness parameter of left ventricle was gained through calculation and curve fitting. After assessment of myocardium stiffness, HE staining and Sirius red staining of myocardium were conducted and endocardium indented by balloon was observed by scan electron microscope in sham group.
Results: Stiffness values of left ventricular anterior and apex wall myocardium during diastasis in heart infarction group were (140.7±30.7) kPa and (49.1±6.2) kPa; those of sham operation group were (34.2±6.5) kPa and (19.3±4.6) kPa. Myocardium strain-stress relation in infarct region was linearity and its correlation coefficient was 0.90 (r= 0.90, P<0.05) and that of sham operation was also linearity and its correlation coefficient was 0.84 (r= 0.84, P<0.05). By HE staining, it showed a large quantity of fibrotic hyperplasia within infarct zone. By Sirius red staining, it showed an amount of collagen hyperplasia. To the anterior wall and the apex of infarction group, the values of CVF, IOD and CVFⅠ/CVFⅢwere 33.0±11.9,10.23±0.79, 17.01±4.2 and 6.6±1.3, 7.22±0.7, 9.0±3.1 separately, while to the sham group, the values of CVF, IOD and CVFⅠ/CVFⅢwere 3.0±0.9, 0.69±0.1, 7.7±1.9 and 3.4±1.1, 0.79±0.09, 7.0±2.01 separately. Content of collagen and the value of CVFⅠ/CVFⅢwere higher in the anterior wall and the apex of infarction group than in the sham group(P<0.05). There wasn’t any damage of endothelial cells detected under electron microscope in the endocardium of the sham group.
Conclusions: The interventional ultrasound indention meter for stiffness detection was able to detect and measure the stiffness of regional myocardium directly in vivo through a safe and reliable method and steps. With the help of detection meter, local diastolic dysfunction of myocardium would be assessed conveniently, while deep tissue stiffness would be assessed easily.
引文
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