肝硬化患者肺微循环多层螺旋CT灌注研究
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摘要
目的采用GE16层螺旋CT灌注成像技术来研究不同程度肝硬化患者肺部微循环灌注参数的改变情况。
材料与方法选取20例正常对照者和43例肝硬化患者(24例代偿期肝硬化患者,19例失代偿期肝硬化患者)行16层螺旋CT肺部同层动态增强扫描。将数据传送到GE AW4.1工作站,并使用perfusion 3软件包对扫描数据进行处理,计算出感兴趣区的时间密度曲线(time-density curve,TDC)和各灌注参数值,包括血流量(blood flow ,BF),血容量(blow volume, BV),对比剂平均通过时间(mean transit time, MTT)和表面渗透积乘积(permeability surface area product ,PS)。采用SPSS11.5软件包进行数据分析。对各组间肺部微循环灌注参数进行ANOVA分析(MTT、PS两组参数不符合正态分布,因此进行了对数转换),并采用LSD-t检验进行两两比较(如各组间方差不齐则采用校正Tamhane法)。
结果肺部微循环灌注参数BF、BV值在各组的总体均数有差别并有统计学意义(P =0.000和0.000)。失代偿期肝硬化组的肺部微循环灌注参数BF、BV值较正常对照组和代偿期肝硬化组都明显增加,组间差别有统计学意义(BF值:P =0.004和0.003;BV值:P =0.004和0.003)。而代偿期肝硬化组的肺部微循环灌注参数BF、BV值与正常对照组比较,还不能认为两组的组间差别有统计学意义(P =0.958和0.998)。
肺部微循环灌注参数MTT值由于不符合正态分布进行了对数转换,其各组的总体均数有差别并有统计学意义(P =0.023)。失代偿期肝硬化组的肺部微循环灌注参数MTT值较正常对照组和代偿期肝硬化组减少,组间差别有统计学意义(P =0.013和0.019)。
肺部微循环灌注参数PS值由于不符合正态分布进行了对数转换,还不能认为组间差别有统计学意义(P =0.337)。
结论1肝硬化时肺部微循环灌注参数BF、BV值升高,MTT值减低, PS值略升高。而且随着肝硬化程度的加重,CT各项灌注指标变化越来越明显。
2肝硬化时肺部微循环各灌注参数尤其BF、BV值的变化,可以在一定程度上反映肝硬化的病变程度。
3 MSCT肺部微循环灌注成像可获得肝硬化患者肺部微循环多项灌注参数,定量分析肝硬化患者肺部血流动力学变化,获得肺部功能学信息。
4 MSCT肺部微循环灌注成像为进一步探讨肝硬化时肺循环改变的演进规律提供了一种新的研究方法。
Purpose: To study perfusion parameters’change of pulmonary microvascular in different severity of liver cirrhosis with GE 16 slices spiral-CT.
Material and Method: Dynamic contrast-enhanced single-location sequences CT scans of the lung were obtained in 20 control subjects and 43 patients of hepatic cirrhosis (24 patients with compensated cirrhosis and 19 patients with decompensate cirrhosis). These data were processed on GE AW4.1 workstation using perfusion 3 software packages. The time-density curve (TDC) of region of interest and perfusion parameters of pulmonary microvascular such as blood flow ( BF),blood volume(BV),mean transit time(MTT)and permeability surface area product(PS)were calculated. Statistics treatment applied SPSS 11.5 software, and the result of perfusion parameters of pulmonary microvascular of each interclass took analysis of variance average (ANOVA) (two group parameters, MTT and PS, mismatched normal distribution,thus made logarithmic transformation), then the multiple comparisons was estimated using LSD test (adjusted Tamhane t test was made if heterogeneity of variance of interclass).
Results: BF、BV of the pulmonary microvascular’s perfusion parameters of three group had significant difference and had statistical significance(P =0.000 and 0.000). Compared to control group and compensated cirrhosis group, the BF and BV of decompensate cirrhosis group were significantly increased, and the difference of interclass had statistical significance(BF :P=0.004 and 0.003; BV: P =0.004 and 0.003). But compared to control group, the BF and BV of compensated cirrhosis group had not significant difference(P =0.958 and 0.998).
MTT of pulmonary microvascular’s perfusion parameters mismatched normal distribution,thus made logarithmic transformation,and the population mean of three group had significant difference (P =0.023 ) . Compared to control group and compensated cirrhosis group, the MTT of decompensate cirrhosis group were decreased, but the difference of interclass had statistical significance(P =0.013 and 0.019).
PS of pulmonary microvascular’s perfusion parameters mismatched normal distribution,thus made logarithmic transformation,and the difference of interclass had not statistical significance(P =0.337).
Conclusion: 1 The significantly increased of BF and BV, the decreased MTT, and the slightly increased of PS were observed in pulmonary microvascular’s perfusion parameters of three groups. In addition , the change of CT perfusion parameters was correlated to the degree of hepatic cirrhosis.
2 In hepatic cirrhosis, the change of pulmonary microvascular’s perfusion parameters,especially BF and BV, can reflect changed degree of liver cirrhosis at some extent.
3 MSCT perfusion imaging of the pulmonary microvascular can get many perfusion parameters of the pulmonary microvascular in liver cirrhosis, quantity analyze the change of the pulmonary microvascular, get information of pulmonary functionology.
4 MSCT perfusion imaging of the pulmonary microvascular provided a new research method for moving forward a single step to probe the rule of liver cirrhosis developing.
材料与方法选取20例正常对照者和43例肝硬化患者(24例代偿期肝硬化患者,19例失代偿期肝硬化患者)行16层螺旋CT肺部同层动态增强扫描。将数据传送到GE AW4.1工作站,并使用perfusion 3软件包对扫描数据进行处理,计算出感兴趣区的时间密度曲线(time-density curve,TDC)和各灌注参数值,包括血流量(blood flow ,BF),血容量(blow volume, BV),对比剂平均通过时间(mean transit time, MTT)和表面渗透积乘积(permeability surface area product ,PS)。采用SPSS11.5软件包进行数据分析。对各组间肺部微循环灌注参数进行ANOVA分析(MTT、PS两组参数不符合正态分布,因此进行了对数转换),并采用LSD-t检验进行两两比较(如各组间方差不齐则采用校正Tamhane法)。
结果肺部微循环灌注参数BF、BV值在各组的总体均数有差别并有统计学意义(P =0.000和0.000)。失代偿期肝硬化组的肺部微循环灌注参数BF、BV值较正常对照组和代偿期肝硬化组都明显增加,组间差别有统计学意义(BF值:P =0.004和0.003;BV值:P =0.004和0.003)。而代偿期肝硬化组的肺部微循环灌注参数BF、BV值与正常对照组比较,还不能认为两组的组间差别有统计学意义(P =0.958和0.998)。
肺部微循环灌注参数MTT值由于不符合正态分布进行了对数转换,其各组的总体均数有差别并有统计学意义(P =0.023)。失代偿期肝硬化组的肺部微循环灌注参数MTT值较正常对照组和代偿期肝硬化组减少,组间差别有统计学意义(P =0.013和0.019)。
肺部微循环灌注参数PS值由于不符合正态分布进行了对数转换,还不能认为组间差别有统计学意义(P =0.337)。
结论1肝硬化时肺部微循环灌注参数BF、BV值升高,MTT值减低, PS值略升高。而且随着肝硬化程度的加重,CT各项灌注指标变化越来越明显。
2肝硬化时肺部微循环各灌注参数尤其BF、BV值的变化,可以在一定程度上反映肝硬化的病变程度。
3 MSCT肺部微循环灌注成像可获得肝硬化患者肺部微循环多项灌注参数,定量分析肝硬化患者肺部血流动力学变化,获得肺部功能学信息。
4 MSCT肺部微循环灌注成像为进一步探讨肝硬化时肺循环改变的演进规律提供了一种新的研究方法。
Purpose: To study perfusion parameters’change of pulmonary microvascular in different severity of liver cirrhosis with GE 16 slices spiral-CT.
Material and Method: Dynamic contrast-enhanced single-location sequences CT scans of the lung were obtained in 20 control subjects and 43 patients of hepatic cirrhosis (24 patients with compensated cirrhosis and 19 patients with decompensate cirrhosis). These data were processed on GE AW4.1 workstation using perfusion 3 software packages. The time-density curve (TDC) of region of interest and perfusion parameters of pulmonary microvascular such as blood flow ( BF),blood volume(BV),mean transit time(MTT)and permeability surface area product(PS)were calculated. Statistics treatment applied SPSS 11.5 software, and the result of perfusion parameters of pulmonary microvascular of each interclass took analysis of variance average (ANOVA) (two group parameters, MTT and PS, mismatched normal distribution,thus made logarithmic transformation), then the multiple comparisons was estimated using LSD test (adjusted Tamhane t test was made if heterogeneity of variance of interclass).
Results: BF、BV of the pulmonary microvascular’s perfusion parameters of three group had significant difference and had statistical significance(P =0.000 and 0.000). Compared to control group and compensated cirrhosis group, the BF and BV of decompensate cirrhosis group were significantly increased, and the difference of interclass had statistical significance(BF :P=0.004 and 0.003; BV: P =0.004 and 0.003). But compared to control group, the BF and BV of compensated cirrhosis group had not significant difference(P =0.958 and 0.998).
MTT of pulmonary microvascular’s perfusion parameters mismatched normal distribution,thus made logarithmic transformation,and the population mean of three group had significant difference (P =0.023 ) . Compared to control group and compensated cirrhosis group, the MTT of decompensate cirrhosis group were decreased, but the difference of interclass had statistical significance(P =0.013 and 0.019).
PS of pulmonary microvascular’s perfusion parameters mismatched normal distribution,thus made logarithmic transformation,and the difference of interclass had not statistical significance(P =0.337).
Conclusion: 1 The significantly increased of BF and BV, the decreased MTT, and the slightly increased of PS were observed in pulmonary microvascular’s perfusion parameters of three groups. In addition , the change of CT perfusion parameters was correlated to the degree of hepatic cirrhosis.
2 In hepatic cirrhosis, the change of pulmonary microvascular’s perfusion parameters,especially BF and BV, can reflect changed degree of liver cirrhosis at some extent.
3 MSCT perfusion imaging of the pulmonary microvascular can get many perfusion parameters of the pulmonary microvascular in liver cirrhosis, quantity analyze the change of the pulmonary microvascular, get information of pulmonary functionology.
4 MSCT perfusion imaging of the pulmonary microvascular provided a new research method for moving forward a single step to probe the rule of liver cirrhosis developing.
引文
[1] Won C, Chon D, Tajik J, et al.CT-based assessment of regional pulmonary microvascular blood flow parameters. J Appl Physiol. 2003,94(6):2483-2493
[2] Fallon MB. Mechanisms of Pulmonary Vascular Complications of Liver Disease: Hepatopulmonary Syndrome. J Clin Gastroenterol,2005,39(4): 138-142
[3] Axel L. Cerebral blood flow determination by rapid-sequence computed tomography: theoretical analysis. Radiology, 1980, 137(3): 679-686
[4] Lee TY. Functional CT: physiological models. Trends in Biotechnology, 2002, 20 (8): 3-10
[5] Krowka MJ, Wiseman GA, Burnett OL,et al. Hepatopulmonary Syndrome:A Prospective Study of Relationships Between Severity of Liver Disease, PaO2 Response to 100% Oxygen, and Brain Uptake After 99mTc MAA Lung Scanning. Chest, 2000,118:615-624
[6] Rodriguez-Roisin R, Krowka MJ, Herve P, et al. Pulmonary-Hepatic vascular Disorders (PHD). Eur Respir J,2004,24(5):861-880
[7] Umeda A,Tagawa M,Kohsaka T,et al. Hepatopulmonary syndrome can show spontaneous resolution: Possible mechanism of portopulmonary hypertension overlap? Respirology, 2006, 11(1):120-123
[8] Wong, F. Portopulmonary hypertension in cirrhosis: the pathogenetic challenge. Gut, 2005,54(2): 309
[9] Kerr R, Stirling D, Ludlam CA. Interleukin 6 and haemostasis. Br J Haematol, 2001,115:3–12
[10] Streetz KL, Tacke F, Leifeld L, et al. Interleukin 6/gp130-dependent pathways are protective during chronic liver diseases. Hepatology, 2003,38:218–229
[11] K?ksal D, Ka?ar S, K?ksal AS, et al. Evaluation of Intrapulmonary Vascular Dilatations With High-Resolution Computed Thorax Tomography in Patients With Hepatopulmonary Syndrome. J Clin Gastroenterol, 2006,40(1):77–83
[12] Hoffman EA, Chon D. Computed Tomography Studies of Lung Ventilation and Perfusion . Proc Am Thorac Soc,2005,2(6):492-498
[1] Fallon MB. Mechanisms of Pulmonary Vascular Complications of Liver Disease: Hepatopulmonary Syndrome. J Clin Gastroenterol,2005,39(4): 138-142
[2] Krowka MJ, Wiseman GA, Burnett OL,et al. Hepatopulmonary Syndrome:A Prospective Study of Relationships Between Severity of Liver Disease, PaO2 Response to 100% Oxygen, and Brain Uptake After 99mTc MAA Lung Scanning. Chest, 2000,118:615-624
[3] Rodriguez-Roisin R, Krowka MJ, Herve P, et al. Pulmonary-Hepatic vascular Disorders (PHD). Eur Respir J,2004,24(5):861-880
[4] Lee KN, Yoon SK, Lee JW, et al. Hepatopulmonary Syndrome Induced by Common Bile Duct Ligation in a Rabbit Model: Correlation between Pulmonary Vascular Dilatation on Thin-Section CT and Angiography and Serum Nitrite Concentration or Endothelial Nitric Oxide Synthase (eNOS) Expression. Korean J Radiol, 2004, 5:149-156
[5] Luo B, Liu L, Tang L, et al. ET-1 and TNF-a in HPS: analysis in prehepatic portal hypertension and biliary and nonbiliary cirrhosis in rats. Am J Physiol Gastrointest Liver Physiol, 2004, 286: 294-303
[6] Sztrymf B, Libert JM, Mougeot C, et al. Cirrhotic rats with bacterial translocation have higher incidence and severity of hepatopulmonary syndrome. J Gastroenterol Hepatol, 2005,20(10):1538-1544
[7] Umeda A,Tagawa M,Kohsaka T,et al. Hepatopulmonary syndrome can show spontaneous resolution: Possible mechanism of portopulmonary hypertension overlap? Respirology, 2006, 11(1):120-123
[8]Wong, F. Portopulmonary hypertension in cirrhosis: the pathogenetic challenge. Gut, 2005,54(2): 309
[9] Kerr R, Stirling D, Ludlam CA. Interleukin 6 and haemostasis. Br J Haematol, 2001,115:3–12
[10] Streetz KL, Tacke F, Leifeld L, et al. Interleukin 6/gp130-dependent pathways are protective during chronic liver diseases. Hepatology, 2003,38:218–229
[11] Samyn M,Bourgois A, Bansal S, et al. Hepatopulmonary syndrome in children: A single centre experience. J Pediatr Gastroenterol Nutr., 2004,39(Suppl 1):199-200
[12] Chevallier P, Novelli L, Motamedi JP, et al. Hepatopulmonary Syndrome Successfully Treated with Transjugular Intrahepatic Portosystemic Shunt: A Three-year Follow-up. J Vasc Interv Radiol, 2004, 15(6):647-648
[13] Tumgor G, Arikan C, Yuksekkaya HA, et al. Childhood cirrhosis, Hepatopulmonary syndrome and liver transplantation: PH1-12. J Pediatr Gastroenterol Nutr, 2005,40(5): 673
[14] Lima BLG, Fran?a AVC, Pazin-Filho A,et al. Frequency, Clinical Characteristics, andRespiratory Parameters of Hepatopulmonary Syndrome. Mayo Clin Proc, 2004, 79(1): 42-48
[15] Koksal D, Kacar S, Koksal AS, et al. Evaluation of Intrapulmonary Vascular Dilatations With High-Resolution Computed Thorax Tomography in Patients With Hepatopulmonary Syndrome. J Clin Gastroenterol, 2006,40(1):77–83
[16] Pavarino PR,Corbucci HAR,Marchi CH,et al. Contrast Echocardiography in the Diagnosis of Intrapulmonary Vascular Dilations in Candidates for Liver Transplantation. Arq Bras Cardiol, 2004, 82(6):519-522
[17] Fernandes A P, Marum S, Ribeiro JP. Hepatopulmonary syndrome as a cause of persistent hypoxaemia. Heart, 2005,91(11):1441
[18] Wesenberg KJ, Lewinsohn D. Hepatopulmonary syndrome unmasked by interstitial pneumonitis. Chest , 2003,124(4 Supple):261
[19] Malagari K, Nikita A, Alexopoulou E,et al. Cirrhosis-related intrathoracic disease, Imaging features in 1038 patients. Hepatogastroenterology, 2005,52(62):558-562
[20] Nagasawa K, Takahashi K, Furuse M, et al. Imaging findings of pulmonary vascular disorders in portal hypertension. Nippon Igaku Hoshasen Gakkai Zasshi, 2004, 64(5): 294-299
[21] Seddon BM,Workman P. The role of functional and molecular imaging in cancer drug discovery and development. Br J Radiol,2003, 76: 128-138
[22] Won C, Chon D, Tajik J, et al.CT-based assessment of regional pulmonary microvascular blood flow parameters. J Appl Physiol. 2003,94(6):2483-2493
[23] Hoffman EA, Chon D. Computed Tomography Studies of Lung Ventilation and Perfusion . Proc Am Thorac Soc,2005,2(6):492-498
[2] Fallon MB. Mechanisms of Pulmonary Vascular Complications of Liver Disease: Hepatopulmonary Syndrome. J Clin Gastroenterol,2005,39(4): 138-142
[3] Axel L. Cerebral blood flow determination by rapid-sequence computed tomography: theoretical analysis. Radiology, 1980, 137(3): 679-686
[4] Lee TY. Functional CT: physiological models. Trends in Biotechnology, 2002, 20 (8): 3-10
[5] Krowka MJ, Wiseman GA, Burnett OL,et al. Hepatopulmonary Syndrome:A Prospective Study of Relationships Between Severity of Liver Disease, PaO2 Response to 100% Oxygen, and Brain Uptake After 99mTc MAA Lung Scanning. Chest, 2000,118:615-624
[6] Rodriguez-Roisin R, Krowka MJ, Herve P, et al. Pulmonary-Hepatic vascular Disorders (PHD). Eur Respir J,2004,24(5):861-880
[7] Umeda A,Tagawa M,Kohsaka T,et al. Hepatopulmonary syndrome can show spontaneous resolution: Possible mechanism of portopulmonary hypertension overlap? Respirology, 2006, 11(1):120-123
[8] Wong, F. Portopulmonary hypertension in cirrhosis: the pathogenetic challenge. Gut, 2005,54(2): 309
[9] Kerr R, Stirling D, Ludlam CA. Interleukin 6 and haemostasis. Br J Haematol, 2001,115:3–12
[10] Streetz KL, Tacke F, Leifeld L, et al. Interleukin 6/gp130-dependent pathways are protective during chronic liver diseases. Hepatology, 2003,38:218–229
[11] K?ksal D, Ka?ar S, K?ksal AS, et al. Evaluation of Intrapulmonary Vascular Dilatations With High-Resolution Computed Thorax Tomography in Patients With Hepatopulmonary Syndrome. J Clin Gastroenterol, 2006,40(1):77–83
[12] Hoffman EA, Chon D. Computed Tomography Studies of Lung Ventilation and Perfusion . Proc Am Thorac Soc,2005,2(6):492-498
[1] Fallon MB. Mechanisms of Pulmonary Vascular Complications of Liver Disease: Hepatopulmonary Syndrome. J Clin Gastroenterol,2005,39(4): 138-142
[2] Krowka MJ, Wiseman GA, Burnett OL,et al. Hepatopulmonary Syndrome:A Prospective Study of Relationships Between Severity of Liver Disease, PaO2 Response to 100% Oxygen, and Brain Uptake After 99mTc MAA Lung Scanning. Chest, 2000,118:615-624
[3] Rodriguez-Roisin R, Krowka MJ, Herve P, et al. Pulmonary-Hepatic vascular Disorders (PHD). Eur Respir J,2004,24(5):861-880
[4] Lee KN, Yoon SK, Lee JW, et al. Hepatopulmonary Syndrome Induced by Common Bile Duct Ligation in a Rabbit Model: Correlation between Pulmonary Vascular Dilatation on Thin-Section CT and Angiography and Serum Nitrite Concentration or Endothelial Nitric Oxide Synthase (eNOS) Expression. Korean J Radiol, 2004, 5:149-156
[5] Luo B, Liu L, Tang L, et al. ET-1 and TNF-a in HPS: analysis in prehepatic portal hypertension and biliary and nonbiliary cirrhosis in rats. Am J Physiol Gastrointest Liver Physiol, 2004, 286: 294-303
[6] Sztrymf B, Libert JM, Mougeot C, et al. Cirrhotic rats with bacterial translocation have higher incidence and severity of hepatopulmonary syndrome. J Gastroenterol Hepatol, 2005,20(10):1538-1544
[7] Umeda A,Tagawa M,Kohsaka T,et al. Hepatopulmonary syndrome can show spontaneous resolution: Possible mechanism of portopulmonary hypertension overlap? Respirology, 2006, 11(1):120-123
[8]Wong, F. Portopulmonary hypertension in cirrhosis: the pathogenetic challenge. Gut, 2005,54(2): 309
[9] Kerr R, Stirling D, Ludlam CA. Interleukin 6 and haemostasis. Br J Haematol, 2001,115:3–12
[10] Streetz KL, Tacke F, Leifeld L, et al. Interleukin 6/gp130-dependent pathways are protective during chronic liver diseases. Hepatology, 2003,38:218–229
[11] Samyn M,Bourgois A, Bansal S, et al. Hepatopulmonary syndrome in children: A single centre experience. J Pediatr Gastroenterol Nutr., 2004,39(Suppl 1):199-200
[12] Chevallier P, Novelli L, Motamedi JP, et al. Hepatopulmonary Syndrome Successfully Treated with Transjugular Intrahepatic Portosystemic Shunt: A Three-year Follow-up. J Vasc Interv Radiol, 2004, 15(6):647-648
[13] Tumgor G, Arikan C, Yuksekkaya HA, et al. Childhood cirrhosis, Hepatopulmonary syndrome and liver transplantation: PH1-12. J Pediatr Gastroenterol Nutr, 2005,40(5): 673
[14] Lima BLG, Fran?a AVC, Pazin-Filho A,et al. Frequency, Clinical Characteristics, andRespiratory Parameters of Hepatopulmonary Syndrome. Mayo Clin Proc, 2004, 79(1): 42-48
[15] Koksal D, Kacar S, Koksal AS, et al. Evaluation of Intrapulmonary Vascular Dilatations With High-Resolution Computed Thorax Tomography in Patients With Hepatopulmonary Syndrome. J Clin Gastroenterol, 2006,40(1):77–83
[16] Pavarino PR,Corbucci HAR,Marchi CH,et al. Contrast Echocardiography in the Diagnosis of Intrapulmonary Vascular Dilations in Candidates for Liver Transplantation. Arq Bras Cardiol, 2004, 82(6):519-522
[17] Fernandes A P, Marum S, Ribeiro JP. Hepatopulmonary syndrome as a cause of persistent hypoxaemia. Heart, 2005,91(11):1441
[18] Wesenberg KJ, Lewinsohn D. Hepatopulmonary syndrome unmasked by interstitial pneumonitis. Chest , 2003,124(4 Supple):261
[19] Malagari K, Nikita A, Alexopoulou E,et al. Cirrhosis-related intrathoracic disease, Imaging features in 1038 patients. Hepatogastroenterology, 2005,52(62):558-562
[20] Nagasawa K, Takahashi K, Furuse M, et al. Imaging findings of pulmonary vascular disorders in portal hypertension. Nippon Igaku Hoshasen Gakkai Zasshi, 2004, 64(5): 294-299
[21] Seddon BM,Workman P. The role of functional and molecular imaging in cancer drug discovery and development. Br J Radiol,2003, 76: 128-138
[22] Won C, Chon D, Tajik J, et al.CT-based assessment of regional pulmonary microvascular blood flow parameters. J Appl Physiol. 2003,94(6):2483-2493
[23] Hoffman EA, Chon D. Computed Tomography Studies of Lung Ventilation and Perfusion . Proc Am Thorac Soc,2005,2(6):492-498