超声二维斑点追踪成像技术评价早期肝硬化患者心室纵向收缩功能
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摘要
第一部分
     超声二维斑点追踪成像技术评价早期肝硬化患者左室纵向收缩功能
     目的:应用超声二维斑点追踪成像技术( two-dimensional speckle tracking imaging ,2D-STI)评价早期肝硬化患者左室局部纵向收缩功能.方法:选取34例早期肝硬化患者作为实验组, 35例健康志愿者作为对照组。常规超声心动图记录左房及左室舒张末期前后径、射血分数(EF)、左室短轴缩短率(FS);心尖长轴切面记录二尖瓣舒张期血流频谱E峰及A峰值,并计算E/A值;记录心尖长轴切面、心尖两腔切面及心尖四腔切面的三个完整心动周期的高帧频二维图像,脱机应用二维应变分析软件测量左室壁各节段收缩期的峰值应变。
     结果:肝硬化组左房收缩期前后径(30.49±4.20mm)、左室舒张末期前后径(44.90±4.33mm)与对照组前后径(28.82±3.67mm,43.25±3.21mm)相比差异无统计学意义(P >0.05)。肝硬化组EF(61.15±4.41%)及FS(32.92±3.34%)与对照组(59.74±5.45% ,32.05±3.71%)比较差异不具有统计学意义(P >0.05)。肝硬化组E/A值(1.03±0.29)较对照组(1.31±2.74)减低,差异具有统计学意义(P <0.05)。肝硬化组左室各节段收缩期纵向峰值应变均低于对照组,除左室后壁基底段、下壁基底段、前壁基底段、前间隔基底段及后间隔中间段和基底段外其他各节段间差异均具有统计学意义(P<0.05)。
     结论:早期肝硬化患者左室舒张功能及左室局部纵向收缩功能均存在异常,利用2D-STI可以较常规超声检查能更早期敏感地反映肝硬化患者左室局部纵向收缩功能改变。
     第二部分
     超声二维斑点追踪成像技术评价早期肝硬化患者右室纵向收缩功能
     目的:应用超声二维应变技术(Speckle Tracking Echocardiograohy)评价早期肝硬化患者右室纵向收缩功能。
     方法:选取34例早期肝硬化患者作为实验组, 35例健康志愿者作为对照组。常规超声心动图心尖四腔切面记录右室及有房舒张末期横径。记录心尖四腔切面的三个完整心动周期的高帧频二维图像,应用二维应变分析软件测量右室游离壁三个节段收缩期的峰值应变(ε),应变率(SRs)及速度(Vs)。测量右室游离壁舒张早期峰值应变率(SRe)和速度(Ve),舒张晚期峰值应变率(SRa)和速度(Va)。
     结果:肝硬化组右房舒张期横径较对照组增大,差异具有统计学意义(P<0.05)。肝硬化组右室舒张末期横径较对照组增大,差异不具有统计学意义(P>0.05)。肝硬化组右室游离壁三个节段的收缩期峰值应变及应变率、舒张早期峰值应变率及舒张晚期峰值应变率较对照组明显减低(P<0.05),肝硬化组右室基底段及中间段收缩期峰值及舒张早期峰值速度较对照组减低,差异具有统计学意义(P<0.005),右室心尖段收缩期峰值速度、舒张早期峰值速度及舒张晚期峰值速度较对照组减低,差异不具有统计学意义(P>0.05)。
     结论:超声二维应变技术可以快速准确的评价肝硬化患者右心功能,提示临床医生诊断和治疗肝硬化性心肌病以改善肝硬化病人预后情况。
Part 1:
     Evaluation of Left Ventricular longitudinal shrinkage Function in Patients with early liver cirrhosis Using two-dimensional speckle tracking imaging
     Objective To assess the left ventricular longitudinal shrinkage function in patients with liver cirrhosis with two-dimensional speckle tracking imaging(2D-STI). Methods Echocardiography and Doppler echocardiography were obtained in 34 patients with hepatic cirrhosis and 35 normal persons of corresponding ages underwent .And high frame rate two-dimensional images were recorded from apical long-axis view,four-chamber view and two-chamber view of left ventricle ,then measuring the left ventricular diameter,left atrium diameter,the peak filling velocity of E wave and A wave,E /A ratio ,EF and FS. The peak systolic strain of left ventricular segment were measured using two-dimensional strain software. Results Compared with healthy subjects,left ventricular diameter,left atrium diameter,EF and FS of hepatic cirrhosis patients were not different(P>0.05) ,but the E /A ratio of hepatic cirrhosis was lower (P<0.05),and the peak systolic strain of most left ventricular segment reduced in hepatic cirrhosis were statistically lower (P<0.05), except base segment of each wall and middle segment of back interventricular septum .
     Conclusions The heart shape ,systolic and diastole function of hepatic cirrhosis were abnormal. Using the 2D-STI can early and accurately evaluate the systolic function of hepatic cirrhosis.
     Part 2:
     Evaluation of Right Ventricular longitudinal shrinkage
     Function in Patients with early liver cirrhosis Using two-dimensional speckle tracking imaging
     Objective To assess the right ventricular longitudinal shrinkage function in patients with liver cirrhosis with Speckle Tracking Echocardiograohy.
     Methods Echocardiography was obtained in 34 patients with hepatic cirrhosis and 35 normal persons of corresponding ages underwent . And high frame rate two-dimensional images were recorded from four-chamber view of left ventricle, then measuring the right ventricular and atrium diameter. The peak strain、strain rate and velocity of right ventricular free wall each segment in systolic、early diastole and during atrial contraction were measured using two-dimensional strain software.
     Results Compared with healthy subjects,right atrium diameter of hepatic cirrhosis patients was statistically augmentation (P<0.05). Peak systolic strain , strain rate and peak strain rate in early diastole and during atrial contraction of all segments in right ventricular free wall reduced significantly in cirrhosis patients when compared with the contrast people (P<0.05). Peak systolic velocity and velocity in early diastole and during atrial contraction of the middle and base segments in right ventricular were reduced significantly when compared with the contrast people (P<0.05). Although Peak systolic velocity and velocity in early diastole and during atrial contraction of the apex segments in right ventricular were not different (P>0.05).
     Conclusions 2D-STI can evaluate the right ventricular function of hepatic cirrhosis patients early and accurately . It can call attention to diagnosis and cure cirrhotic cardiomyopathy then improved the prognosis of hepatic cirrhosis patients.
引文
[1] Baik SK ,Fouad TR ,Lee SS. Cirrhotic cardiomyopathy[J] . Orphanet J Rare Dis , 2007 ,3 (2) :1172-1186.
    [2]孟庆国,尹立雪,李春梅,等。超声斑点成像技术评价左心室长轴心肌节段应变与位移。中华超声影像学杂志,2006 ,15 :721-724。
    [3] Ma Z. Cirrhotic cardiomopathy : Getting to the heart of the matter, Hepatology, 1996, 24(2):451-459.
    [4] Lee SS , Myers RP ,et a1.Liver Transpl: official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society,2000 Jul ,6 (4 Suppl 1) :S44-52.
    [5]李瑞珍罗卓琼周平,等。彩色多普勒超声对肝硬化体循环血流动力学变化的评价。中国超声医学杂志,2002,18(4):246-248
    [6]王爱鱼,候培珍,高军。肝硬化所致心脏损害:附96例尸解分析[ J]。中华消化杂志, 1998, 18( 3) : 184。
    [7] Hashimoto I ,Li X ,Hemadi Bhat A ,et al . Myocardial strain rate is a superior method for evaluation of left ventricular subendocardial function compared with tissue Doppler imaging. J Am Coll Cardiol, 2003,42 :1574-1583.
    [8] Sutherland GR,Di Salvo G, Claus P, et al . Strain and strain rate imaging :a new clinical approach to quantifying regional myocardial function. J Am Soc Echocardiogr,2004 ,17 :788-802.
    [9]姜志荣,李大海,张小花。应变率显像评价高血压患者左室功能。中国医学影像技术,2006 ,22 :244-247。
    [10]余芬,邓又斌.二维超声应变成像的临床应用。中华超声影像学杂志,2007,6(3) :269-271。
    
    [1] Baik SK , Fouad TR ,Lee SS. Cirrhotic cardiomyopathy[J] . Orphanet J Rare Dis , 2007 ,3 (2) :1172-1186.
    [2] Ma Z. Cirrhotic cardiomopathy : Getting to the heart of the matter Hepatology,1996,24(2):451-459.
    [3] Grosmann RJ.Hyerdynannc circulation of liver disease 40 year later:patholysiology and clinical consequences.Hepatology,1994,20:1359.
    [4]杨颖,陈峰,张宝娓,等.二维应变对左心室整体应变与应变率的研究[J],中国医学影像技术,2006 ,22 (7) :1018-1020.
    [5] Azoulay D , Castaing D ,Dennison A , et al . Transjugular intrahepatic po-rtosystemic shunt worsens the hyperdynamic circulatory state of the irrh-otic patient :preliminary report of a prospective study[J ] . Hepatology,1994 ,19 (2) :129-132.
    [6]苏军芳,张军,张海滨,等。正常中老年人心室壁应变率及应变成像的临床研究[J],中国医学影像技术,2006 ,22 (5) :705-707.
    [7]余芬,邓又斌.二维超声应变成像的临床应用.中华超声影像学杂志,2007 ,16(3): 269-271.
    [8] Amundsen BH , Helle Valle T , Edvardsen T , et al1 Noninvasive myocardial strain measurement by speckle t racking echocardiography : validation against sonomicrometry and tagged magnetic resonance imaging[J ]1J Am Coll Cardiol ,2006 ,47 (4) :789-793.
    [9]徐希岳,王启之,吴炎,等.肝硬化时右心功能的变化.临床消化病杂志,2000,12(1):35-37
    [10]米润昭.肝肺综合症.国外医学流行病学传染病学分册.1995,22(1):16.
    [1] Kowalski HJ, Abelmann WH. The cardiac output at rest in Laennec cirrhosis. J Clin Invest 1953;32:1025–1033
    [2] Laffi G, Barletta G, La Villa G, Del Bene R, Riccardi D, Ticali P, et al. Altered cardiovascular responsiveness to active tilting in nonalcoholic cirrhosis. Gastroenterology 1997;113:891–898
    [3] Moreau R, Hadengue A, Soupison T, Mechin G, Assous M, Roche-Sicot J, et al. Abnormal pressor response to vasopressin in patients with cirrhosis: evidence for impaired buffering mechanism. Hepatology 1990;12:7–12
    [4] Wong F, Liu P, Lilly L, Bomzon A, Blendis L. The role of cardiac structural and functional abnormalities in the pathogenesis of hyperdynamic circulation and renal sodium retention in cirrhosis. Clin Sci 1999;97:259–267
    [5] Pozzi M, Carugo S, Boari G, Pecci V, de Ceglia S, Maggiolini S,et al. Functional and structural cardiac abnormalities in cirrhotic patients with and without ascites.Hepatology 1997;26:1131–1137
    [6] Finucci G, Desideri A, Sacerdoti D, Bolognesi M, Merkel C, Angeli P, et al. Left ventricular diastolic dysfunction in liver cirrhosis. Scan J Gastroenterol 1996;31:279–284
    [7]Bernardi M, Calandra S, Colantoni A, Trevisani F, Raimondo ML, Sica G, et al. QT interval prolongation in cirrhosis: prevalence, relationship with severity, and etiology of the disease and possible pathogenetic factors. Hepatology 1998;27:28–34
    [8]Lee SS. Cardiac abnormalities in liver cirrhosis. West J Med 1989;151:530–539
    [9]Caramelo C, Fernandez-Munoz D, Santos JC, Blanchart A,Rodriguez-Puyol D, Lo′pez-Novoa JM, et al. Effect of volume expansion on hemodynamics, capillary permeability and renal function in conscious, cirrhotic rats. Hepatology 1986;6:129–134
    [10]Castro A, Jimenez W, Claria J, Ros J, Martinez JM, Bosch M, et al. Impaired responsiveness to angiotensin-II in experimental cirrhosis: role of nitric oxide.Hepatology 1993;18:367–372
    [11]Grose RD, Nolan J, Dillon JF, Errington M, Hannan WJ, Bouchier IAD, et al. Exercise-induced left ventricular dysfunction in alcoholic and non-alcoholic cirrhosis. J Hepatology 1995;22:326–332
    [12]Lunzer MR, Newman SP, Bernard AG, Manghani KK, Sherlock SP, Ginsburg J. Impaired cardiovascular responsiveness in liver disease. Lancet 1975;2:382–385
    [13]Bernardi M, Rubboli A, Trevisani F, Cancellieri C, Ligabue A,Baraldini M, et al. Reduced cardiovascular responsiveness to exercise-induced sympathoadrenergic stimulation in patients with cirrhosis. J Hepatol 1991;12:207–216
    [14]Henriksen JH, Fuglsang S, Bendtsen F, Christensen E, Moller S.Dyssynchronous electrical and mechanical systole in patients with cirrhosis. J Hepatol 2002;36:513–520
    [15]Henriksen JH, Gotze JP, Fuglsang S, Christensen E, Bendtsen F,Moller S. Increased circulating pro-brain natriuretic peptide (proBNP) and brain natriuretic peptide (BNP) in patients with cirrhosis: relation to cardiovascular dysfunction and severity of disease. Gut 2003;52:1511–1517
    [16]La Villa G, Romanelli RG, Casini Raggi V, Tosti-Guerra C, De Feo ML, Marra F, et al. Plasma levels of brain natriuretic peptide in patients with cirrhosis. Hepatology 1992;16:156–161
    [17]Yildiz R,YildirimB, KarincaogluM,HarputluogluM,Hilmioglu F. Brain natriuretic peptide and severity of disease in non-alcoholic cirrhotic patients. J Gastroenterol Hepatol 2005;20:1115–1120
    [18]Bodor GS, Porter S, Landt Y, Ladenson JH. Development of monoclonal antibodies for an assay of cardiac troponin-I and preliminary results in suspected cases of myocardial infarction. Clin Chem 1992;38:2203–2214
    [19]Pateron D, Beyne P, Laperche T, Logeard D, Lefilliatre P, Sogni P, et al. Elevated circulating cardiac troponin I in patients with cirrhosis. Hepatology 1999;29:640–643
    [20]Guevara M, Gines P, Jimenez W, Sort P, Fernandez-Esparrach G, Escorsell A, et al. Increased adrenomedullin levels in cirrhosis: relationship with hemodynamic abnormalities and vasoconstrictor systems. Gastroenterology 1998;114:336–343
    [21]Jougasaki M, Wei CM, McKinley LJ, Burnett JCJ. Elevation of circulating and ventricular adrenomedullin in human congestive heart failure. Circulation 1995;92:286–289
    [22]Hirano S, Imamura T, Matsuo T, Ishiyama Y, Kato J, Kitamura K, et al. Differential responses of circulating and tissue adrenomedullin and gene expression to volume overload. J Card Fail 2000;6:120–129
    [23]Parkes DG. Cardiovascular actions of adrenomedullin in conscious sheep. Am J Physiol 1995;268:H2574–H2578
    [24]Ikenouchi H, Kangawa K, Matsuo H, Hirata Y. Negative inotropic effects of adrenomedullin in isolated adult rabbit cardiac ventricular myocytes. Circulation 1997;95:2318–2324
    [25]Pan CS, Jin SJ, Cao CQ, Zhao J, Zhang J, Wang X, et al. The myocardial response to adrenomedullin involves increased cAMP generation as well as augmented Akt phosphorylation. Peptides 2007;28:900–909
    [26]Ishimitsu T, Ono H, Minami J, Matsuoka H. Pathophysiologic and therapeutic implications of adrenomedullin in cardiovascular disorders. Pharmacol Ther 2006;111:909–927
    [27]M?ller S, Henriksen JH. Cardiovascular complications of cirrhosis. Gut 2008;57:268–278
    [28]Alqahtani SA, Fouad TR, Lee SS. Cirrhotic cardiomyopathy Sem Liver Dis 2008;28:59–69
    [29]Ma Z, Lee SS, Meddings JB. Effects of altered cardiac membrane fluidity on beta-adrenergic receptor signalling in rats with cirrhotic cardiomyopathy. J Hepatol 1997;26:904–912
    [30]Caraceni P, Domenicali M, Bernardi M. The endocannabinoid system and liver diseases. J Neuroendocrinol 2008;20(Suppl 1):47–52
    [31]Gaskari SE, Liu H, Moezi L, Li Y, Baik SK, Lee SS. Role of endocannabinoids in the pathogenesis of cirrhotic cardiomyopathy in bile duct ligated rats. Br J Pharmacol 2005;146:315–323
    [32]Batkai S, Mukhopadhyay P, Harvey-White J, Kekrid R, Pacher P, Kunos G. Endocannabinoids acting at CB1 receptors mediate the cardiac contractiledysfunction in vivo in cirrhotic rats. Am J Physiol Heart Circ Physiol 2007;293:H1689–H1695
    [33]Liu H, Ma Z, Lee SS. Contribution of nitric oxide to the pathogenesis of cirrhotic cardiomyopathy in bile duct-ligated rats. Gastroenterology 2000;118:937–944
    [34]Liu H, Song D, Lee SS. Role of heme oxygenase-carbon monoxide pathway in pathogenesis of cirrhotic cardiomyopathy in the rat. Am J Physiol Gastrointest Liver Physiol 2001;280:G68–G74
    [35]Liu H, Lee SS. Nuclear factor-kappaB inhibition improves myocardial contractility in rats with cirrhotic cardiomyopathy. Liver Int 2008;28:640–648
    [36]Piper RD. Myocardial dysfunction in sepsis. Clin Exp Pharmacol Physiol 1998;25:951–954
    [37]Lunseth JH, Olmstead EG, Abboud F. A study of heart disease in one hundred eight hospitalized patients dying with portal cirrhosis.Arch Intern Med 1958;102:405–413
    [38]Meggs LG, Ben-Ari J, Gammon D, Goodman AI. Myocardial hypertrophy: the effects of sodium and the role of sympatheticnervous activity. Am J Hypertens 1988;1:1–11
    [39]Leenen FHH, Yuan B. Dietary-sodium-induced cardiac remodelingin spontaneously hypertensive rat versus Wistar-Kyoto rat. J Hypertens 1998;16:885–892
    [40]Weber KT, Sun Y, Tyagi SC, Cleutjens JP. Collagen network of the myocardium: function, structural remodeling and regulatory mechanisms. J Mol Cell Cardiol 1994;26:279–292
    [41]Van Wamel AJ, Ruwhof C, van der Valk-Kokshoom LE, Schrier PI, van der Laarse A. The role of angiotensin II endothelin-1 and transforming growth factor-beta as autocrine/paracrine mediators of stretch-induced cardiomyocyte hypertrophy. Mol Cell Biochem 2001;218:113–124
    [42]Yamazaki T, Komuro I, Kudoh S, Zou Y, Shiojima I, Hiroi Y, et al. Endothelin-1 is involved in mechanical stress-induced cardiomyocyte hypertrophy. J Biol Chem 1996;271:3221–3228
    [43]Schmieder RE. Salt intake is related to the process of myocardial hypertrophy in essential hypertension. JAMA 1989;262:1187–1188
    [44]Raizada V, Skipper B, Luo W, Griffith J. Intracardiac and intrarenal renin-angiotensin systems: mechanisms of cardiovascular and renal effects. J Investig Med 2007;55:341–359
    [45]Dostal DE, Hunt RA, Kule CE, Bhat GJ, Karoor V, McWhinney CD, et al. Molecular mechanisms of angiotensin II in modulating cardiac function: intracardiac effects and signal transduction pathways. J Mol Cell Cardiol 1997;29:2893–2902
    [46]Booz GW, Dostal DE, Baker KM. Paracrine actions of cardiac fibroblasts on cardiomyocytes: implications for the cardiac reninangiotensin system. Am J Cardiol 1999;83:44H–47H
    [47]Zierhut W, Zimmer HG. Significance of myocardial a- and b-adrenoreceptors in catecholamine induced cardiac hypertrophy. Circ Res 1989;65:1417–1425
    [48]Ward CA, Ma Z, Lee SS, Giles WR. Potassium currents in atrial and ventricular myocytes from a rat model of cirrhosis. Am J Physiol 1997;273:G537–G544
    [49]Lin RS, Lee FY, Lee SD, Tsai YT, Lin HC, Lu RH, et al. Endotoxemia in patients with chronic liver diseases: relationship to severity of liver diseases, presence of esophageal varices, and hyperdynamic circulation. J Hepatol 1995;22:165–172
    [50]Magyar J, Iost N, Kortvely A, Banyasz T, Virag L, Szigligeti P, et al. Effects of endothelin-1 on calcium and potassium currents in undiseased human ventricular myocytes. Pflugers Arch 2000;441: 144–149
    [51]Kuddus RH, Nalesnik MA, Subbotin VM, Rao AS, Gandhi CR. Enhanced synthesis and reduced metabolism of endothelin-1 (ET-1) by hepatocytes—an important mechanism of increased endogenous levels of ET-1 in liver cirrhosis. J Hepatol 2000;33:725–732
    [52]Gazawi H, Ljubuncic P, Cogan U, Hochgraff E, Ben-Shachar D, Bomzon A. The effects of bile acids on beta-adrenoceptors, fluidity, and the extent of lipid peroxidation in rat cardiac membranes. Biochem Pharmacol 2000;59:1623–1628
    [54]胡望月,孙晓枫,何家春等,肝硬化患者心脏结构和功能的超声改变及其与肝功能的关系,临床消化病杂志,2005,17(6):286-288
    [55]张洁,黄灿亮,刘新娟等,高排低阻型血流动力学改变对肝硬化患者的心功能影响,天津医药,2002,9(30):558-559
    [56]李瑞珍,罗卓琼,周平,等,彩色多普勒超声对肝硬化体循环血流动力学变化的评价,中国超声医学杂志,2002,18(4):246-248
    [57]彭敏霞,郑笑娟,史小龙等,组织速度成像技术评价肝硬化患者心功能,中国超声诊断杂志,2005,6(8):589-592
    [58]金蓉,柴云生,贾国英,等,声学密度定量分析技术(AD)在心肌梗塞中的临床应用.中国超声诊断杂志,2002 ,3(6) :419
    [59]杨晓英王润兰张静,应用AD技术评价晚期肝硬化患者心肌改变,中国医学影像杂志,2005,13(5):375-377
    [60]张玉奇,陈宝树,多普勒超声Tei指数估测心功能的研究[J ],国外医学:儿科学分册, 2003 , 30 (2) : 57-59。
    [61]王润兰,杨晓英,杨松青等,应用超声心动图Tei指数评价晚期肝硬化患者心功能,吉林大学学报医学版,2006,32(2):350-352

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