超声三维斑点追踪评价不同心脏起搏方式对健康犬左心室功能的影响
详细信息    本馆镜像全文|  推荐本文 |  |   获取CNKI官网全文
摘要
目的:应用超声三维斑点追踪成像技术评价并比较不同位点心室单点双极起搏对健康犬左心室壁机械同步性和左心室功能的影响,为临床优化人工心脏起搏位点提供基础实验数据。
     材料与方法:分别采集10只健康开胸比格犬基础状态和右心室心尖、左心室心尖、左心室侧壁起搏状态一个完整心动周期的左心室全容积实时图像;同步记录左心室压力变化时间曲线并获取左心室射血压力和收缩期压力最大上升速率。用超声三维斑点追踪分析软件分别提取不同状态左心室壁径向三维应变图、左心室壁径向三维应变峰值和左心室收缩末期容积、舒张末期容积、射血分数、每搏输出量、心输出量。定性观察并比较不同状态左心室壁不同心肌节段的径向三维应变同步性。采用相应的参数检验或非参数检验方法比较不同状态同类定量参数;不同状态左心室壁整体径向三维应变峰值分别与左心室容量参数、压力参数之间进行直线相关分析。
     结果:(1)定性观察结果:①基础状态左心室壁16个不同心肌节段的径向三维应变的时空变化并非完全同步,表现为“有序不同步”。②各个不同起搏状态左心室壁16个心肌节段的径向三维应变的时空变化均失去基础状态的“有序不同步”特征,且左心室心尖或侧壁起搏状态左心室壁不同心肌节段的径向三维应变不同步程度较右心室心尖起搏状态明显。(2)定量分析结果:①与基础状态比较:右心室心尖起搏状态左心室壁基底后间隔和基底下壁的径向三维应变峰值减低(P<0.05);左心室心尖起搏状态整个左心室壁心尖部、中后壁、中侧壁、中前壁、中前间隔和中后间隔等9个心肌节段的径向三维应变峰值减低(P<0.05);左心室侧壁起搏状态整个左心室壁心尖部、中后壁、中侧壁、中前壁、中前间隔和基底前壁等9个心肌节段的径向三维应变峰值减低(P<0.05);各个不同起搏状态左心室壁部分心肌节段的径向三维应变峰值较基础状态略有增高,但差异无统计学意义(P>0.05)。②左心室心尖或侧壁起搏状态左心室壁径向三维应变峰值较基础状态显著减低的心肌节段数多于右心室心尖起搏状态(均为9/16对2/16, P<0.05)。③左心室心尖或侧壁起搏状态左心室壁整体径向三维应变峰值和左心室每搏输出量、射血分数、心输出量均低于右心室心尖起搏状态(P<0.05)。不同起搏状态间左心室压力参数差异无统计学意义(P>0.05)。④不同状态左心室壁整体径向三维应变峰值分别与左心室每搏输出量、射血分数、心输出量呈线性正相关(P<0.05),但未能与左心室压力参数建立直线相关关系(P>0.05)。
     结论:基于超声三维斑点追踪成像技术的左心室功能评价结果提示:(1)不同位点心室单点双极起搏均会破坏健康犬左心室壁各心肌节段的机械同步性,且左心室心尖或侧壁起搏的破坏作用较右心室心尖起搏明显。(2)不同位点心室单点双极起搏均导致左心室壁部分心肌节段收缩功能减低,且左心室心尖或侧壁起搏导致左心室壁节段收缩功能减低的范围较右心室心尖起搏广。(3)左心室心尖或侧壁起搏对健康犬左心室功能的损害超过右心室心尖起搏。(4)超声三维斑点追踪成像技术为医学工作者洞察左心室功能状态提供了新视窗,有望在心脏疾病电生理治疗的基础研究和临床应用方面发挥作用。
Objective: To evaluate and to compare the effects of the one point dipolar pacing at various ventricular sites on the mechanical synchrony of left ventricular wall and its effects on the left ventricular function using echocardiographic three-dimensional (3D) speckle tracking, so as to provide basic experimental database for optimizing the sites of the artificial cardiac pacing in clinic conditions.
     Method: The open-chest modes for cardiac pacing were prepared in 10 healthy beagles. The full volumetric real-time images of the left ventricle in one completed cardiac cycle were acquired respectively during baseline (BASE) and at the right ventricular apex pacing (RVAP), the left ventricular apex pacing (LVAP), the left ventricular lateral wall pacing (LVLP) states. The left ventricular pressure-time curves were recorded simultaneously for achieving left ventricular ejection pressure and the maximal upstroke velocity of left ventricular systolic pressure. The radial 3D strain maps and the peak radial 3D strain of the left ventricular wall, as well as the left ventricular end systolic volume, end diastolic volume, stroke volume, ejection fraction, cardiac output at different states were extracted respectively using echocardiograic 3D speckle tracking analysis software. The radial 3D strain synchrony of left ventricular wall during different states was qualitatively observed and compared. The pertinent parameter test and non-parameter test were applied for comparing the same kind quantitative parameters of the various states; and the linear correlation analyses were applied respectively between the peak global radial 3D strain of the left ventricular wall and the left ventricular volumetric parameters, as well as the pressure parameters.
     Results: (1) The results of the qualitative observation:①The temporospatial changes of the radial 3D strain in the 16 myocardial segments of the left ventricular wall was not completely synchronic at the BASE, and embodied the characteristic of“orderly asynchrony”.②The“orderly asynchrony”in the 16 myocardial segments of the left ventricular wall disappeared at all the various pacing states. Further more, the temporospatial asynchrony in the different myocardial segments of the left ventricular wall was worse at the LVAP or the LVLP state than that of the RVAP state. (2) The results of the quantitative analysis:①To be compared with the BASE: The peak radial 3D strain decreased significantly in the left ventricular basal post-septum and the basal inferior wall at the RVAP state (P < 0.05). The peak radial 3D strain decreased significantly in 9 myocardial segments of the left ventricular wall at the LVAP state; including the whole left ventricular apex, the middle-post wall, the middle-lateral wall, the middle-anterior wall, the middle anterior-septum, and the middle post-septum (P<0.05). The peak radial 3D strain decreased significantly in 9 myocardial segments of the left ventricular wall at the LVLP state; including the whole left ventricular apex, the middle-post wall, the middle-lateral wall, the middle-anterior wall, the middle anterior-septum, and the basal anterior wall (P<0.05). The peak radial 3D strain in some myocardial segments of the left ventricular wall increased at various pacing states, but has no statistical significance (P>0.05).②There were more parafunctional myocardial segments,which peak radial 3D strain decreased significantly, within the left ventricular wall at the LVAP or the LVLP state than those of the RVAP state (both comparisons are 9/16 vs 2/16,P<0.05).③To be compared with the RVAP state; the peak global radial 3D strain of the left ventricular wall and the left ventricular stroke volume, ejection fraction, cardiac output decreased at the LVAP or the LVLP state (P<0.05). But the comparisons of the left ventricular pressure parameters between various pacing states has no statistical significance (P>0.05).④There were statistic significant linear correlations between the peak global 3D strain of the left ventricular wall with the left ventricular stroke volume, and the ejection fraction, as well as the cardiac output in different states (P<0.05); but the linear correlation with the left ventricular pressure parameters was not established in all states (P>0.05).
     Conclusion:The study results of the left ventricular function, which based on the echocardiographic 3D speckle tracking technique, hint that: (1) All the one point dipolar pacing modes at the various ventricular sites in our study have destructive effects on the mechanical synchrony of the left ventricular wall, and the destructive effects of the LVAP or the LVLP are stronger than those of the RVAP. (2) All the one point dipolar pacing modes at the various ventricular sites have negatively affects on the systolic function of some myocardial segments within the left ventricular wall, and the region of pacing-induced dysfunction within the left ventricular wall is wider during the LVAP or the LVLP than that of the RVAP. (3) AS far as the destructive effects on the left ventricular function of healthy canine are concerned, the LVAP or the LVLP mode is more harmful than the RVAP mode. (4) Echocardiographic 3D speckle tracking technique provides medical workers with new visual pathway for insighting the left ventricular function, and may contribute its advantages to the electrophysilogical therapy of heart diseases at the scope of basic studies and clinical applications.
引文
[1]尹立雪.超声在心脏电机械矫正术中的应用[J].中华医学超声杂志(电子版), 2004; 1(2): 92~94
    [2]Leclercq C, Faris O, Tunin R, et al. Systolic improvement and mechanical resynchronization does not require electrical synchrony in the dilated failing heart with left bundle-branch block[J]. Circulation. 2002; 106(14): 1760~1763
    [3]Trohman RG, Kim MH, Pinski SL. Cardiac pacing: the state of the art[J]. Lancet, 2004; 364(9446): 1701~1719
    [4]Birnie DH, Tang AS. If it is not broken, don't fix it: avoidance of right ventricular pacing in cardiac resynchronization therapy[J]. J Cardiovasc Electrophysiol, 2007; 18(5): 505~506
    [5]Healey JS, Yee R, Tang A. Right ventricular apical pacing: a necessary evil[J]? Curr Opin Cardiol, 2007; 22(1): 33~38
    [6]Gillis AM. Redefining physiologic pacing: lessons learned from recent clinical trials[J]. Heart Rhythm, 2006; 3(11): 1367~1372
    [7]Padeletti L, Lieberman R, Valsecchi S, et al. Physiologic pacing: new modalities and pacing sites[J]. Pacing Clin Electrophysiol. 2006; 29(Suppl 2): S73-77
    [8]Vanagt WY, Prinzen FW, Delhaas T. Physiology of cardiac pacing in children: the importance of the ventricular pacing site[J]. Pacing Clin Electrophysiol. 2008; 31(S uppl 1): S24-27
    [9]Peschar M, de Swart H, Michels KJ, ey al. Left ventricular septal and apex pacing for optimal pump function in canine hearts[J]. J Am Coll Cardiol. 2003; 41(7): 1218-1226.
    [10]Vanagt WY, Verbeek XA, Delhaas T, et al. The left ventricular apex is the optimal site for pediatric pacing: correlation with animal experience[J]. Pacing Clin Electrophysiol, 2004; 27(6): 837~843
    [11]Mills RW, Cornelussen RN, Mulligan LJ, et al. Left ventricular septal and left ventricular apical pacing chronically maintain cardiac contractile coordination, pump function and efficiency[J]. Circ Arrhythm Electrophysiol. 2009; 2(5): 571-579
    [12]Faris OP, Evans FJ, Dick AJ, et al. Endocardial versus epicardial electricalsynchrony during LV free-wall pacing[J]. Am J Physiol Heart Circ Physiol, 2003; 285(5): H1864~1870
    [13]尹立雪.超声三维斑点跟踪成像与心肌力学评价[J].中华医学超声杂志(电子版), 2009; 6(5): 1~2
    [14]姚泰.生理学[M].第6版.北京:人民卫生出版社, 2004: 93~94
    [15]Kutty S, Deatsman SL, Nugent ML, et al. Assessment of regional right ventricular velocities, strain, and displacement in normal children using velocity vector imaging. Echocardiography[J]. 2008; 25(3): 294~307
    [16]Wyman BT, Hunter WC, Prinzen FW, et al. Mapping propagation of mechanical activation in the paced heart with MRI tagging[J]. Am J Physiol, 1999; 276(3): H881~891
    [17]Lafitte S, Garrigue S, Perron JM, et al. Improvement of left ventricular wall synchronization with multisite ventricular pacing in heart failure:a prospective study using Doppler tissue imaging[J]. Eur J Heart Fail, 2004; 6(2): 203~212
    [18]Helmer GA, McKirnan MD, Shabetai R, et al. Regional deficits of myocardial blood flow and function in left ventricular pacing-induced heart failure[J]. Circulation, 1996; 94(9): 2260~2267
    [19]Prinzen FW, Hunter WC, Wyman BT, et al. Mapping of regional myocardial strain and work during ventricular pacing: experimental study using magnetic resonance imaging tagging[J]. J Am Coll Cardiol, 1999: 33(6): 1735~1742
    [20]Prinzen FW, Peschar M. Relation between the pacing induced sequence of activation and left ventricular pump function in animals[J]. Pacing Clin Electrophysiol, 2002; 25(4): 484~498
    [21]Kavanagh KM, Belenkie I, Duff HJ. Transmural temporospatial left ventricular activation during pacing from different sites: potential implications for optimal pacing[J]. Cardiovasc Res, 2008; 77(1): 81~88
    [22]De Pauw M, Vilaine JP, Heyndrickx GR. Role of force-frequency relation during AV-block, sinus node block and beta-adrenoceptor block in conscious animals[J]. Basic Res Cardiol, 2004; 99(5): 360~371
    [23]钟毓,尹立雪,王志刚,等.犬左心室不同激动顺序收缩容量与压力的超声研究[J].中华超声影像学杂志, 2009; 18(2): 153~158
    [24]Tanaka M, Sakamoto T, Sugawara S, et al. Blood flow structure and dynamics, and ejection mechanism in the left ventricle: Analysis using echo-dynamography[J]. J Cardiol, 2008, 52(2): 86~101
    [25]Ritter MA, Ringelstein EB. The Venturi effect and cerebrovascular ultrasound[J]. Cerebrovasc Dis, 2002; 14(2): 98~104
    [26]Crosby J, Amundsen BH, Hergum T, et al. 3-D speckle tracking for assessment of regional left ventricular function[J]. Ultrasound Med Biol, 2009; 35(3): 458~471
    [27]Chen X, Xie H, Erkamp R, et al. 3-D correlation-based speckle tracking. Ultrason Imaging, 2005; 27(1): 21~36
    [28]Kawagishi T. Speckle tracking for assessment of cardiac motion and dyssynchrony[J]. Echocardiography, 2008; 25(10): 1167~1171
    [29]Pérez de Isla L, Balcones DV, Fernández-Golfín C, et al. Three-dimensional-wall motion tracking: a new and faster tool for myocardial strain assessment: comparison with two-dimensional-wall motion tracking[J]. J Am Soc Echocardiogr. 2009; 22(4): 325~330
    [30]尹立雪.现代超声心脏电生理学[M].第1版.北京:人民军医出版社, 2007: 103~104
    [31]周永昌,郭万学.超声医学[M].第5版.北京:科学教育出版社, 2006: 3
    [32]Johnson L, Kim HK, Tanabe M, et al. Differential effects of left ventricular pacing sites in an acute canine model of contraction dyssynchrony[J]. Am J Physiol Heart Circ Physiol. 2007; 293(5): H3046-3055
    [33]Tomaske M, Breithardt OA, Bauersfeld U. Preserved cardiac synchrony and function with single-site left ventricular epicardial pacing during mid-term follow-up in paediatric patients[J]. Europace. 2009; 11(9): 1168-1176
    [34]Nesser HJ, Winter S. Speckle tracking in the evaluation of left ventricular dyssynchrony. Echocardiography[J]. 2009; 26(3): 324~336
    [35]Nesser HJ, Mor-Avi V, Gorissen W, et al. Quantification of left ventricular volumes using three-dimensional echocardiographic speckle tracking: comparison with MRI[J]. Eur Heart J. 2009; 30(13): 1565~1573
    [1] Christoffels VM, Burch JBE, Moorman AFM. Architectural plan for the heart: early patterning and delineation of the chambers and the nodes[J]. Trends Cardiovasc Med. 2004; 14(8): 301~307
    [2] Bmneau BG. Transcriptional regulation of vertebrate cardiac morphogenesis[J]. Circ Res. 2002; 90(5): 509~519
    [3] Bartman T, Hove J. Mechanics and function in heart morphogenesis[J]. Dev Dyn 2005; 233(2): 373~381
    [4] Kokubo H, Tomita-Miyagawa S, Hamada Y, et al. Hesr1 and Hesr2 regulate atrioventricular boundary formation in the developing heart through the repressionof Tbx2[J]. Development. 2007; 134(4): 747~755
    [5] Restivo A, Piacentini G, Placidi S, et al. Cardiac outflow tract: a review of some embryogenetic aspects of the conotruncal region of the heart[J]. Anat Rec A Discov Mol Cell Evol Biol. 2006; 288(9): 936~943
    [6]Bradley B. New Insights into the developmental biomechanics of the atrioventricular valves[J]. Circ Res. 2007; 100(10): 1399~1401
    [7]Olsen EN, Srivastava D. Molecular pathways controlling heart development[J]. Science. 1996; 272(5262): 671~676
    [8]Eisenberg LM, Markwald RR. Molecular regulation of atrioventricular valvuloseptal morphogenesis[J]. Circ Res. 1995; 77(1): 216~219
    [9] Tam PP, Parameswaran M, Kinder SJ, et al. The allocation of epiblast cells to the embryonic heart and other mesodermal lineages: the role of ingression and tissue movement during gastrulation[J]. Development. 1997; 124(9): 1631~1642
    [10]Brand T. Heart development: molecular insights into cardiac specification and early morphogenesis[J]. Dev Biol. 2003; 258(1):1~19
    [11]Grepin C, Nemer G, Nemer M. Enhanced cardiogenesis in embryonic stem cells overexpressing the GATA-4 transcription factor[J]. Development. 1997; 124(12): 2387~2395
    [12]Rosenquist GC. Location and movements of cardiogenic cells in the chick embryo: the heart-forming portion of the primitive streak[J]. Dev Biol. 1970; 22(3): 461-475
    [13]Buckingham M, Meilhac S,Zaffran S. Building the mammalian heart from two sources of myocardial cells[J]. Nat Rev Genet. 2005;6(11): 826~835.
    [14]Abu-Issa R, Waldo K, Kirby ML. Heart fields: one, two or more[J]? Dev Biol. 2004; 272(2): 281~285
    [15]Kelly RG, Brown NA, Buckingham ME. The arterial pole of the mouse heart forms from Fgf10-expressing cells in pharyngeal mesoderm[J]. Dev Cell. 2001; 1(3): 435~440
    [16]Klaus A, Saga Y, Taketo MM, et al. Distinct roles of Wnt/beta-catenin and Bmp signaling during early cardiogenesis[J]. Proc Natl Acad Sci U S A. 2007; 104(47): 18531~18536
    [17]Ryckebusch L, Wang Z, Bertrand N, et al. Retinoic acid deficiency alters secondheart field formation[J]. Proc Natl Acad Sci U S A. 2008; 105(8): 2913~2918
    [18]Sedmera D, Pexieder T, Vuillemin M, et al. Developmental patterning of the myocardium[J]. Anat Rec. 2000; 258(4):319~337
    [19]Harvey RP. Patterning the vertebrate heart[J]. Nat Rev Genet. 2002; 3(7): 544~556
    [20]Schultheiss TM, Xydas S, Lassar AB. Induction of avian cardiac morphogenesis by anterior endoderm[J]. Development. 1995; 121(12): 4203~4214
    [21]Srivastava D, Olson EN. A genetic blueprint for cardiac development[J]. Nature. 2000; 407(6801): 221~226
    [22]Eisenberg LM, Moreno R, Markwald RR. Multiple stem cell populations contribute to the formation of the myocardium[J]. Ann N Y Acad Sci. 2005; 1047: 38~49
    [23]Monzen K, Shiojima I, Hiroi Y, et al. Bone morphogenetic proteins induce cardiomyocyte differentiation through the mitogen-activated protein kinase TAK1 and cardiac transcription factors Csx/Nkx-2.5 and GATA-4[J]. Mol Cell Biol. 1999; 19(10): 7096~7105
    [24]Vrancken-Peeters MP, Gittenberger-de Groot AC, Mentink MM, et al. Smooth muscle cells and fibroblasts of the coronary arteries derive from epithelial-mesenchymal transformation of the epicardium[J]. Anat Embryol. 1999; 199(4): 367~378
    [25]Itasaki N, Nakamura H, Sumida H, et al. Actin bundles on the right side in the caudal part of the heart tube play a role in dextro-looping in the embryonic chick heart[J]. Anat Embryol. 1991; 183(1): 29~39
    [26]Sedmera D, Thomas PS. Trabeculation in the embryonic heart[J]. Bioessays, 1996, 18(7): 607
    [27]Lee KF, Simon H, Chen H, et al. Requirement for neuregulin receptor erbB2 in neural and cardiac development[J]. Nature. 1995; 378(6555): 394~398
    [28]Gittenberger-de Groot AC, Bartelings MM, de Ruiter MC, et al. Basics of cardiac development for the understanding of congenital heart malformations[J]. Pediatr Res. 2005; 57(2): 169~176
    [29]Lewis FT. The question of sinusoids[J]. Anat Anz. 1904; 25: 261~279
    [30]Valdes-Dapena M, Gilbert-Barness E. Cardiovascular causes for sudden infant death[J]. Pediatr Pathol Mol Med. 2002; 21(2): 195~211
    [31]Cserjesi P, Brown D, Lyons GE, etal. Expression of the novel basic-helix-loop-helix gene eHAND in neural crest derivatives and extraembryonic membranes during mouse development[J]. Dev Biol. 1995; 170(2): 664~678
    [32] M?nner J. The development of pericardial villi in the chick embryo. Anat Embryol [J]. 1992; 186(4): 379~385
    [33]MacNeill C, French R, Evans T, et al. Modular regulation of cGATA-5 gene expression in the developing heart and gut[J]. Dev Biol. 2000; 217(1): 62~76
    [34]Fossett N, Schulz RA. Conserved cardiogenic functions of the multitype zinc-finger proteins:U-shaped and FOG-2[J]. Trends Cardiovasc Med. 2001; 11(5): 185~190
    [35]Morabito CJ, Dettman RW, Kattan J, et al. Positive and negative regulation of epicardial-mesenchymal transformation during avian heart development[J]. Dev Biol. 2001; 234(1): 204~215
    [36]Lu J, Chang P, Richardson JA, et al. The basic helix-loop-helix transcription factor capsulin controls spleen organogenesis[J]. Proc Natl Acad Sci U S A. 2000; 97(17): 9525~9530
    [37]Reese DE, Zavaljevski M, Streiff NL, et a. Bves: A novel gene expressed during coronary blood vessel development[J]. Dev Biol. 1999; 209(1): 159~171
    [38]Viragh S, Challice CE. The origin of the epicardium and the embryonic myocardial circulation in the mouse[J]. Anat Rec. 1981; 201(1): 157~168
    [39]Bogers AJJC, Gittenberger-de Groot AC, Poelmann RE, et al. Development of the origin of the coronary arteries, a matter of ingrowth or outgrowth[J]? Anat Embryol. 1989; 180(5): 437~441
    [40]Vrancken Peeters MP, Gittenberger-de Groot AC, Mentink MM, et al. The development of the coronary vessels and their differentiation into arteries and veins in the embryonic quail heart[J]. Dev Dyn. 1997; 208(3): 338~348
    [41]Agmon Y, Connolly HM, Olson LJ, et al. Noncompaction of the ventricular myocardium[J].J Am Soc Echocardiogr. 1999; 12(10): 859~863.
    [42]Chin TK, Perloff JK, Williams RG, et al. Isolated noncompaction of the left ventricular myocardium. A study of eight cases[J]. Circulation. 1990; 82(2): 507~513
    [43]Sadoulet-Puccio HM, Feener CA, Schaid DJ, et al. The genomic organization ofhuman dystrobrevin[J]. Neurogenetics. 1997; 1(1): 37~42
    [44]Ishiwata T, Nakazawa M, Pu WT, et al. Developmental changes in ventricular diastolic function correlate with changes in ventricular myoarchitecture in normal mouse embryos[J]. Circ Res,2003; 193(9): 857~865
    [45]Franco D, Meilhac SM, Christoffels VM, et al. Left and right ventricular contributions to the formation of the interventricular septum in the mouse heart[J]. Dev Biol,2006; 294(2): 366~375
    [46]Sedmera D. Form follows function: developmental and physiological view on ventricular myocardial architecture[J]. Eur J Cardiothorac Surg,2005,28(4): 526~528
    [47]Kang J,Sucov H. Convergent proliferative response and divergent morphogenic pathways induced by epicardial and endocardial signaling in fetal heart development[J]. Mech Dev, 2005, 122(1): 57~65
    [48]Xavier-Neto J, Shapiro MD, Houghton L, et al. Sequential programs of retinoic acid synthesis in the myocardial and epicardial layers of the developing avian heart[J]. Dev Biol, 2000; 219(1): 129~141
    [49]Tobita K, Garrison JB, Liu LJ, et al. Three-dimensional myofiber architecture of the embryonic left ventricle during normal development and altered mechanical loads[J]. Anat Rec A Discov Mol Cell Evol Biol, 2005, 283(1): 193~201
    [50]Pennisi DJ, Rentschler S, Gourdie RG, et al. Induction and patterning of the cardiac conduction system[J]. Int J Dev Biol. 2002; 46(6): 765~775
    [51]Harris BS, Jay PY, Rackley MS, et al. Transcriptional regulation of cardiac conduction system development: 2004 FASEB cardiac conduction system minimeeting, Washington, DC[J]. Anat Rec A Discov Mol Cell Evol Biol. 2004; 280(2): 1036~1045
    [52]Mommersteeg MT, Hoogaars WM, Prall OW, et al. Molecular pathway for the localized formation of the sinoatrial node[J]. Circ Res. 2007; 100(3): 354~362
    [53]Harris BS, Brien TX, Gourdie RG. Coronary arteriogenesis and differentiation of periarterial Purkinje fibers in the chick heart: is there a link[J]? Tex Heart Inst J. 2002; 29(4): 262~270
    [54]Harris BS, Spruill L, Edmonson AM, et al. Differentiation of cardiac purkinje fibersrequires precise spatiotemporal regulation of Nkx2-5 expression[J]. Dev Dyn. 2006; 235(1): 38~49
    [55]Thomas PS, Kasahara H, Edmonson AM, et al. Elevated expression of Nkx-2.5 in developing myocardial conduction cells[J]. Anat Rec. 2001; 263(3): 307~313
    [56]Jay PY, Harris BS, Maguire CT, et al. Nkx2-5 mutation causes anatomic hypoplasia of the cardiac conduction system[J]. J Clin Invest. 2004; 113:1130~1137
    [57]Stroud DM, Gaussin V, Burch JBE, et al. Abnormal conduction and morphology in the atrioventricular node of mice with atrioventricular canal-targeted deletion of Alk3/Bmpr1a receptor[J]. Circulation. 2007; 116: 2535~2543
    [58]Sedmera D, KurkováD. Functional and developmental view on Purkinje fibers system[J]. Cas Lek Cesk. 2007; 146(9): 673~676
    [59]Yang HT, Tweedie D, Wang S, et al. The ryanodine receptor modulates the spontaneous beating rate of cardiomyocytes during development[J]. Proc Natl Acad Sci U S A. 2002; 99(14): 9225~9230
    [60]Guimaraes H, Costa L, Araujo E, et al. Comparison of two- and three-dimensional ultrasonography in the evaluation of fetal heart: image quality and time spent in the exam[J]. Arch Gynecol Obstet. 2007; 276(3): 231~235
    [61]Allan LD, Santos R, Pexieder T. Anatomical and echocardiographic correlates of normal cardiac morphology in the late first trimester fetus[J]. Heart. 1997; 77(1): 68~72
    [62]Wloch A, Rozmus-Warcholinska W, Czuba B, et al. Doppler study of the embryonic heart in normal pregnant women[J]. J Matern Fetal Neonatal Med. 2007; 20(7): 533~539
    [63]Gembruch U, Shi C, Smrcek JM. Biometry of the fetal heart between 10 and 17 weeks of gestation[J]. Fetal Diagn Ther. 2000; 15(1): 20~31.
    [64]Smrcek JM, Berg C, Geipel A, et al. Early fetal echocardiography: heart biometry and visualization of cardiac structures between 10 and 15 weeks' gestation[J]. J Ultrasound Med. 2006; 25(2): 173~182
    [65]Goncalves LF, Lee W, Chaiworapongsa T, et al. Fourdimensional ultrasonography of the fetal heart with spatiotemporal image correlation[J]. Am J Obstet Gynecol. 2003; 189(6): 1792~1802
    [66]Wu Y, Liu T, Xiong Y, et al. Application of spatio-temporal image correlation in normal fetal heart ultrasonography[J]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2008; 30(1): 75~79
    [67]Messing B, Cohen SM, Valsky DV, et al. Fetal cardiac ventricle volumetry in the second half of gestation assessed by 4D ultrasound using STIC combined with inversion mode[J]. Ultrasound Obstet Gynecol. 2007; 30(2): 142~151
    [68]Hata T, Dai SY, Inubashiri E, et al. Four-dimensional sonography with B-flow imaging and spatiotemporal image correlation for visualization of the fetal heart[J]. J Clin Ultrasound. 2008; 36(4): 204~207
    [69]Szymkiewicz-Dangel J, Hamela-Olkowska A, W?asienko P, et al. The possibility of evaluation of the myocardial performance index in fetuses at 11.0 to 13.6 week of gestation. Ginekol Pol[J]. 2007; 78(3): 218~222
    [70]Mori A, Uchida N, Ishiguro Y, et al. Evaluation of cardiac function of the fetus by inferior vena cava diameter pulse waveform. Am Heart J. 2007; 154(4): 789~794
    [71]Steinhard J, Heinig J, Schmitz R, et al. Tissue Doppler imaging of the fetal heart--a new parametric ultrasound technique in prenatal medicine[J]. Ultraschall Med. 2007; 28(6): 578~583
    [72]Perles Z, Nir A, Gavri S, et al. Assessment of fetal myocardial performance using myocardial deformation analysis[J]. Am J Cardiol. 2007; 99(7): 993~996
    [73]Rizzo G, Capponi A, Cavicchioni O, et al. Fetal cardiac stroke volume determination by four-dimensional ultrasound with spatio-temporal image correlation compared with two-dimensional and Doppler ultrasonography[J]. Prenat Diagn. 2007; 27(12): 1147~1150
    [74]Ta-Shma A, Perles Z, Gavri S, et al. Analysis of segmental and global function of the fetal heart using novel automatic functional imaging[J]. J Am Soc Echocardiogr. 2008; 21(2): 146~150
    [75]Lee W, Dorewwamy A, Comstock C, et al. Fetal cardiac ventricular strain using velocity vector imaging[J]. Ultrasound Obstet Gynecol. 2007; 30(4): 624~625
    [76]Selbing A, ?nghagen O, Bylund B, et al. Velocity vector imaging to assess fetal myocardial function[J]. Ultrasound Obstet Gynecol. 2007; 30(4): 625
    [77]Chia EL, Ho TF, Rauff M, et al. Cardiac time intervals of normal fetuses using noninvasive fetal electrocardiography[J]. Prenat Diagn. 2005; 25(7): 546-555
    [78]Kahler C, Grimm B, Schleussner E, et al. The application of fetal magnetocardiography(FMCG) to investigate fetal arrhythmias and congenital heart defects(CHD) [J]. Prenat Diagn. 2001; 21(3): 176~182
    [79]Fouron JC. Fetal arrhythmias: the Sainte-Justine hospital experience[J]. Prenatal Diagn. 2004; 24(13): 1068~1080
    [80]Carvalho JS, Prefumo F, Ciardelli V, et al. Evaluation of fetal arrhythmias from simultaneous pulsed wave Doppler in pulmonary artery and vein[J]. Heart. 2007; 93(11): 1448~1453
    [81]Rein AJJT, Donnell CO, Geva T, et al. Use of tissue velocity imaging in the diagnosis of fetal cardiac arrhythmias[J]. Circulation. 2002; 106(14): 1827~1833
    [82]Nii M, Hamilton RM, Fenwick L, et al. Assessment of fetal atrioventricular time intervals by tissue Doppler and pulsed Doppler echocardiography: normal values and correlation with fetal echocardiography[J]. Heart. 2006; 92(12): 1831~1837
    [83]Yu Q, Leatherbury L, Tian X, et al. Cardiovascular assessment of fetal mice by in utero echocardiography[J]. Ultrasound Med Biol. 2008; 34(5): 741~752
    [84]Colin K, Phoon M. Imaging tools for the developmental biologist: ultrasound biomicroscopy of mouse embryonic development[J]. Pediatric Research. 2006; 60(1): 14~21
    [85]Brown AS, Reid AD, Leamen L, et al. Biological effects of high-frequency ultrasound exposure during mouse organogenesis[J]. Ultrasound Med Biol. 2002; 30(9): 1223~1232
    [86]Jones EAV, Baron MH, Fraser SE, et al. Measuring hemodynamic changes during mammalian development[J]. Am J Physiol Heart Circ Physiol. 2004; 287(4): 1561~1569
    [87]McQuinn TC, Bratoeva M, Dealmeida A, et al. High-frequency ultrasonographic imaging of avian cardiovascular development[J]. Dev Dyn. 2007; 236(12): 3503~3513
    [88]Phoon CK, Aristizabal O, Turnbull DH. 40 MHz Doppler characterization of umbilical and dorsal aortic blood flow in the early mouse embryo[J]. Ultrasound Med Biol. 2000; 26(8):1275~1283
    [89]Fechner S, Busch C, Oppitz M, et al. The chick embryo as a model for intrauterine ultrasound-guided heart intervention Ultrasound[J]. Obstet Gynecol. 2008; 31(3):277~283
    [90]Weiss EC, Lemor RM, Pilarczyk G, et al. Imaging of focal contacts of chicken heart muscle cells by high-frequency acoustic microscopy[J]. Ultrasound Med Biol. 2007; 33(8): 1320~1326
    [91]Schneider JE, Bamforth SD, Farthing CR, et al. High-resolution imaging of normal anatomy,and neural and adrenal malformations in mouse embryos using magnetic resonance microscopy[J]. J Anat. 2003; 202(2): 239~247
    [92]Schneider JE, Bose J, Bamforth SD, et al. Identification of cardiac malformations in mice lacking Ptdsr using a novel high-throughput magnetic resonance imaging technique[J]. BMC Dev Biol. 2004; 4: 16
    [93]Bain MM, Fagan AJ, Mullin JM, et al. Noninvasive monitoring of chick development in ovo using a 7T MRI system from day 12 of incubation through to hatching[J]. J Magn Reson Imaging. 2007;26(1):198~201
    [94]Wadghiri YZ, Schneider AE, Gray EN, et al. Contrast-enhanced MRI of right ventricular abnormalities in Cx43 mutant mouse embryos[J]. NMR Biomed. 2007; 20(3): 366~374
    [95]Yelbuz TM, Choma MA, Thrane L, et al. Optical coherence tomography. A new high-resolution imaging technology to study cardiac development in chick embryos[J]. Circulation. 2002; 106(22): 2771~2774
    [96]Sharpe J. Optical projection tomography[J]. Annu Rev Biomed Eng. 2004; 6: 209~228
    [97]Jonathan T, Sedmera D, Robert E. Quantitative volumetric analysis of cardiac morphogenesis assessed through micro-computed tomography[J]. Developmental Dynamics. 2007; 236(3): 802~809
    [98]Muhler MR, Rake A, Schwabe M, et al. Truncus arteriosus communis in a midtrimester fetus: comparison of prenatal ultrasound and MRI with postmortem MRI and autopsy[J]. Eur Radiol. 2004; 14(11): 2120~2124
    [99]Gorincour G, Bourlie B, Bonello B, et al. Feasibility of fetal cardiac magnetic resonance imaging: preliminary experience[J]. Ultrasound Obstet Gynecol. 2007; 29(1): 105~108
    [100]M?nner J. Ontogenetic development of the helical heart:concepts and facts[J]. Eur J Cardiothorac Surg. 2006; 29(Suppl 1): 69~74
    [111]Dunwoodie SL. Combinatorial signaling in the heart orchestrates cardiac induction, lineage specification and chamber formation[J]. Semin Cell Dev Biol. 2007; 18(1): 54~66
    [112]Mitchell ME, Sander TL, Klinkner DB, et al. The molecular basis of congenital heart disease[J]. Semin Thorac Cardiovasc Surg. 2007; 19(3): 228~237
    [113]Durocher D, Nemer M. Combinatorial interactions regulating cardiac transcription[J]. Dev Genet. 1998; 22(3): 250~262

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700