孤立性左室心肌致密化不全的高场MRI多序列成像及与血浆NT-proBNP含量的相关性研究
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摘要
第一部分孤立性左室心肌致密化不全的MRI与超声心动图、病理对照研究
     目的MRI多序列联合应用以探讨孤立性左室心肌致密化不全(Isolated left ventricular non-compaction, IVNC)的形态学特征,并与超声心动图表现、病理表现进行对照,评价MRI诊断左室心肌致密化不全的临床价值。
     材料与方法由临床资料和超声心动图诊断为IVNC的27例患者(男性26例,女性1例。年龄18~73岁,平均年龄51.1±15.7岁)、14例扩张型心肌病患者、15例健康对照者进行了MRI检查。采用Siemens Magnetom Avanto 1.5T设备扫描,胸前置体部相控阵线圈,心电门控R波触发成像。扫描项目包括:黑血技术采用半傅里叶采集单次激发自旋回波(HASTE)序列、白血技术采用真实稳态进动快速成像(TrueFISP)序列、心脏电影成像(Cine MRI)采用真实稳态进动快速成像(TrueFISP)序列,进行四腔位、两腔位、长轴位成像。超声心动图检查使用2D、M型显像技术探查胸骨旁左心室长轴切面、胸骨旁左心室短轴切面、心尖两腔、三腔、四腔多切面扫描。一例心脏移植的离体心脏标本垂直于心脏长轴方向由心尖至心底部进行切片,进行病理解剖对照。MRI图像处理采用AHA/ACC标准17节段分段法,统计致密化不全心肌节段的部位、累及心肌节段的总数。在左心室舒张末期短轴位左心室壁最厚处测量致密化心肌厚度(compacted myocardium, C)和非致密心肌厚度(noncompacted myocardium, N)计算得到最大N/C值。目测判断左心室各节段心肌的室壁运动状态。
     结果①所有27例IVNC患者的MRI和超声心动图检查均能显示左心室心肌受累,左心室内膜增厚、左室壁分层改变。内层非致密心肌由多发、呈网格状或栅栏状排列的肌小梁以及深陷的小梁间隐窝构成。外层致密心肌层变薄。②其它的MRI征象包括:肌小梁间隐窝内血栓形成1例、节段性室壁收缩功能不良11例、左心室普遍性收缩功能不良7例、二尖瓣关闭不全17例、心包腔积液8例、单侧胸腔积液5例、双侧胸腔积液4例。③27例IVNC患者的非致密心肌节段共159段。常见受累节段为:尖部侧壁27段、中部下侧壁23段、心尖帽22段、中部前侧壁22段。每例IVNC患者非致密心肌节段数均值为9±3段,N/C均值为3.21±1.08。扩张型心肌病组(14例)的非致密心肌节段数均值为6±3段,N/C均值为1.22±0.48。健康对照组(15例)的非致密心肌节段数均值为4±3段,N/C均值为1.02±0.38。IVNC组与扩张型心肌病组、健康对照组之间的非致密心肌节段数均值、N/C均值有统计学差异(P<0.01)。④对于IVNC组患者,MRI显示的非致密心肌节段共159段,N/C均值为3.21±1.08。超声心动图显示的非致密心肌节段共131段,N/C均值为2.66±0.67。MRI在心脏基底部下侧壁、前侧壁的非致密心肌节段与超声心动图相比有显著差异(P<0.05),在其它节段中无统计学差异。MRI测得N/C均值大于超声心动图,Bland-Altmen结果显示MRI和超声心动图所测的N/C值有一致性。⑤心脏离体标本经病理解剖显示左心室受累,左心室腔内多发异常粗大的肌小梁和深陷交错的小梁间隐窝,主要分布于左心室中部和心尖部的前壁、侧壁、下壁和心尖帽,室间隔未见受累。逐层对比病理断面标本与MRI图像,两者间显示的非致密心肌节段的部位、范围、N/C值的一致性较好。
     结论MRI多序列、多方位成像能清晰显示IVNC的形态学特征,有效显示非致密心肌的节段分布范围、精确定量N/C值。MRI显示的非致密心肌范围、对心肌分层的界面定位优于超声心动图。病理解剖对照证实MRI显示的非致密心肌节段的范围、N/C值与离体解剖标本的病变特征基本一致。
     第二部分MR I心肌延迟灌注增强评价IVNC心肌纤维化的研究
     目的对孤立性左室心肌致密化不全的心肌进行心肌延迟灌注增强MRI(Delayedenhancement DE-MRI)检查并与组织病理对照研究,探讨IVNC患者心肌纤维化的程度和范围。
     材料与方法由临床资料和超声心动图诊断为IVNC的27例患者(男性26例,女性1例。年龄18~73岁,平均年龄51.1±15.7岁)和15例健康对照者进行MRI心肌延迟灌注增强检查。采用Siemens Magnetom Avanto 1.5T设备扫描,胸前置体部相控阵线圈,心电门控R波触发成像。心肌延迟灌注增强采用相位敏感反转恢复序列(Phase-sensitive Inversion Recovery, PSIR)。高压注射器团注Gd—DTPA(0.2mmol/kg,速率2ml/s)注药后延迟10分钟采集心脏两腔、四腔、短轴位层面。MRI图像处理采用AHA/ACC标准17节段分段法,统计延迟灌注增强为阳性的心肌节段数量、计算延迟灌注强化的心肌质量。将心脏标本固定、切片、取组织块后进行固定、脱水、石蜡包埋制作组织切片、苏木精-伊红(HE)染色、Massion染色、天狼星染色后分别在普通显微镜和偏振光显微镜下观察。
     结果①27例IVNC患者中,16例心肌延迟灌注增强为阳性。94/459段(20.4%)的心肌节段延迟强化。延迟强化节段最常见部位:中部下侧壁11段、中部前侧壁11段、尖部侧壁9段、心尖帽9段。其中69/94段(73.4%)为非致密心肌节段,25/94段(26.5%)为致密心肌节段。87/94段(92.5%)表现为心内膜下延迟强化,7/94(7.4%)表现为透壁型延迟强化。IVNC组延迟灌注增强心肌质量均值为5.72±4.36(g)。15例健康对照组中3例延迟强化,3/255段(1.2%)的心肌节段延迟强化。表现为小灶样轻度强化。延迟灌注增强心肌质量均值0.73±3.23(g),与IVNC组相比有统计学差异(t值3.679,P值0.001)。②病理结果:所有延迟增强为阳性的心肌节段,组织切片显微镜下观察均有不同程度的心肌细胞变性、坏死。HE染色示心肌间质内和心内膜下胶原纤维明显增加。Massion染色示染色为绿色的胶原纤维在心肌间质内和心内膜下明显增多。天狼星染色切片在偏振光显微镜下观察示:红染和黄染的Ⅰ型胶原纤维显著增多;绿染的Ⅲ型胶原纤维轻度增加;对照组染色为阴性。
     结论MRI心肌延迟灌注增强能无创性地、在活体内定量评估IVNC心肌纤维化的范围和延迟增强的心肌质量。IVNC患者延迟强化的心肌节段多分布于左心室中部、尖部的侧壁和室间隔。主要位于非致密的心肌节段,致密心肌节段中也可出现。其强化类型多为心内膜下强化。病理组织染色研究证实IVNC患者存在延迟灌注强化的心肌节段与镜下显示存在胶原纤维增生的心肌节段有较好的一致性。
     第三部分IVNC的MRI左心室功能定量分析研究
     目的采用4D MRI左心室心功能成像定量分析IVNC患者的左室心功能相关参数值,评价心肌致密化不全的非致密心肌的节段数量、N/C比值、心肌延迟灌注强化节段评分值与左室心功能参数值之间的相关性。
     材料与方法由临床资料和超声心动图诊断为IVNC的27例患者(男性26例,女性1例。年龄18~73岁,平均年龄51.1±15.7岁)和15例健康对照组进行MRI左室心功能分析检查。将所有受试者分为:A组5例,临床NYHA分级为Ⅰ-Ⅱ级;B组22例,临床NYHA分级为Ⅲ-Ⅳ级;C组15例,为正常对照组。采用Siemens Magnetom Avanto 1.5T设备扫描,胸前置体部相控阵线圈,心电门控R波触发成像。扫描序列包括Cine MRI序列进行左室心功能成像、相位敏感反转恢复序列进行心肌延迟灌注增强扫描。采集心脏两腔、四腔和短轴位。MRI图像处理采用Argus 4D软件包进行左心室功能分析,计算得到舒张末期容积EDV、收缩末期容积ESV、每搏输出量SV、心输出量CO、左心室射血分数LVEF、左心室心肌质量LV MASS、左心室最大充盈率PFR、最大射血率PER、峰值充盈时间TPFR、峰值射血时间TPER。统计IVNC组的非致密心肌的节段数量、最大N/C值、计算延迟灌注强化节段评分值与上述左室心功能参数值之间的相关性。
     结果①A、B、C三组之间的LVEDV、LVESV、LVEF、PER和PFR值有统计学差异(P<0.05); LV MASS、CO、SV、TPER、TPFR值无统计学差异(P>0.05),A、B组的LVEDV(均值168.67±55.31、257.84±87.53)、LVESV(均值101.73±74.29167.78±69.04)、LVEF(均值42.76±8.72、24.79±11.17)、PER(均值2.85±0.71、2.45±0.49)、PFR(均值1.27±0.51、1.17±0.31)分别与C组的LVEDV(均值104.57±21.20)、LVESV(均值35.76±13.37)、LVEF(均值66.39±7.69)、PER(均值3.54±0.68)、PFR(均值3.31±0.65)相比有统计学差异。(P<0.05)。A组和B组间的LVEDV、LVESV、LVEF、PER、PFR值有统计学差异。②LVEF与非致密心肌节段数量、N/C值、左心室延迟强化评分值均呈负相关。非致密心肌节段数量、N/C值、左心室心肌延迟灌注强化评分值与LVEF值的相关系数r值分别为(0.376、0.45、0.501),有统计学意义。(P<0.05)。
     结论采用4D MRI左心室功能定量分析能获得LVEDV、LVESV、LVEF、SV、CO、PER、PFR、TPER、TPFR的左心功能参数值,结合左心室容积-时间曲线,定量评价左心室的收缩和舒张功能。A、B、C各组的LVEDV、LVESV、LVEF、PER、PFR参数值存在显著差异,MRI左心室心功能参数值的变化与临床NYHA分级升高相一致。LVEF值是反映IVNC患者左心室收缩功能的重要参数值,它与非致密心肌节段数量、N/C值、MRI延迟强化心肌节段评分值负相关。
     第四部分IVNC患者MRI左心室功能及心肌延迟灌注增强与血浆NT-proBNP含量的相关性研究
     目的测量IVNC患者血浆NT-proBNP (N-terminal pro-B-type natriuretic peptide)含量,并探讨其与MRI左心室功能参数值、MRI延迟灌注增强评分值之间的相关性。
     材料与方法由超声心动图诊断为IVNC的21例患者(年龄33-73岁,平均年龄47±13.9岁,男性20例,女性1例)、年龄与性别匹配的15例正常对照组进行MRI检查。采用Siemens Magnetom Avanto 1.5T设备扫描,胸前置体部相控阵线圈,心电门控R波触发成像。扫描序列包括Cine MRI序列左心功能成像、相位敏感反转恢复序列心肌延迟灌注增强扫描两腔、四腔、短轴位。MRI图像处理采用Argus 4D软件包进行左心室功能分析,计算得到左心室舒张末期容积EDV、收缩末期容积ESV、每搏输出量SV、心输出量CO、左心室射血分数LVEF、左心室心肌质量LV MASS。计算延迟灌注强化心肌节段评分值。用放射免疫法测定IVNC患者血浆NT-proBNP含量。
     结果①IVNC组与正常对照组的血浆NT-proBNP含量均值分别为2559±2300.6ng/L、23.55±17.9 ng/L,两组均值间存在统计学差异(P值=0.001)。②MRI测得左心室心功能参数值LVEDV、LVESV与NT-proBNP含量呈正相关、LVEF与NT-proBNP含量呈负相关。LVEDV、LVESV、LVEF与血浆NT-proBNP的相关系数r值分别为(0.69、0.749、0.48),有统计学意义(P<0.01)。
     结论血浆NT-proBNP含量是反映左心室心功能不全的敏感性指标,具有高度的特异性。IVNC组患者的血浆NT-proBNP含量与正常对照组相比有显著性差异。左心室容量负荷增加促使NT-proBNP合成、释放增加,血浆NT-proBNP含量与左心室功能状态密切相关。LVEDV、LVESV值与NT-proBNP含量正相关,LVEF值与NT-proBNP含量负相关。
PARTⅠ:Assessment of isolated ventricular noncompaction:Comparison of cardiac MR imaging with echocardiography manifestation and with a pathological study
     Objective Compare with 2D echocardiography and to describe morphologic feature with cardiac MRI in the evaluation of patients with noncompaction of left ventricular myocardium
     Materials and Methods Twenty-seven IVNC patients diagnosed by echocardiography underwent MRI, scanning of black-blood sequence, white-blood sequence and Cine MRI, included four chamber view, two chamber view and short axis view of left ventricle.
     Results Noncompacted myocardium was characterized by prominent and excessive myocardial trabeculations and deep intratrabecular recesses.All segments could be analysed by Cardiac MRI whereas only 131(82.3%) could be showed by echocardiography. CMRI identified a higher rate of NC/C maximum ratio compared with echocardiography. No significant difference was observed of two-layered structures except in the anterolateral and inferolateral segments. One case eventually underwent heart transplantation because of severe congestive heart failure. Gross findings demonstrated prominent muscular trabeculations, with deep intratrabecular recesses into lesion heart. Noncompaction of ventricular myocardium showed a thin, compacted epicardial and an extremely thickened endocardium, which coincided well with MRI findings.
     Conclusion Cardiac MRI appears superior to standard echocardiography in assessing the extent of noncompaction and provides supplemental morphological information beyond that obtained with conventional echocardiography.
     PART II:Delayed contrast enhancement of MRI in ventricular noncompaction:Emphasis on segmental fibrosis
     Objective The purpose of this study is to describe the delayed contrast-enhancement pattern feature of the noncompaction of the left ventricle in cardiac magnetic resonance imaging
     Materials and Methods Twenty-seven IVNC patients diagnosed by echocardiography underwent delayed contrast enhancement MRI, scanning of Phase-sensitive Inversion Recovery (PSIR) sequence, included four chamber view, two chamber view and short axis view of left ventricle.
     Results Noncompaction was seen in 16 cases. CMRI demonstrated 94(20.4%) segments contrast enhancement mostly in the apical and midventricular lateral segment. Delayed contrast enhancement was seen not only involved noncompaction segments (73.4%) but also normal segments of the heart (26.5%). Myocardial fibrosis was demonstrated predominates subendocardial patterns (92.5%) and transmural patterns (7.4%).More segments (20.4%) occurred in IVNC patients with increased fibrosis mass (5.72±4.36g) compared to normal control. Histological findings demonstrated interstitial fibrosis in all delayed contrast enhanced segments with endomyocardial thickening and subendocardial fibroelastosis.
     Conclusion Fibrosis is a common finding in ventricular noncompaction. Delayed contrast enhancement CMRI is a valuable imaging method in patients with ventricular concompaction by showing fibrosis.
     PART III:Quantification of left ventricular function in left ventricular noncompaction with cardiac MRI
     Objective The aim of the study was to evaluate the clinic value of MRI for quantitative assessment of systolic and diastolic left ventricular function in IVNC patients.
     Materials and Methods Twenty-seven IVNC patients diagnosed by echocardiography underwent MRI. All patients were divided by their heart function.There were 5 patients in NYHA classⅠorⅡ,22 patients in NYHA classⅢorⅣ,15 in normal group. ECG gated trueFISP and Phase-sensitive Inversion Recovery imaging were performed, including four chamber view, two chamber view and short axis view of left ventricle. Left ventricular end diastole volume (LVEDV), Left ventricular end systole volume (LVESV), Left ventricular myocardial mass (LV MASS), Left ventricular ejection fraction (LVEF),cardiac output(CO), stroke volume(SV),peak filling rate(PFR),peak ejection rate(PER), time of PFR(TPFR) and time of PER(TPER) were estimated.
     Results Significant differences among clinical severity groups (A, B, C) divided by NYHA class were noted in left ventricular function quantitative by MRI. The means of LVESV,LVEDV, LVEF,PER,PFR in group A, B and C had significant difference(P< 0.05),no significant differences occurred on means of LVMM,SV,CO,TPFR,TPER(P> 0.05).The extent of left ventricular noncompaction, NC/C maximum ratioand the degree of trabecular delayed hyper enhancement correlated significantly with ejection fraction (LVEF),(r=0.376、0.45、0.501, P<0.05).
     Conclusion Cardiac MRI allows for reliable assessment of systolic and diastolic left ventricular function. Evaluating the extent and severity of left ventricular noncompaction and delayed hyperenhancement may improve the ability of predict LVEF of IVNC.
     PARTⅣ:Elevated plasma N-terminal pro-B-type natriuretic peptide level in isolated ventriclar noncompaction:Correlation with left ventricular function and delayed contrast enhancement of cardiac MRI
     Objective To determine the correlation between the plasma NT-proBNP and left ventricular function, delayed contrast-enhancement extent of cardiac MRI and to evaluate the diagnosis values of NT-proBNP in IVNC patient with heart failure.
     Materials and Methods Twenty-one IVNC patients diagnosed by echocardiography underwent MRI,ECG gated trueFISP and Phase-sensitive Inversion Recovery imaging were performed, including four chamber view, two chamber view and short axis view of left ventricle. Plasma NT-proBNP concentrations were measured with immunoradiometric assay and MRI were detected in all patients to measure left ventricular function and extent of delayed contrast-enhancement.
     Results Plasma NT-proBNP was increased in patients with IVNC compared to control subjects. NT-proBNP were correlated with LVEDV, LVESV and LVEF in IVNC patients(r=0.69、0.749、0.48, P<0.01).
     Conclusion The plasma NT-proBNP levels showed significant correlation with LVEDV, LVESV and LVEF. It suggests that NT-proBNP might be used to evaluate the heart failure and to predict prognosis.
引文
[1]Moon JC, Fisher NG, McKenna WJ, et al. Detection of apical hypertrophic cardiomyopathy by cardiovascular magnetic resonance in patients with non-diagnostic echocardiography. Heart,2004,90(6):645-649
    [2]Petersen SE, Selvanayagam JB, Wiesmann F, et al.Left ventricular non-compaction:insights from cardiovascular magnetic resonance imaging, J Am Coll Cardiol.2005,46(1):101-105.
    [3]Jenni R, Goebel N, Tartini R, et al. Persisting myocardial sinusoids of both ventricles as an isolated anomaly:echocardiographic, angiographic, and pathologic anatomical findings. Cardiovasc Intervent Radiol,1986, 9(3):127-131.
    [4]Angelini A, Melacini P, Barbero F, et al. Evolutionary persistence of spongy myocardium in humans. Circulation.1999,99(18):2475.
    [5]Agmon Y, Connolly HM, Olson LJ, et al. Noncompaction of the ventricular myocardium. J Am Soc Echocardiogr.1999,12(10):859-863.
    [6]Freedom RM, Yoo SJ, Perrin D, et al.The morphological spectrum of ventricular noncompaction. Cardiol Young.2005,15(4):345-364.
    [7]Bellet S, Goulet BA. Congenital heart disease with multiple cardiac anomalies:report of a ease showing aortic atresia, fibrous scar in myocardium and embryonal sinusoidal remains. Am J Med Sci,1932,183:458-465
    [8]Feldt RH, Rahimtoola SH, Davis GD, et al. Anomalous ventricular myocardial patterns in a child with complex congenital heart disease. Am J Cardiol, 1969,23 (5):732-734.
    [9]Captur G, Nihoyannopoulos P. Left ventricular non-compaction: Genetic heterogeneity, diagnosis and clinical course. Int J Cardiol.2009,5 (8):1-11
    [10]Richardson P, McKenna W, Bristow M, et al. Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of cardiomyopathies. Circulation,1996,93(5):841-842.
    [11]Engberding R, Bender F. Identification of a rare congenital anomaly of the myocardium by two-dimensional echocardiography:persistence of isolated myocardial sinusoids. Am J Cardiol,1984,53(11):1733-1734.
    [12]Chin TK, Perloff JK, Williams RG, et al. Isolated noncompaction of left ventricular myocardium. A study of eight cases. Circulation,1990,82 (2):507-513.
    [13]Thuny F, Jacquier A, Jop B, et al. Assessment of left ventricular non-compaction in adults:side-by-side comparison of cardiac magnetic resonance imaging with echocardiography. Clinical research,2010,1(15) [Epub ahead of print]
    [14]Bax JJ, Atsma DE, Lamb HJ, Rebergen SA, et al. Noninvasive and invasive evaluation of noncompaction cardiomyopathy. J Cardiovasc Magn Reson. 2002,4(3):353-357
    [15]Stollberger C, Kopsa W, Tscherney R, et al. Diagnosing left ventricular noncompaction by echocardiography and cardiac magnetic resonance imaging and its dependency on neuromuscular disorders. Clin Cardiol,2008,31 (8):383-387.
    [16]Alhabshan F, Smallhorn JF, Golding F, et al. Extent of myocardial non-compaction:comparison between MRI and echocardiographic evaluation. Pediatr Radiol,2005,35(11):1147-1151.
    [17]Boyd MT, Seward JB, Tajik AJ, et al. Frequency and location of prominent left ventricular trabeculations at autopsy in 474 normal human hearts: implications for evaluation of mural thrombi by two-dimensional echocardiography. J Am Coll Cardiol,1987,9(2):323-326.
    [18]Asinger RW, Mikell FL, Sharma B, et al. Observations on detecting left ventricular thrombus with two dimensional echocardiography:emphasis on avoidance of false positive diagnoses. Am J Cardiol,1981,47(1):145-156
    [19]Marcus FI, Fontaine G. Arrhythmogenic right ventricular dysplasia/ cardiomyopathy:a review. Pacing Clin Electrophysiol,1995,18(6):1298-1314.
    [20]Sjoberg G, Chow CW, Cooper S, et al. X-linked cardiomyopathy presenting as contracted endocardial fibroelastosis. J Heart Lung Transplant, 2007,26(3):293-295.
    [21]何怡华,李治安,张惠信,等.心肌致密化不全的超声心动图与病理检查对照研究.中华超声影像学杂志,2003,12(10):581-584
    [22]Hansen MW, Merchant N. MRI of hypertrophic cardiomyopathy:part I, MRI appearances. AJR Am J Roentgenol,2007,189(6):1335-1343.
    [1]Weiford BC, Subbarao VD, Mulhern KM, et al. Noncompaction of the ventricular myocardium. Circulation,2004,109(24):2965-2971.
    [2]Maron BJ, Olivotto I, Spirito P, et al. Epidemiology of hypertrophic cardiomyopathy-related death:revisited in a large non-referral-based patient population. Circulation,2000,102(8):858-864.
    [3]Basso C, Thiene G, Corrado D, et al. Hypertrophic cardiomyopathy and sudden death in the young:pathologic evidence of myocardial ischemia. Hum Pathol, 2000,31 (8):988-998.
    [4]Bogaert J, Goldstein M, Tannouri F, et al. Late myocardial enhancement in hypertrophic cardiomyopathy with contrast-enhanced MR imaging. AJR Am J Roentgenol,2003,180(4):981-985.
    [5]Moon JC, McKenna WJ, McCrohon JA, et al. Toward clinical risk assessment in hypertrophic cardiomyopathy with gadolinium cardiovascular magnetic resonance. J Am Coll Cardiol,2003,41(9):1561-1567
    [6]Dodd JD, Holmvang G, Hoffmann U, et al. Quantification of left ventricular noncompaction and trabecular delayed hyperenhancement with cardiac MRI: correlation with clinical severity. Am J Roentgenol,2007,189 (4):974-980.
    [7]Weber KT. Cardiac interstitium in heart and disease:the fibrillar collagen network. J Am Coll Cardiol,1989,13(7):1637-1752
    [8]. Strauss DG, Wu KC. Imaging myocardial scar and arrhythmic risk prediction--a role for the electrocardiogram? J Electrocardiol,2009, 42(2):138. e1-8
    [9]Sato Y, Matsumoto N, Matsuo S, et al. Subendomyocardial perfusion abnor mality and necrosis detected by magnetic resonance imaging in a patient with isolated noncompaction of the ventricular myocardium associated with ventricular tachycardia. Cardiovasc Revasc Med,2009,10 (1):66-68
    [10]Sato Y, Matsumoto N, Matsuo S, et al. Myocardial perfusion abnormality and necrosis in a patient with isolated noncompaction of the ventricular myocardium:evaluation by myocardial perfusion SPECT and magnetic resonance imaging. Int J Cardiol,2007,120(2):e24-26
    [11]Jenni R, Oechslin E, Schneider J, et al. Echocardiographic and pathoana tomical characteristics of isolated left ventricular non-compaction:a step towards classification as a distinct cardiomyopathy. Heart,2001, 86(6):666-671
    [12]Burke A, Mont E, Kutys R, et al. Left ventricular noncompaction:a patho logical study of 14 cases. Hum Pathol,2005,36(4):403-411
    [13]Finsterer J, Stollberger C, Feichtinger H. Histological appearance of left ventricular hypertrabeculation/noncompaction. Cardiology,2002,98(3):1 62-164.
    [14]Conraads V, Paelinck B, Vorlat A, et al.Isolated non-compaction of the left ventricle:a rare indication for transplantation. J Heart Lung Transplant,2001,20(8):904-907
    [15]Dursun M, Agayev A, Nisli K, et al.MR imaging features of ventricular noncompaction:Emphasis on distribution and pattern of fibrosis. Eur J Radiol,2009,5(26):1-5
    [16]Matsumoto N, Sato Y, Kasama S, et al. Myocardial necrosis in both left and right ventricles detected by delayed-enhanced magnetic resonance imaging in a patient with isolated noncompaction of the ventricular myocardium. Int J Cardiol,2009,133(3):e94-96.
    [17]Alsaileek AA, Syed I, Seward JB, et al. Myocardial fibrosis of left ventricle:magnetic resonance imaging in noncompaction. J Magn Reson Imaging,2008,27(3):621-624.
    [18]Fieno DS, Kim RJ, Chen EL, et al. Contrast-enhanced magnetic resonance imaging of myocardium at risk:distinction between reversible and irreversible injury throughout infarct healing. J Am Coll Cardiol,2000, 36(6):1985-1991.
    [19]Toyono M, Kondo C, Nakajima Y, et al. Effects of carvedilol on left ventricular function, mass, and scintigraphic findings in isolated left ventricular non-compaction. Heart,2001,86(1):E4.
    [20]Soler R, Rodriguez E, Monserrat L, et al.MRI of subendocardial perfusion deficits in isolated left ventricular noncompaction. J Comput Assist Tomogr,2002,26 (3):373-375.
    [21]Jenni R, Wyss CA, Oechslin EN, et al. Isolated ventricular noncompaction is associated with coronary microcirculatory dysfunction. J Am Coll Cardiol,2002,39(3):450-454.
    [22]Junga G, Kneifel S, Von Smekal A, et al. Myocardial ischaemia in children with isolated ventricular non-compaction. Eur Heart J,1999,20(12): 910-916.
    [1]Glockner JF, Johnston DL, McGee KP. Evaluation of cardiac valvular disease with MR imaging:qualitative and quantitative techniques. Radiographics. 2003,23(3):686
    [2]Jenni R, Oechslin E, Schneider J, et al. Echocardiographic and pathoanato-mical characteristics of isolated left ventricular non-compaction:a step towards classification as a distinct cardiomyopathy. Heart,2001,86(6): 666-671.
    [3]Dodd JD, Holmvang G, Hoffmann U, et al. Quantification of left ventricular noncompaction and trabecular delayed hyperenhancement with cardiac MRI: correlation with clinical severity. Am J Roentgenol,2007,189 (4):974-980.
    [4]Chin TK, Perloff JK, Williams RG, et al. Isolated noncompaction of left ventricular myocardium. A study of eight cases. Circulation.1990,82 (2):507-513.
    [5]Kovacevic-Preradovic T, Jenni R, Oechslin EN, et al. Isolated left ventri cular noncompaction as a cause for heart failure and heart transplantation: a single center experience. Cardiology,2009,112(2):158-164.
    [6]Yousef ZR, Foley PW, Khadjooi K, et al. Left ventricular non-compaction: clinical features and cardiovascular magnetic resonance imaging. BMC Cardiovasc Disord.2009,9(8):37-45
    [7]Duncan RF, Brown MA, Worthley SG, et al. Increasing identification of isolated left ventricular non-compaction with cardiovascular magnetic resonance:a mini case series highlighting variable clinical presentation. Heart Lung Circ,2008,17(1):9-13
    [8]Fazio G, Novo G, Casalicchio C, Left ventricular non-compaction cardiomyo pathy in children:Is segmental fibrosis the cause of tissue Doppler alterations and of EF reduction?Int J Cardiol.2009,132(2):278-280.
    [9]Belanger AR, Miller MA, Donthireddi UR, New classification scheme of left ventricular noncompaction and correlation with ventricular perfor mance. Am J Cardiol.2008,102(1):92-96.
    [10]Agmon Y, Connolly HM, Olson LJ, et al. Noncompaction of the ventricular myocardium. J Am Soc Echocardiogr,1999,12(10):859-863.
    [11]Weiford BC, Subbarao VD, Mulhern KM. Noncompaction of the ventricular myocardium. Circulation,2004,109(24):2965-2971
    [12]Toyono M, Kondo C, Nakajima Y, et al. Effects of carvedilol on left ventricular function, mass, and scintigraphic findings in isolated left ventricular non-compaction. Heart,2001,86(1):E4.
    [13]Jenni R, Wyss CA, Oechslin EN, et al. Isolated ventricular noncompaction is associated with coronary microcirculatory dysfunction. J Am Coll Cardiol,2002,39(3):450-454.
    [14]Soler R, Rodriguez E, Monserrat L, et al.MRI of subendocardial perfusion deficits in isolated left ventricular noncompaction. J Comput Assist Tomogr,2002,26(3):373-375.
    [15]Junga G, Kneifel S, Von Smekal A, et al. Myocardial ischaemia in children with isolated ventricular non-compaction.Eur Heart J,1999,20(12): 910-916.
    [16]Zaragoza MV, Arbustini E, Narula J. Noncompaction of the left ventricle: primary cardiomyopathy with an elusive genetic etiology. Curr Opin Pediatr. 2007,19 (6):619-627.
    [17]Matsuda M, Tsukahara M, Kondoh O, et al. Familial isolated noncompaction of ventricular myocardium. J Hum Genet,1999;44(2):126-128.
    [18]Murphy RT, Thaman R, Blanes JG, et al. Natural history and familial characteristics of isolated left ventricular non-compaction. Eur Heart J,2005,26 (2):187-192.
    [19]Gabrielli FA, Lombardo A, Natale L, et al. Myocardial infarction in isolated ventricular non-compaction:contrast echo and MRI. Int J Cardiol. 2006,111(2):315-317.
    [20]Burke A, Mont E, Kutys R, et al. Left ventricular noncompaction:a patho logical study of 14 cases. Hum Pathol.2005,36(4):403-411
    [21]Finsterer J, Stollberger C, Feichtinger H. Histological appearance of left ventricular hypertrabeculation/noncompaction. Cardiology,2002,98(3):1 62-164.
    [22]Conraads V, Paelinck B, Vorlat A, et al.Isolated non-compaction of the left ventricle:a rare indication for transplantation. J Heart Lung Transplant,2001,20(8):904-907
    [23]Dursun M, Agayev A, Nisli K, et al. MR imaging features of ventricular noncompaction:Emphasis on distribution and pattern of fibrosis. Eur J Radiol.2009 Mar 26. [Epub ahead of print]
    [1]Tsutamoto T, Wada A, Maeda K, et al. Attenuation of compensation of endogenous cardiac natriuretic peptide system in chronic heart failure: prognostic role of plasma brain natriuretic peptide concentration in patients with chronic symptomatic left ventricular dysfunction. Circulation,1997,96(2):509-516
    [2]Boomsma F, van den Meiracker AH. Plasma A-and B-type natriuretic peptides: physiology, methodology and clinical use. Cardiovasc Res,2001, 51 (3):442-449
    [3]Omland T, Persson A, Ng L, et al. N-terminal pro-B-type natriuretic peptide and long-term mortality in acute coronary syndromes. Circulation,2002, 106(23):2913-2918.
    [4]刘梅林,李继敏,胡大一,等.心绞痛患者血浆N-proBNP水平的变化及其临床意义.中华心血管病杂志.2004,32(6):497-500
    [5]Toyono M, Kondo C, Nakajima Y, et al. Effects of carvedilol on left ventricular function, mass, and scintigraphic findings in isolated left ventricular non-compaction. Heart,2001,86(1):E4.
    [6]Bogaert J, Goldstein M, Tannouri F, et al. Late myocardial enhancement in hypertrophic cardiomyopathy with contrast-enhanced MR imaging. AJR Am J Roentgenol,2003,180(4):981-985
    [7]Moon JC, McKenna WJ, McCrohon JA, et al. Toward clinical risk assessment in hypertrophic cardiomyopathy with gadolinium cardiovascular magnetic resonance. J Am Coll Cardiol,2003,41(9):1561-1567
    [8]Dodd JD, Holmvang G, Hoffmann U, et al. Quantification of left ventricular noncompaction and trabecular delayed hyperenhancement with cardiac MRI: correlation with clinical severity. Am J Roentgenol,2007,189 (4):974-980.
    [9]McCullough PA, Nowak RM, McCord J, et al. B-type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure:analysis from Breathing Not Properly (BNP) Multinational Study. Circulation,2002,106 (4):416-422
    [10]Nakamura M, Endo H, Nasu M, Value of plasma B type natriuretic peptide measurement for heart disease screening in a Japanese population. Heart. 2002,87 (2):131-135.
    [11]Hunt SA, Abraham WT, Chin MH, ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult:a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation.2005,112(12):e154-235.
    [12]Moe GW. BNP in the diagnosis and risk stratification of heart failure. Heart Fail Monit,2005,4(4):116-122.
    [13]Moe GW. B-type natriuretic peptide in heart failure. Curr Opin Cardiol. 2006,21(3):208-214.
    [14]Adams KF Jr, Mathur VS, Gheorghiade M. et al. B-type natriuretic peptide: from bench to bedside. Am Heart J,2003,145(2):S34-46.
    [1]Sarma RJ, Chana A, Elkayam U. Left ventricular noncompaction. Prog Cardio vase Dis,2010,52(4):264-273.
    [2]Maron BJ, Towbin JA, Thiene G, et al.Contemporary definitions and classification of the cardiomyopathies:an American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. Circulation,2006,113(14):1807-1816.
    [3]Bellets S, Goulet BA. Congenital heart disease with multiple cardiac anomalies:report of a ease showing aortic atresia, fibrous scar in myocardium and embryona sinusoidal remains. Am J Med Sci,1932,183:458-465
    [4]Chin TK, Perloff JK, Williams RG, et al. Isolated noncompaction of left ventricular myocardium. A study of eight cases. Circulation.1990,82 (2):507-513.
    [5]Stollberger C, Finsterer J. Left ventricular hypertrabeculation /noncompaction. J Am Soc Echocardiogr,2004,17(1):91-100
    [6]Weiford BC, Subbarao VD, Mulhern KM. Noncompaction of the ventricular myocardium. Circulation,2004,109(24):2965-2971.
    [7]Burke A, Mont E, Kutys R, Left ventricular noncompaction:a pathological study of 14 cases. Hum Pathol,2005,36(4):403-411
    [8]Oechslin EN, Attenhofer Jost CH, et al. Long-term follow-up of 34 adults with isolated left ventricular noncompaction:a distinct cardiomyopathy with poor prognosis. J Am Coll Cardiol,2000,36(2):493-500
    [9]Duncan RF, Brown MA, Worthley SG, et al. Increasing identification of isolated left ventricular non-compaction with cardiovascular magnetic resonance:a mini case series highlighting variable clinical presentation. Heart Lung Circ,2008,17(1):9-13.
    [10]Ritter M, Oechslin E, Sutsch G, et al. Isolated noncompaction of the myocardium in adults. Mayo Clin Proc,1997,72(1):26-31.
    [11]兰天,刘玉清.成人孤立性心室心肌致密化不全.国外医学临床放射学杂志.2007:30(6):403-405
    [12]Engberding R, Bender F. Identification of a rare congenital anomaly of the myocardium by two-dimensional echocardiography:persistence of isolated myocardial sinusoids. Am J Cardiol.1984,53(11):1733-1734.
    [13]Bartram U, Bauer J, Schranz D. Primary noncompaction of the ventricular myocardium from the morphogenetic standpoint. Pediatr Cardiol,2007,28 (5):325-332.
    [14]Wagner M, Siddiqui MA. Signal transduction in early heart development (Ⅱ):ventricular chamber specification, trabeculation, and heart valve formation. Exp Biol Med (Maywood),2007,232(7):866-880.
    [15]Sedmera D, Pexieder T, Vuillemin M, et al. Developmental patterning of the myocardium. Anat Rec,2000,258(4):319-337
    [16]Captur G, Nihoyannopoulos P. Left ventricular non-compaction:Genetic heterogeneity, diagnosis and clinical course. Int J Cardiol.2009 Aug 5.[Epub ahead of print]
    [17]Lee KF, Simon H, Chen H, et al. Requirement for neuregulin receptor erbB2 in neural and cardiac development. Nature,1995,378(6555):394-398.
    [18]Viragh S, Challice CE. The origin of the epicardium and the embryonic myocardial circulation in the mouse. Anat Rec,1981,201(1):157-168.
    [19]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, Dev Dyn,1997,208(3):3 38-348
    [20]Petersen SE, Selvanayagam JB, Wiesmann F, et al. Left ventricular non-compaction:insights from cardiovascular magnetic resonance imaging,J Am Coll Cardiol.2005,46(1):101-105.
    [21]Zambrano E, Marshalko SJ, Jaffe CC, et al. Isolated noncompaction of the ventricular myocardium:clinical and molecular aspects of a rare cardiomyopathy. Lab Invest,2002,82(2):117-122.
    [22]Finsterer J. Cardiogenetics, neurogenetics, and pathogenetics of left ventricular hypertrabeculation/noncompaction. Pediatr Cardiol.2009,30 (5):659-681
    [23]Toyono M, Kondo C, Nakajima Y, et al. Effects of carvedilol on left ventricular function, mass, and scintigraphic findings in isolated left ventricular non-compaction. Heart,2001,86(1):E4.
    [24]Sasse-Klaassen S, Gerull B, Oechslin E, et al. Isolated noncompaction of the left ventricular myocardium in the adult is an autosomal dominant disorder in the majority of patients. Am J Med Genet A,2003,119A (2):162-167.
    [25]Zaragoza MV, Arbustini E, Narula J. Noncompaction of the left ventricle: primary cardiomyopathy with an elusive genetic etiology. Curr Opin Pediatr. 2007,19(6):619-627.
    [26]Matsuda M, Tsukahara M, Kondoh 0, et al. Familial isolated noncompaction of ventricular myocardium. J Hum Genet,1999;44(2):126-128.
    [27]Biagini E, Ragni L, Ferlito M, et al. Different types of cardiomyopathy associated with isolated ventricular noncompaction. Am J Cardiol. 2006,98 (6):821-824.
    [28]Shirahama M, Yamano M, Kawasaki T, et al. Biventricular noncompaction detected by magnetic resonance imaging:a case report. J Cardiol,2007 50(2):149-154.
    [29]Chin TK, Perloff JK, Williams RG, et al. Isolated noncompaction of left ventricular myocardium. A study of eight cases. Circulation,1990,82 (2):507-513.
    [30]Bleyl SB, Mumford BR, Brown-Harrison MC, et al. Xq28-linked noncompaction of the left ventricular myocardium:prenatal diagnosis and pathologic analysis of affected individuals. Am J Med Genet,1997,72(3):257-265
    [31]Stollberger C, Finsterer J, Blazek G. et al.Left ventricular hypertr abeculation/noncompaction and association with additional cardiac abnormalities and neuromuscular disorders. Am J Cardiol,2002,90 (8):899-902.
    [32]Kohli SK, Pantazis AA, Shah JS, et al. Diagnosis of left-ventricular non-compaction in patients with left-ventricular systolic dysfunction: time for a reappraisal of diagnostic criteria? Eur Heart J.2008,29 (1):89-95.
    [33]Yousef ZR, Foley PW, Khadjooi K, et al.Left ventricular non-compaction: clinical features and cardiovascular magnetic resonance imaging. BMC Cardiovasc Disord.2009,9(8):37-45
    [34]Agmon Y, Connolly HM, Olson LJ, et al. Noncompaction of the ventricular myocardium. J Am Soc Echocardiogr,1999,12(10):859-863.
    [35]Liberthson RR.Sundden death from cardiac causes in children and young adults. N.Engl J Med,1996,334(16):1039-1044
    [36]Yasukawa K, Terai M, Honda A, et al. Isolated noncompaction of ventricular myocardium associated with fatal ventricular fibrillation. Pediatr Cardiol.2001,22(6):512-514.
    [37]Buonanno C, Variola A, Dander B, et al. Isolated noncompaction of the myocardium:an exceedingly rare cardiomyopathy. A case report. Ital Heart J.2000,1(4):301-305.
    [38]Stollberger C, Finsterer J. Thrombi in left ventricular hypertra beculation/noncompaction--review of the literature. Acta Cardiol. 2004,59(3):341-344.
    [39]Stollberger C, Winkler-Dworak M, Blazek G, et al. Prognosis of left ventricular hypertrabeculation/noncompaction is dependent on cardiac and neuromuscular comorbidity.Int J Cardiol.2007,121(2):189-193.
    [40]Ichida F, Hamamichi Y, Miyawaki T, et al. Clinical features of isolated noncompaction of the ventricular myocardium:long-term clinical course, hemodynamic properties, and genetic background. J Am Coll Cardiol. 1999,34 (1):233-240.
    [41]Hook S, Ratliff NB, Rosenkranz E, et al. Isolated noncompaction of the ventricular myocardium. Pediatr Cardiol,1996,17(1):43-45.
    [42]Finsterer J, Stollberger C. Cardiac MRI versus echocardiography in assessing noncompaction in children without neuromuscular disease. Pediatr Radiol,2006,36(7):720-721.
    [43]Jenni R, Oechslin E, Schneider J, et al. Echocardiographic and patho anatomical characteristics of isolated left ventricular non-compaction: a step towards classification as a distinct cardiomyopathy,Heart,2001 86(6):666-671
    [44]Boyd MT, Seward JB, Tajik AJ, et al. Frequency and location of prominent left ventricular trabeculations at autopsy in 474 normal human hearts: implications for evaluation of mural thrombi by two-dimensional echocardiography. J Am Coll Cardiol,1987,9(2):323-326
    [45]Finsterer J, Stollberger C. Definite, probable, or possible left ventricular hypertrabeculation/noncompaction. Int J Cardiol,2008,123 (2):175-176.
    [46]McCrohon JA, Richmond DR, Pennell DJ, et al. Images in cardiovascular medicine. Isolated noncompaction of the myocardium:a rarity or missed diagnosis?Circulation,2002,106(6):e22-3.
    [47]Alhabshan F, Smallhorn. JF, Golding F, et al. Extent of myocardial non-compaction:comparison between MRI and echocardiographic evaluation. Pediatr Radiol.2005,35(11):1147-1151.
    [48]Dodd JD, Holmvang G, Hoffmann U, et al. Quantification of left ventricular noncompaction and trabecular delayed hyperenhancement with cardiac MRI: correlation with clinical severity. Am J Roentgenol,2007,189 (4):974-980.
    [49]Fazio G, Visconti C, D' Angelo L, et al. Delayed MRI hyperenhancement in noncompaction:sign of fibrosis correlated with clinical severity. Am J Roentgenol,2008,190(4):W273
    [50]Sen-Chowdhry S, McKenna WJ.Left ventricular noncompaction and cardiomyopathy:cause, contributor, or epiphenomenon? Curr Opin Cardiol. 2008,23 (3):171-175.
    [51]Conces DJ Jr, Ryan T, Tarver RD. Noncompaction of ventricular myocardium: CT appearance. Am J Roentgenol.1991,156(4):717-718.
    [52]Sarma RJ, Chana A, Elkayam U. Left ventricular noncompaction. Prog Cardiovasc Dis.2010,52(4):264-273.
    [53]Sato Y, Matsumoto N, Matsuo S, Right ventricular involvement in a patient with isolated noncompaction of the ventricular myocardium. Cardiovasc Revasc Med.2007,8(4):275-277
    [54]Asinger RW, Mikell FL, Sharma B, et al. Observations on detecting left ventricular thrombus with two dimensional echocardiography:emphasis on avoidance of false positive diagnoses. Am J Cardiol,1981,47(1):145-156
    [55]Conraads V, Paelinck B, Vorlat A, et al. Isolated non-compaction of the left ventricle:a rare indication for transplantation. J Heart Lung Transplant,2001,20(8):904-907
    [56]Fazio G, Corrado G, Zachara E, et al. Anticoagulant drugs in noncompaction: a mandatory therapy?J Cardiovasc Med (Hagerstown),2008,9(11):1095-1097.
    [57]Pignatelli RH, McMahon CJ, Dreyer WJ, et al. Clinical characterization of left ventricular noncompaction in children:a relatively common form of cardiomyopathy. Circulation.2003,108(21):2672-2678.
    [58]Rigopoulos A, Rizos IK, Aggeli C, et al. Isolated left ventricular noncompaction:an unclassified cardiomyopathy with severe prognosis in adults. Cardiology.2002,98(1-2):25-32.
    [59]Murphy RT, Thaman R, Blanes JG, et al. Natural history and familial characteristics of isolated left ventricular non-compaction. Eur Heart J.2005,26(2):187-192.
    [60]Finsterer J, Stollberger C, Blazek G. Neuromuscular implications in left ventricular hypertrabeculation/noncompaction. Int J Cardiol.2006,110 (3):288-300.

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