超声心动图评价以右心室病变为主的心肌病

目的 探讨以右心室病变为主的心肌病的彩色多普勒超声显像特点。方法 应用彩色多普勒超声心动图诊断以右心室病变为主的心肌病患者13例。结果 11例患者右心房明显增大,所有患者均有不同程度的三尖瓣关闭不全,1例患者左心室轻度增大。超声心动图观察右心室形态变化,8例以右心室显著增大为主要特点,表现为右心室弥漫性扩大或局限性扩张,右室壁变薄,右室壁普遍性或局限性运动减弱,心尖小梁部和右室流入部肌小梁粗大,回声增强。5例以右室心尖小梁部闭塞为主要特点,表现为右室腔缩小、变形,心尖小梁部明显缩小或完全闭塞,右室流出道正常或扩张,增厚的右室壁回声增强,心包膜厚度正常。结论 以右心室病变为主的心肌病超声显像特点为右室扩大、室壁变薄、运动减弱或右室腔缩小、变形,心尖小梁部明显缩小或完全闭塞等两种表现。这些特征对以右心室病变为主的心肌病具有较高的诊断价值。     

超声心动图诊断右心型心内膜心肌纤维化的临床价值

目的探讨超声心动图在右心型心内膜心肌纤维化（EMF）诊断中的临床价值。方法回顾分析10例右心型EMF患者的临床和超声心动图检查资料。结果10例右心型EMF患者中,均有右心房明显增大,右室腔缩小变形,右室流入道及右室内膜增厚,回声增强。其中7例伴有右室心尖小梁部闭塞,8例伴有不同程度三尖瓣关闭不全。结论超声心动图能准确显示右心型EMF患者的右心房、右心室的形态变化及右室心尖小梁部闭塞及心脏的血流动力学改变,为临床诊断提供可靠依据。     

超声心动图在诊断心尖肥厚型心肌病中的应用

目的：探讨超声心动图检测心尖肥厚型心肌病的特征性改变和诊断价值。方法：采用彩色多普勒超声诊断仪对26例心尖肥厚性心肌病患者和28例正常对照组的超声心动图、心电图进行对比检测。结果：对28例心尖肥厚型心肌病的患者检测左室心尖部厚度与正常组比较有明显差异，P〈0．05；左房径增大与正常组比较有明显差异，P〈0．05。其中室间隔心尖水平肥厚者12例，乳头肌水平以下左室游离壁肥厚者5例，室间隔心尖段＋乳头肌水平以下左室游离壁肥厚者7例，乳头肌水平以下右室游离壁肥厚者2例。结论：超声心动图是准确诊断心尖肥厚性心肌病的主要方法之一，能为临床提供有价值的诊断依据。     

非典型肥厚型心肌病7例的超声心动图及临床特点分析

目的总结7例非典型肥厚型心肌病患者的超声心动图及临床特点,旨在加强超声诊断医生对该病的认识,以提高诊断率。方法回顾性描述该7例患者二维及多普勒超声心动图及临床特点,以及部分心电图资料。结果 7例非典型肥厚型心肌病患者中,心尖部肥厚4例,其中心尖部室间隔及心尖部左室游离壁肥厚3例,单纯心尖部室间隔肥厚1例,均匀肥厚型1例,室间隔中部肥厚并前壁节段性运动异常1例,单纯右室游离壁肥厚1例。结论非典型肥厚型心肌病发病率低,超声特征相对不典型,应结合临床资料特别是心电图综合判断,从而减少漏诊或误诊。     

无创性诊断致心律失常性右心室发育不良心肌病的超声心动图与磁共振对比研究

目的致心律失常性右心室发育不良心肌病(ARVC)是一种累及右心室心肌组织的心肌病,其右心室的解剖结构和组织病理发生改变,从而导致各种心律失常。本研究旨在运用超声心动图与核磁共振(MRI)无创性手段对ARVC进行检查,并进行对比分析,以期提高临床诊断ARVC的准确性。方法9例符合ARVC诊断标准的患者行超声心动图和MRI检查,男7例,女2例,平均年龄(42．6±14．8)岁。记录临床资料,如家族史、心悸、晕厥、室性早搏(PVB)、室性心动过速(VT)和Epsilon波。由一位医师盲法进行超声心动图检查,记录右心室壁、右室流出道(RVOT>30 mm)、调节束、异常肌小梁、憩室和囊袋。MRI检查用EKG触发,从冠状面、矢状面和轴向面进行扫描,层厚10 mm,记录动态模式,用“黑血”技术行右室壁心肌检查,记录脂肪和纤维脂肪组织,同时记录右心室壁、右室流出道、调节束、异常肌小梁、憩室和囊袋等解剖结构异常。对两种检查方法的结果用Fisher’s精确检验行统计学分析。结果2例患者有家族史,8例有心悸症状,2例有晕厥,9例有PVB,7例有VT,3例有Epsilon波。超声心动图检查示2例患者右心室壁变薄、6例右室流出道扩张,6例患者有调节束、4例有异常肌小梁、1例有瘤样膨出．MRI检查示4例患者右心室壁变薄、7例右室流出道扩张,6例患者有调节束、4例有异常肌小梁、3例有憩室和囊袋、2例有脂肪替代心肌。在右室流出道扩张、调节束和异常肌小梁方面,两者检出率相似,MRI在室壁变薄、小憩室和脂肪替代心肌方面优于超声心动图,由于样本量较小,两者差异无统计学意义。结论超声心动图和MRI技术可发现ARVC患者右心室壁变薄、右室流出道扩张、调节束、异常肌小梁、憩室和囊袋等解剖结构异常,MRI在确诊微小结构异常和心肌组织脂肪化方面优于超声心动图。     

非典型肥厚型心肌病7例的超声心动图及临床特点分析

目的 总结7例非典型肥厚型心肌病患者的超声心动图及临床特点,旨在加强超声医师对该病的认识,提高诊断率.方法 分析7例患者二维及多普勒超声心动图及临床特点,以及部分心电图资料.结果 7例非典型肥厚型心肌病患者中,心尖部肥厚4例,其中心尖部室间隔及心尖部左室游离壁肥厚3例,单纯心尖部室间隔肥厚1例;均匀肥厚型1例,室间隔中部肥厚并前壁节段性运动异常1例,单纯右室游离壁肥厚1例.结论 非典型肥厚型心肌病发病率低,超声特征相对不典型,应结合临床资料特别是心电图综合判断,从而减少漏诊或误诊.     

彩超对扩张型心肌病与缺血性心肌病对比分析

目的探讨超声心动图对扩张型心肌病(DCM)与缺血性心肌病(ICM)的鉴别诊断的临床意义.方法对38例扩张型心肌病和26例缺血性心肌病患者的超声检查结果进行对比分析.结果 DCM组心脏多个房室腔扩大多呈"球形",室壁变薄及弥漫性减弱,心尖部心肌不变薄及EPSS增大,多瓣膜反流,以收缩功能降低较明显为其特点.ICM组以左房室腔扩大多呈"圆拱门形",心尖圆钝变薄,室壁活动呈节段性障碍,主动脉及根部钙化、主动脉增宽,单瓣膜反流,以舒张功能障碍较明显为其特点.结论彩超结合患者病史是对扩张型心肌病与缺血性心肌病进行鉴别的简便无创性可靠方法.     

超声心动图对心尖肥厚型心肌病及早期心尖肥厚型心肌病的诊断价值分析

目的评价超声心动图对典型心尖肥厚型心肌病（T-AHCM）及早期心尖肥厚型心肌病（P-AHCM）的诊断价值。方法对T-AHCM患者68例和P-AHCM患者42例行超声心动图检查,并结合检测结果同30例正常者进行比较分析。结果本组68例典型T-AHCM患者中单纯心尖部肥厚48例,同时累及乳头肌20例,其中8例收缩末心尖部心腔缩小近于闭塞;42例P-AHCM中单纯心尖部肥厚36例,同时累及乳头肌6例。T-AHCM组及P-AHCM组的舒张末期心尖段室壁厚度（LVAW）,舒张末期心尖段室壁厚度与舒张末期基底段室间隔厚度的比值（LVAW/IVS）以及左房内径与正常组患者比较均有统计学差异（均P〈0.05）。T-AHCM组中有93%（63例）,P-AHCM组中有41%（17例）患者测及二尖瓣血流频谱E峰/A峰〈1,正常组仅2例二尖瓣血流频谱E峰/A峰〈1。全部110例病患左室内径均无明显增大。本组患者不管是T-AHCM组还是P-AHCM组,肥厚的心尖部心肌回声均尚均匀或略增粗。结论超声心动图是早期明确诊断P-AHCM、T-AHCM的有效方法。     

成人孤立性心肌致密化不全的超声诊断分析

目的:探讨超声心动图对心肌致密化不全的诊断价值及临床意义。方法:用超声心动图多切面探查心脏形态、结构及血流改变特征,重点观察近心尖处心室壁结构特点。结果:8例患者超声心动图特点均为多发过度隆起肌小梁和深陷的小梁隐窝,病变部位主要在心尖部1/3处、心室侧壁,基底部未见受累心肌;彩色多普勒示深陷的肌小梁隐窝有低速血流与心腔交通,本组患者隐窝内未见血栓;射血分数均<40%。结论:心肌致密化不全超声心动图具有特征性改变,是目前诊断该病的首选检查方法。     

致心律失常性右室发育不良的影像学特点(2例报告并文献复习)

目的:探讨致心律失常性右室发育不良(ARVD)的超声心动图及磁共振(MRI)图像表现,以提高对其认识.方法:对2例完全符合欧洲心脏病学会/国际心脏病学会ARVD诊断标准的患者,分别进行超声心动图及MRI检查,重点观察右心室形态结构及功能改变,并在心脏三维电解剖标测系统(Carto)标测下构建右心室电解剖图,进行心内电生理检查及射频消融治疗.结果:超声心动图检查显示2例患者均右心室腔扩张,右室壁有局限性室壁瘤,调节束回声增强.MRI也提示右心腔扩大,右心室肌小梁排列紊乱.2例患者影像学检查所提示的病变区与Carto标测的低电压区一致.结论:超声心动图及MRI检查可无创性检测ARVD患者右心室形态结构及功能改变,为ARVD的临床诊断提供重要依据.     

超声心动图对心肌致密化不全的诊断价值

目的分析超声心动图在心肌致密化不全（Noncompaction of Ventricular Myocardium NVM）诊断中的应用价值及临床意义。方法彩色多普勒超声心动图对临床心功能不全和心脏扩大的患者进行多切面的探查,总结心肌致密化不全患者的超声心动图特征,分析病变区域的分布特点。结果 15例超声诊断为心肌致密化不全,其中14例为左室受累,1例为左右室均受累。采用jenni等提出的诊断标准：①病变区域心室壁为双层结构,外层较薄为致密层,内层较厚为非致密化心肌,非致密化心肌中间可见深隐窝。②心室收缩末期内层非致密化心肌厚度与外层致密化心肌厚度比值〉2.0。③彩色多普勒显示深隐窝内有血流与心室腔相通,患者的超声心动图均显示受累室壁由丰富的肌小梁和深陷的隐窝构成,隐窝内血流与心室腔相通,室间隔及左室前壁无受累。结论心肌致密化不全具有特征性超声心动图表现,是诊断心肌致密化不全可靠首选的方法。     

原发性心肌病心电图的分析与探讨

本文对４０例确诊为原发性心肌病的心电图进行了回顾性分析。结果发现，在扩张型心肌病中，左室腔增大、左室游离壁变薄时，胸前导联ＱＲＳ波电压增高及ＳＴ－Ｔ的改变与常规心电图中左室肥厚及劳损的改变类似；左房扩大时Ｐ波时限并未≥０．１１ｓ，心尖肥厚型心肌病以多导联持续的尖、深、窄、双肢对称的倒置Ｔ波及下垂型ＳＴ段为其典型特征。空间隔肥厚型心肌病以持续下垂型ＳＴ段下移及负正双向Ｔ波为显著表现。作者提出对原发性心肌病不能用常规心电图标准来判断其左室游离壁厚度及左房扩大。     

缺血性心肌病与扩张型心肌病超声比较分析

目的：探讨彩色多普勒超声对缺血性心肌病与扩张型心肌病的鉴别诊断价值。方法：将15例缺血性心肌病和43例扩张型心肌病患者的超声检查结果进行比较分析。结果：室壁局限性变薄及室壁节段性运动异常，主动脉瓣区退行性变是缺血性心肌病的超声特征。扩张型心肌病则表现为室壁弥漫性变薄，运动弥漫性减弱，右房室扩大，多瓣膜反流，与前者对比有显著性差异。结论：彩超结合患者病史是对缺血性心肌病和扩张型心肌病进行鉴别的简便可靠方法。     

Clinical and familial study of arrhythmogenic right ventricular cardiomyopathy

Objective　To explore the characteristics of arrhythmogenic right ventricular cardiomyopathy (ARVC). Methods　Seven patients with arrhythmogenic right ventricular cardiomyopathy and 34 members of three families were studied. All patients and family members underwent history collection, clinical examination, electrocardiogram (ECG), two-dimensional echocardiography (2-DE) and a signal averaging electrocardiogram. Programmed ventricular stimulation was performed in five patients. Results　All patients and family members had normal morphologic characteristics and normal function of the left ventricular by 2-DE. Fourteen persons had abnormal findings indicating ARVC. Five had enlargement of the right ventricular with diffused hypocontractility, eight had thin and systolic bulging in the focal anterior wall with hypokinesia and one had bulging of the inferior wall. Twenty-five persons (seven patients and 18 family members) had abnormal findings in ECG. Positive ventricular late potential was recorded in 13 persons (six patients). Two to three monomorphic ventricular tachycardia (VT) with left bundle branch block (LBBB) configurations were induced in five patients. Ventricular fibrillation was induced in two patients during the electrophysiologic study (EPS). Five patients had very high pacing threshold and/or ineffective pacing in one or many regions of the right ventricle. Two members of one family died suddenly. One member was a dwarf with ARVC. Spontaneous VT with a left bundle branch block (LBBB) configuration was recorded in five patients, polymorphic VT with extremely short coupling interval in one, and premature ventricular complexes with LBBB configuration in 12 (six patients). Conclusion　Our familial study strongly suggests that ARVC may be a hereditary disease and it is helpful in the diagnosis and detection of ARVC. The most common manifestations were abnormal structure and function of the right ventricle and abnormal ECG of repolarization and ventricular arrhythmia which originates from the right ventricle.     

Pacemaker implantation in a patient with noncompaction and aneurysm of right ventricular combination with postclosure of atrial septal defect

To the editor:Noncompaction of the ventricular myocardium (NVM) can be an isolated condition or co-existed with other congenital cardiac malformations.We report a NVM patient presenting with localized right ventricular aneurysm (VA) formation,atrial septal defect (ASD),and bradycardia,and describe a new tactics by which a dual-chamber pacemaker (PM) was implanted successfully. A 37-year-old male with palpitation and lightheadedness was referred to our hospital for further diagnostic procedures.Two years ago,transthoracic echoeardiography showed dilated ventricle and right atrium (RA),globally hypokinetic left ventricle (LV),thinning hypokinetic myocardium in the apex and outflow tract of right ventricle (RV) and formation of local VA,prominent trabecularization in the lateral wall of right ventricle,and ASD with the diameter of about 10 mm.Deep intertrabecular recesses with flow coming out from RV cavity by color Doppler flow imaging.     

Right ventricular endomyocardial fibrosis – A case report

Endomyocardial fibrosis (EMF) is a progressive type of restrictive cardiomyopathy. It affects inflow portion of right and/or left ventricle and apex. It is a neglected tropical disease. Here we report a rare case of right ventricular endomyocardial fibrosis. A 70-year-old female presented to us with history suggestive of right-sided heart failure of two months duration. There was no eosinophilia. Chest X-ray showed cardiomegaly. Echocardiogram showed dilated right atrium and obliteration of the apex of the right ventricle. A diagnosis of Right ventricular Endomyocardial fibrosis was made. She was treated with diuretics and anticoagulants and she improved.     

双脉冲波多普勒组织速度超声成像评价正常成年人心室不同水平面心肌机械运动时空特征

目的应用双脉冲波多普勒组织速度超声成像评价正常人心室短轴不同水平面心肌机械运动特征及表达时间差异,探讨其临床应用价值。方法应用双脉冲波多普勒组织速度超声成像同步采集100例健康成年人3个连续心动周期内二尖瓣、乳头肌及心尖3个水平左心室标准短轴切面,两两同步获取右心室游离壁、前间隔及左心室后壁心肌的双脉冲波多普勒组织速度超声图像。观察同一水平面左右心室心肌及同一室壁不同节段心肌机械运动特征。测量左心室短轴二尖瓣、乳头肌及心尖3个水平右心室游离壁、前间隔及左心室后壁共6个节段心肌在收缩期、快速充盈期及心房收缩期机械运动达峰时间(Ts、Te、Ta),分析同一水平面不同室壁心肌以及同一室壁不同节段心肌的机械同步顺序状态。结果双脉冲波多普勒组织速度图像显示:左心室短轴切面,同一水平的右心室游离壁与前间隔心肌运动方向一致,左心室后壁心肌与前两个室壁心肌运动方向相反。左心室短轴3个标准水平面,同一水平不同室壁心肌达峰时间:①前间隔心肌Ts最短;基底段和中间段,左心室后壁心肌较前间隔分别延迟约14和19ms,较右心室游离壁分别延迟约11和12ms(P均<0.001);心尖段,右心室游离壁心肌Ts最大,3个室壁心肌间差异无统计学意义(P>0.05)。②左心室后壁心肌Te最短,前间隔心肌Te最长,并且3个室壁心肌两两间的Te值差均有统计学意义(P均<0.001)。③左心室后壁心肌Ta最短,前间隔心肌Ta最长。前间隔和右心室游离壁心肌Ta值较左心室后壁延迟均约10ms(P均<0.001)。同一室壁心肌在左室不同水平面机械运动表达时间差异性:左心室后壁心肌从基底段至心尖段Ts值逐渐延长,中间段心肌较基底段延迟14ms,心尖段心肌较基底段延迟17ms(P<均0.001);心尖段心肌较中间段延迟仅3ms(P>0.05)。结论正常成年人心脏收缩及舒张期机械运动空间及时间上均具有不对称性;同一室壁不同节段心肌从心尖至基底收缩时间逐渐延长,舒张时间保持高度一致。双脉冲波多普勒组织速度超声成像能更客观的评价心脏收缩期及舒张早、晚期表达时间差异性。     

胎儿心肌致密化不全的超声心动图诊断与病理对比研究

目的：研究胎儿心肌致密化不全心肌病(ventricular non-compaction cardiomyopathy,NCCM)的产前超声心 动图诊断及其病理特征和心肌超微结构的特点。方法：2004年到2013年产前超声诊断9例胎儿NCCM,观察其产前超 声心动图表现,与产后超声心动图或尸体解剖进行对比,并取心肌组织进行病理检查,观察NCCM心肌超微结构特 点。结果：NCCM心肌的超声心动图表现为异常粗大的肌小梁、肌小梁隐窝和心肌非致密层厚度/致密层厚度≥2。 产前超声心动图诊断9例胎儿NCCM中,6例累及左心室,2例累及双心室,1例累及右心室。其中2例胎儿继续妊娠至 分娩,并经产后超声心动图证实,其他7例均选择终止妊娠并经尸体解剖病理证实,心肌组织活检显示NCCM心肌的 线粒体和肌小节发育不良、心肌纤维化。结论：通过产前超声心动图诊断NCCM是可行的。胎儿NCCM可以累及左 心室、右心室或两个心室。NCCM心肌的线粒体和肌小节成熟度低并伴有心肌纤维化。     

RETROSPECTIVE ANALYSIS OF MAGNETIC RESONANCE MYOCARDIAL DELAYED ENHANCEMENT

Objective To explore the imaging and related clinical characteristics of magnetic resonance （MR） delayed enhancement in patients with ischemic or nonischemic heart disease. Methods Thirty-two cases who underwent MR myocardial cine and delayed enhancement imaging from January 2004 to October 2006 were retrospectively analyzed. The cine sequence imaging included the four-chamber view and the left ventricular short axis view. The delayed enhancement imaging was taken 10 minutes after the infusion of gadolinium from the antecubital vein with a segmented inversion-recovery-prepared Tl-weighted fast gradient echo sequence. Patients underwent coronary computed tomography angiography （CTA） two weeks before or after the MR imaging examination. Combined with clinical history, the clinical and MR imaging characteristics of the patients who had delayed enhancement were analyzed. Results MR delayed enhancement could be found in 16 cases. Among them, 12 cases had ischemic heart disease. Their coronary CTA showed one to three vessel diseases. The delayed enhancement was transmural or subendocardium, and the area of delayed enhancement corresponded well with one or more coronary arteries which had severe stenosis or occlusion. Four cases had nonischemic heart diseases One case was dilated cardiomyopathy, with diffuse small midwall spots in delayed enhancemen and only 30% stenosis of the anterior descending coronary artery in coronary CTA. One case was hypertrophic cardiomyopathy, with delayed enhancement of strip- and patch-shaped at midwall of the hypertrophic myocardiurn. One case was restrictive cardiomyopathy, and the delayed enhancement was located in the area of subendocardium of both the right and left ventricles. Coronary CTA of these two cases were normal The other case was a mass of the lateral wall of the left ventricle, and the delayed enhancement with a clumpy shape was located in the lateral wall of the left ventricle. Conclusions MR myocardial delayed enhancement is not a specific sign of myocardial infarction of ischemic heart disease. Nonischemic heart diseases including all kinds of primary cardiomyopathy and some other diseases affecting myocardium can also cause delayed enhancement, but their characteristics are different. The differentiation of the etiology of the nonischemic heart disease with delayed enhancement relies upon the intimate connection with clinical history and the cine sequence MR images.