应用超声斑点追踪成像技术研究缺血心肌的收缩期峰值圆周应变的变化规律

目的:应用超声斑点追踪成像技术研究心肌缺血患者的左心室各节段心肌收缩期峰值圆周应变的变化规律,探讨其诊断心肌缺血的临床应用价值.方法:应用超声心动图仪获得31例对照组及56例冠心病(组)患者的高频帧二维图像,用二维斑点追踪软件测量左心室短轴基底部及乳头肌水平的收缩期峰值圆周应变.结果:与对照组比较,冠心病组冠脉狭窄50%～75%者后壁基底段、间隔基底段、前间隔基底段、后壁中间段减低,差异均有统计学意义(P<0.05).与对照组比较,冠心病组冠脉狭窄76%～98%者侧壁基底段、后壁基底段、下壁基底段、间隔基底段、前间隔基底段、前壁中间段、侧壁中间段、后壁中间段、前间隔中间段减低,差异均有统计学意义(P<0.05～0.01).与对照组比较,冠心病组冠脉次全及完全闭塞者各节段均减低,差异均有统计学意义(P<0.05～0.01).相关分析显示冠状动脉狭窄程度与乳头肌各节段心肌平均收缩期峰值圆周应变绝对值呈负相关(r=0.547,P<0.01).结论:当冠状动脉高度狭窄时,二维超声心动图无明显改变,但收缩期峰值圆周应变已明显降低.超声斑点追踪成像技术能精确评价缺血心肌的局部应变功能.     

面积应变定量评价无室壁运动异常的左心室缺血心肌的局部功能

目的利用三维斑点追踪成像面积应变评价常规超声心动图检查无明显节段性室壁运动异常的左心室缺血心肌的局部功能。方法本研究包括30例对照组和78例病例组,常规超声心动图检查左心室未见明显节段性运动异常,冠状动脉造影检查对照组所有分支狭窄均小于50%,病例组至少一条主要分支狭窄大于70%,利用三维斑点追踪成像测量左心室17节段的面积应变,比较缺血心肌节段和正常心肌节段面积应变的差异。结果左前降支供血区域前壁中间段、前间隔基底段与中间段、心尖部面积应变和平均面积应变较对照组明显减低(P0.05);左回旋支供血区域侧壁心尖段、后壁基底段与中间段面积应变和平均面积应变较对照组明显减低(P0.05);右冠状动脉供血区域下壁中间段与心尖段面积应变和平均面积应变较对照组明显减低(P0.05)。结论面积应变是可以作为定量评价左心室局部心肌功能的一种可用指标。     

组织速度成像评价冠心病不同程度缺血心肌的左室局部收缩功能

目的 应用组织速度成像技术分析冠心病(CAD)不同程度冠脉狭窄缺血心肌及心梗后缺血心肌纵轴方向运动速度、运动位移、应变及应变率的特点,评价其对不同程度心肌缺血的诊断价值.方法 对72例CAD患者采用TVI技术检测心室各节段心肌收缩期纵轴方向运动速度及运动位移、组织形变及形变速率,并比较定量组织速度成像(QTVI)、组织追踪成像(TTI)、应变(SI)及应变率成像(SRI),检测冠心病心肌缺血的临床应用价值.结果 随着冠状动脉左前降支狭窄程度加重,TVI各曲线变得紊乱,收缩期波峰显著降低,非心梗1级组、2 级组、3级组及心梗组各收缩期峰值参数逐渐降低,心梗组明显下降(P<0.05).运动立称(SD)、运动速度(SV)各组间比较:心梗组与非心梗1级组、心梗组与非心梗2级组比较,左前降支所支配的各基底段、中间段及前壁心尖段SV、SD均降低(P<0.05);非心梗3级组与1级组比较,3个节段(前间隔基底段、前壁基底段及中间段)SV、SD降低(P<0.05);心梗组与非心梗3级组比较,11个节段SV、SD降低(P>0.05).S、SR各组间比较:心梗组与非心梗1级组比较,11个节段组织应变(S)、应变速度(SR)降低(P<0.05);心梗组与非心梗2级组比较,除侧壁心尖段外,余10个节段S、SR降低(P<0.05);心梗组与非心梗3级组比较,5个节段(前间隔基底段、中间段及前壁基底段、中间段、心尖段)S、SR降低(P<0.05);非心梗3级组与1级组比较,5个节段(前间隔基底段、中间段及前壁基底段、中间段、心尖段)S、SR降低(P<0.05).结论 随着冠状动脉狭窄程度加重,缺血心肌节段的定量组织速度成像、组织追踪成像、应变及应变率成像四项收缩期峰值参数逐渐减低,有一定的变化规律.     

超声组织同步检测评价老年心肌梗死伴传导阻滞致左心室收缩不同步的研究

目的探讨超声组织同步显像技术评价老年心肌梗死患者不同传导阻滞所造成的心室各壁收缩不同步性的临床价值。方法选择老年心肌梗死患者52例,根据心电图传导阻滞情况分为右束支阻滞组14例,左束支阻滞组21例,房室传导阻滞组17例,采用超声组织同步显像技术对所有患者的3个左心室心尖长轴观的后间隔、侧壁、前壁、下壁、前间隔、后壁的基底段和中间段进行心肌收缩达峰时间(TTP)的检测,并进行比较与分析。结果右束支阻滞组TTP延长部位位于前间隔中段、基底段以及后间隔中段。左束支阻滞组TTP延长部位主要位于后间隔中段及基底段、左心室下壁中段及基底段、左心室后壁中段及基底段,前间隔中段及基底段、左心室前壁基底段TTP也轻度延迟。房室传导阻滞组TTP延长部位位于左心室侧壁中段及基底段、后间隔中段、左心室后壁中段及基底段。结论老年心肌梗死后伴不同传导阻滞所产生的左心室收缩不协调部位不同,超声组织同步显像技术能直观并且准确检测出左心室收缩不同步的部位,并进行量化。     

组织速度成像评价经皮冠状动脉介入术前后左室局部收缩功能

目的应用组织速度成像(TVI)技术分析经皮冠状动脉介入术(PCI)前后不同时间点心室心肌纵轴方向运动速度、运动位移、应变、应变率变化规律,研究其评价冠心病(CAD)介入治疗疗效的价值。方法对接受PCI治疗的15例冠心病患者于术前、术后1周、术后1个月以及3个月时采用TVI技术检测心室各节段心肌收缩期纵轴方向运动速度及运动位移、组织形变及形变速率,并比较术前及术后不同时间点差异。结果术前、术后定量组织速度成像(QTVI)、组织追踪成像(TTI)、应变(SI)及应变率成像(SRI)曲线各节段收缩期峰值参数随着时间的延长逐渐增高。与术前比较,术后1个月2个节段(前壁基底段与中间段)收缩期峰值速度(SV)、收缩期峰值位移(SD)增高(P<0.05);术后3个月,8个节段(除前间隔心尖段、侧壁心尖段、后间隔心尖段)SV、SD增高更为显著(P<0.05)。术后3个月6个节段(前间隔基底段及中间段、前壁基底段及中间段、后间隔中间段、后壁心尖段)SV、SD与术后1周相比明显增高(P<0.05)。与术前比较,术后1周3个节段(前壁基底段、中间段、心尖段)收缩期最大应变值(S)及SRI的收缩期最大应变率值(SR)增高(P<0.05);术后1个月5个节段(前壁基底段、中间段、心尖段及前间隔基底段、中间段)S、SR增高(P<0.05)。术后3个月9个节段(除侧壁心尖段、后间隔心尖段)S、SR与术前、术后1周相比均明显增高(P<0.05)。结论 TVI技术能准确地定量评价冠心病患者缺血心肌的局部功能,动态观察PCI前、后局部心肌功能变化,可评价PCI的治疗效果。     

二维斑点成像技术评价扩张型心肌病患者心脏的纵向扭转

目的 运用二维斑点成像技术评价扩张型心肌病患者(dilated cardiomyopathy,DCM)与健康人间各参数的差异,证实DCM患者心脏纵向扭转的存在.方法 搜集温州医学院附属第一医院2008年6月至2009年9月期间就诊的42例DCM患者作为DCM组和35例健康人作为对照组.两组均行常规超声心动图,检测左心房内径、左心室射血分数、过二尖瓣口舒张早期血流速度及舒张晚期血流速度.应用GE Echopac软件测量得到DCM组和对照组患者心尖四腔心的左心室壁的径向应变、应变率,左心室侧壁、室间隔、心尖及左心室整体纵向峰值扭转角度,对比两组间各参数的差异.结果 (1) DCM组患者左心房内径、左心室收缩末期容积及左心室舒张末期容积均明显大于对照组(P均＜0.01),左心室射血分数明显低于对照组(P＜0.0l),过二尖瓣口舒张早期血流峰速度/舒张晚期血流峰速度两组比较差异无统计学意义(P＞0.05).(2) DCM组患者径向收缩期峰值应变以及收缩期、舒张早期、舒张晚期径向峰值应变率均明显低于对照组(P均＜0.01).(3)对照组左心室侧壁的中间段、基底段以及心尖段呈逆时针扭转,而室间隔的基底段、中间段呈顺时针扭转,DCM组患者左心室侧壁的中间段呈逆时针扭转,而左心室侧壁基底段、心尖段、室间隔的基底段及中间段均呈顺时针扭转.DCM组患者左心室侧壁中间段和基底段、心尖段以及室间隔基底段的扭转角度均明显低于对照组(P均＜0.01).对照组左心室呈较小角度的纵向逆时针扭转(0.76°±2.63°),而DCM组患者左心室呈纵向顺时针扭转(- 1.58°±3.42°),两组扭转角度的差异有统计学意义(P＜0.01).(4)DCM组患者左心室侧壁基底段、中间段与室间隔基底段扭转达峰时间差均与左心室的纵向峰值扭转角度具有相关性(r=0.409,P=0.007; r=0.396,P=0.009).结论 应用二维斑点成像技术,通过分析各节段应变、应变率及纵向扭转角度等参数,证实DCM患者心脏存在着一定角度的纵向顺时针扭转,DCM患者左心室侧壁基底段、中间段与室间隔基底段扭转达峰时间差可能是形成DCM患者心脏纵向扭转的一个原因.     

肥厚型梗阻性心肌病扩大室间隔切除术后左心室心肌收缩后缩短的变化规律

目的:分析肥厚型梗阻性心肌病(HOCM)患者扩大室间隔切除术前及术后左心室心肌收缩后缩短(PSS)的变化规律,探讨HOCM患者术后左心室心肌舒张功能的改善情况。方法:纳入2012年至2017年在中国医学科学院阜外医院接受扩大室间隔切除术的39例HOCM患者。应用二维斑点追踪技术,分析左心室壁18个节段(前壁、下壁、前室间隔、后壁、后室间隔、侧壁的基底段、中间段及心尖段)的应变曲线。计算心肌收缩后应变指数(PSI),以PSI≥20%判定为该节段发生了PSS。对比分析术前基底段、中间段、心尖段PSS分布情况以及术后各节段PSS的变化情况。结果:39例HOCM患者,共702个节段。术前共44个节段发生了PSS,其中基底段31个、中间段10个、心尖段3个。基底段、中间段、心尖段PSS发生率以及PSI依次递减,差异均有统计学意义(P均0.05)。扩大室间隔切除术后,患者左心房内径、室间隔厚度、左心室后壁厚度、左心室射血分数、左心室流出道最大压差以及二尖瓣反流均较术前明显缩小,左心室舒张末期内径及收缩末期内径均较术前增大,差异均有统计学意义(P均0.05)。二尖瓣舒张期血流E峰减速时间(DT)缩短(P0.05)、二尖瓣舒张晚期运动速度a’较术前增快(P0.05)。术后共19个节段发生了PSS,其中基底段10个、中间段6个、心尖段3个。与术前相比,术后总PSS发生率(2.71%vs. 6.27%)以及平均PSI[(2.34±2.33)%vs.(3.68±2.79)%]均显著降低(P均0.05),其中以基底段PSS发生率以及平均PSI降低最为明显,差异均有统计学意义(P均0.05)。结论:HOCM患者的PSS发生率及PSI增高以室间隔基底段为著。扩大室间隔切除术后PSS发生率及PSI均较术前降低,以基底段为著,提示扩大室间隔切除术后HOCM患者的左心室舒张功能有改善。     

心肌致密化不全患者心肌收缩运动同步性研究

目的 利用定量组织速度成像(quantitative tissue velocity imganig,QTVI)技术分析探讨心肌致密化不全患者的心肌收缩同步性运动情况.方法 采集18例心肌致密化不全患者(NVM组)和30例健康对照组的常规二维图像,启动组织多普勒(DTI)程序,获取标准心尖位左心室长轴观、两腔观和四腔观共3个切面的QTVI图像.分别描绘左心室侧壁、后间隔、前壁、下壁、前间隔和后壁等6个室壁的基底段及中间段共12个节段的组织速度曲线.测量左心室12个节段的QRS波起始点至各节段收缩期达峰时间(Q-Ts),计算48例检查者左心室12个节段的Ts最大差值(Max-△Ts).结果 NVM组和健康对照组相比,左心室各壁基底段Q-Ts均明显长(P均<0.001),且以左心室侧壁、后壁、下壁延迟为重;左心室各壁中间段Q-Ts均明显长(P均<0.001),且以左心室下壁、侧壁、后壁延迟为重.NVM组左心室12个节段的Max-△Ts为(161.9±93.2)ms,显著大于正常对照组的(61.2±27.4)ms,P<0.001.结论 左心室心肌致密化不全患者存在心肌收缩运动的不同步性.且左心室各壁中间段Q-Ts最延迟的部位依次为下壁、侧壁、后壁,有别于既往文献报道的其他原因所致心力衰竭时左心室各壁中间段Q-Ts最延迟的部位依次为侧壁、后壁、下壁.     

二维纵向应变对室壁运动正常患者冠状动脉左主干和三支病变的预测价值

目的:应用二维斑点追踪显像(2D-STI)技术评价室壁运动正常的不同程度冠状动脉病变患者左心室心肌纵向应变,探讨不同应变参数对冠状动脉左主干和三支病变的预测价值。方法:选取92例可疑冠心病患者,根据冠状动脉造影结果分为:冠心病高危组(左主干或三支病变)24例,冠心病低危组(单支或双支病变)36例和对照组(无冠心病)32例。应用自动功能成像技术获取左心室基底段纵向应变、中间段纵向应变、心尖段纵向应变、基底段+中间段纵向应变以及左心室整体纵向应变。比较三组间各常规超声参数和二维纵向应变参数的差异,利用受试者工作特征(ROC)曲线分析各应变参数对冠状动脉左主干和三支病变的预测价值。结果:随着冠状动脉病变程度加重,对照组、冠心病低危组、冠心病高危组的左心室基底段纵向应变、中间段纵向应变、心尖段纵向应变、基底段+中间段纵向应变以及左心室整体纵向应变均逐渐减低,上述指标冠心病低危组均低于对照组,冠心病高危组均低于冠心病低危组(P均0.01)。ROC曲线分析显示,左心室基底段+中间段纵向应变预测冠状动脉左主干和三支病变的曲线下面积最大,为0.870,最佳界值为-18.1%(敏感度83.3%,特异度76.5%)。结论:在静息状态下室壁运动正常的冠心病患者中,左心室各水平及整体纵向应变随冠状动脉病变程度加重逐渐减低,二维纵向应变可较敏感地发现心肌缺血,左心室基底段+中间段纵向应变对冠状动脉左主干及三支病变的预测价值最大。     

应变成像定量评价冠心病病人局部心肌收缩功能

目的 应用应变成像技术定量评价冠心病局部心肌收缩能.方法 应用应变成像对冠心病病人53例和正常人42名左心室前间隔与后壁径向、各室壁节段纵向收缩期峰值应变进行测定,并以冠状动脉造影结果为标准进行对比分析.结果 冠心病病人缺血心肌的收缩期峰值应变表现为明显减低、消失,甚至倒置.冠心病组各室壁缺血节段收缩期径向、纵向峰值应变测值均较对照组相应节段明显减低.结论 冠心病缺血心肌收缩期峰值应变明显减低,应变成像技术是临床无创、定量评价冠心病局部心肌功能的新方法.     

Serial changes in left ventricular configuration and function in hypertrophic cardiomyopathy

Fifteen patients, 12 males and three females, with hypertrophic cardiomyopathy (HCM) including three of obstructive type (HOCM) were investigated to observe the long-term course of HCM. Left ventriculography and bi-ventriculography were performed twice serially in all cases. We studied the correlations between the serial ECG changes, especially the negative T wave, and the left ventricular configuration, wall thickness, and left ventricular function. Serial ECG changes included: 1) negativity of the T wave which developed or increased concomitantly with increased voltages of SV1 + RV5 (A-1 group: five cases), 2) the negativity decreased or resolved with decreased voltages of SV1 + RV5 (A-2 group: four cases), and 3) insignificant changes of both T waves and SV1 + RV5 (B group: six cases). In the right oblique views at end-diastole, the configuration of the left ventricle was classified in three forms; (1) spade form (S), (2) round form (R), and (3) intermediate form (SR). The results were as follows: 1. The A-1 group showed increased thickness of the apical and anterior walls, but the thickness of the posterior wall and interventricular septal wall did not change serially. In three cases, the thickness of the interventricular septum showed mild hypertrophy at the initial and final observations. The configuration changed from the R or SR form to the S form. Diastolic dysfunction (peak dV/dt/V, peak dV/dt/EDV) was progressive, but end-diastolic volume and ejection fraction did not change. 2. The A-2 group showed the significantly decreased thickness of the apical and anterior walls. The thicknesses of the posterior wall and interventricular septal wall tended to decrease in all cases. In three cases (75%), the interventricular septal wall was markedly hypertrophied on the initial observation. The configuration changed from the S or SR form to the R form. Left ventricular diastolic function and ejection fraction decreased significantly and end-diastolic volume increased. Two cases showed clinical pictures of dilated cardiomyopathy at the final observation. 3. In the B group, there were no marked changes in wall thickness, left ventricular configuration, or systolic and diastolic functions. In conclusion, serial changes in left ventricular configuration, wall thickness, especially of the anterior and apical walls, and left ventricular function were all compatible with the serial changes of the ECG in hypertrophic cardiomyopathy.(ABSTRACT TRUNCATED AT 400 WORDS)     

Thrombotic occlusion of a large septal perforator presenting as ST-segment elevation in V1-V2 and treated with aspiration thrombectomy: a brief review of the literature

The interventricular septum constitutes approximately one-third of the mass of the left ventricle, and the bulk of the anterior septum is supplied by septal branches of the left anterior descending coronary artery. Ischemia of the interventricular septum results in angina, infarction, biventricular failure and ventricular arrhythmias. While the majority of septal infarctions are due to occlusions of the proximal left anterior descending coronary artery, a large first septal branch thrombosis can rarely be the culprit. Given the paucity of data pertaining to septal perforator disease, a thorough discussion on septal perforator coronary artery interventions and an illustrative case will be provided.     

Left ventricular performance in patients with left ventricular hypertrophy caused by systemic arterial hypertension.

To assess the adaptation of the left ventricle to a chronic pressure overload we used echocardiography to study 18 patients with left ventricular hypertrophy caused by systemic arterial hypertension. Increased values for either posterior wall or interventricular septal thickness or both confirmed the presence of left ventricular hypertrophy in all patients and an increase in the average wall thickness to radius ratio was consistent with the development of concentric hypertrophy. No patient had clinical evidence of ischaemic heart disease. Ejection phase indices of left ventricular performance (mean Vcf, fractional per cent of shortening, normalised posterior wall velocity, and ejection fraction) were within the normal range in the basal state in 16 of the 18 patients. The hypothesis is advanced that patients with concentric left ventricular hypertrophy resulting from systemic arterial hypertension usually have normal left ventricular performance in the basal state because values for wall stress remain within the normal range. We conclude that the hypertrophic response to a chronic increase in systemic arterial pressure does not per se result in depression of the basal inotropic state of the left ventricle.     

Left ventricular performance in patients with left ventricular hypertrophy caused by systemic arterial hypertension.

To assess the adaptation of the left ventricle to a chronic pressure overload we used echocardiography to study 18 patients with left ventricular hypertrophy caused by systemic arterial hypertension. Increased values for either posterior wall or interventricular septal thickness or both confirmed the presence of left ventricular hypertrophy in all patients and an increase in the average wall thickness to radius ratio was consistent with the development of concentric hypertrophy. No patient had clinical evidence of ischaemic heart disease. Ejection phase indices of left ventricular performance (mean Vcf, fractional per cent of shortening, normalised posterior wall velocity, and ejection fraction) were within the normal range in the basal state in 16 of the 18 patients. The hypothesis is advanced that patients with concentric left ventricular hypertrophy resulting from systemic arterial hypertension usually have normal left ventricular performance in the basal state because values for wall stress remain within the normal range. We conclude that the hypertrophic response to a chronic increase in systemic arterial pressure does not per se result in depression of the basal inotropic state of the left ventricle.     

应用应变率成像技术对尿毒症患者左心室功能的评价

目的 应用应变率成像技术评价尿毒症患者左室的局部收缩与舒张功能。方法 40例尿毒症患者,左室肥厚(LVH)组25例,非左室肥厚(NLVH)组15例及30例正常对照组。取心尖四腔、心尖两腔、心尖左室长轴切面测量左室各室壁心肌收缩期、舒张早期、房缩期的峰值速度(VS、VE、VA)、峰值应变率(SRS、SRE、SRA)、最大应变及位移。结果 速度Vs、VA:尿毒症患者较正常对照组无显著性差异,VE:尿毒症患者NLVH组后间隔、下壁较正常对照组显著性减低,LVH组除后壁外余左室各壁较正常对照组显著性减低。尿毒症患者两组间仅在前间隔有显著性差异。应变率SRS:尿毒症患者LVH组左室侧壁较正常对照组显著性减低。SRE:尿毒症患者NLVH组左室侧壁、下壁、后壁较正常对照组显著性减低,LVH组除后间隔外左室各壁较正常对照组显著性减低。LVH组前间隔及前壁的SRE较NLVH组显著性减低。SRA:尿毒症患者较正常对照组无显著性差异。应变S:尿毒症患者NLVH组仅有左室侧壁较正常对照组有显著性差异,LVH组除后间隔外其余左室壁较对照组显著性减低。LVH组前壁的应变较NLVH组显著性减低。位移D:尿毒症患者NLVH组仅在后间隔较正常对照组显著性减低,LVH组后间隔、后壁、前间隔、下壁较正常对照组显著性减低(分别P<0.05和0.01)。结论 应变率成像技术能够早期评尿毒症患者左室的心肌运动功能。     

Systolic anterior motion of the mitral valve with and without asymmetric septal hypertrophy. Role of left ventricular posterior wall motion

Abnormal systolic anterior (SAM) motion of the mitral valve without asymmetric hypertrophy of the interventricular septum was observed in 16 patients (group 1). 5 of the 16 patients had no other evidence of heart disease and the remaining 11 had a variety of cardiac disorders. Left ventricular dimensions, septal and posterior wall thickness, left ventricular ejection fraction, the mean velocity of circumferential fiber shortening, and the mean velocity of the posterior wall and septal contraction was measured by echocardiography in all patients in group 1. These measurements were compared with similar measurements in 14 patients with idiopathic hypertrophic subaortic stenosis (group 2) and in 11 normal subjects (group 3) to evaluate the role of the left ventricular contractility with particular reference to the left ventricular posterior wall motion in production of SAM. All patients with SAM (groups 1 and 2) showed significantly higher indexes of left ventricular contractility, particularly posterior wall velocity, and normalized mean posterior wall velocity, when compared to the normal subjects. The significantly higher posterior wall and the normalized mean posterior wall velocities in all patients with SAM suggest that the exaggerated systolic anterior motion of the left ventricular posterior wall plays an important role in production of SAM in the presence or absence of asymmetric septal hypertrophy.     

So-called "ampulla" cardiomyopathy associated with coronary vasospasm compared with acute myocardial infarction showing similar abnormal left ventricular wall motion: two case reports

So-called "ampulla" cardiomyopathy is characterized by transient abnormal left ventricular wall motion showing hypokinesia around the apical area and hyperkinesia at the basal area, without any detectable coronary lesion. We recently treated a patient with "ampulla" cardiomyopathy (Case 1) and a patient with acute myocardial infarction showing similar abnormal left ventricular wall motion (Case 2). A 75-year-old female (Case 1) presented with "ampulla" cardiomyopathy without coronary lesion. Vasospasm was induced at segment 8 on the left anterior descending (LAD) coronary artery by intracoronary administration of acetylcholine. A 58-year-old male (Case 2) presented with acute myocardial infarction due to occlusion at segment 8 and underwent successful coronary reperfusion therapy by direct percutaneous transluminal coronary angioplasty. Both Case 1 and Case 2 revelaed similar abnormal left ventricular wall motion, with hypokinesia around the apical area and hyperkinesia at the basal area by echocardiography, in the acute phase. Furthermore, these two patients showed elevated ST segment at both anterior and inferior leads by electrocardiography, and markedly reduced uptake of beta-methyl-p-iodophenyl-pentadecanoic acid around the apical area in the acute phase by scintigraphy. Interestingly, the LAD perfused a relatively wide area including the anterior, apical and part of the inferior area of the left ventricle in both patients by coronary angiography. The abnormal wall motion of Case 1 disappeared 4 weeks after onset, but that of Case 2 did not disappear. Although the diagnoses of Case 1 and Case 2 were different, abnormal wall motion of these cases might be due to myocardial ischemia due to distal LAD lesion. "Ampulla" cardiomyopathy might develop from transient myocardial ischemia induced by coronary vasospasm at the distal LAD which perfuses a relatively wide area.     

心室重塑患者瘦素抵抗与胰岛素抵抗及其相关性研究

目的:探讨不同基础病因的心室重塑患者血浆瘦素、可溶性瘦素受体水平的改变及其与胰岛素抵抗的关系.方法:选择心室重塑患者(心室重塑组,η=180)和体检正常者(对照组,η=60)采用酶联免疫吸附法测定血浆瘦素及可溶性瘦素受体、空腹胰岛素的浓度,同时常规测空腹血糖、甘油三酯、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、体重指数、腰臀比等指标.采用彩色多普勒超声诊断仪测量心室重塑患者左心室舒张末期间隔厚度、左心室后壁厚度、左心室舒张末期内径及左心室射血分数值,计算左心室质量指数.结果:心室重塑组血浆瘦素、空腹胰岛素均高于对照组[(12.22±6.10)ng/ml vs(8.89±5.27)ng/ml,P<0.01];[(14.37±7.19)ng/ml vs(10.48±5.17)ng/ml,P<0.01],可溶性瘦素受体水平低于对照组[(124.08±62.12)ng/ml v8(164.23±69.60)ng/ml,P<0.01],差异均有统计学显著意义;其中缺血性心肌病患者血浆瘦素和空腹胰岛素水平最高,较高血压性心脏病和扩张型心肌病患者差异有统计学显著意义(P<0.01).可溶性瘦素受体呈现相反的变化,以对照组最高,其次为扩张型心肌病、高血压性心脏病和缺血性心肌病患者.结论:心室重塑患者存在高胰岛素血症和胰岛素抵抗.瘦素抵抗和胰岛素抵抗与心室重塑密切相关.     

Color Doppler echocardiography in emergency diagnosis of ventricular septal rupture after acute myocardial infarct

A 58-year-old man developed a rupture of the interventricular septum after acute posterior myocardial infarction. The two-dimensional echocardiographic features of the ruptured interventricular septum included akinesia of posterior wall, hyperkinesia of the interventricular septum and anterior wall, inferior basal septum aneurysm and visualization of the ventricular septum defect. Injection of echocardiographic contrast (Gelatin solution) into the right atrium showed a small right-to-left shunt, injection into the left ventricle (during heart catheterization) demonstrated massive crossing of echocontrast similar to the results of cineventriculography of the left ventricle. By coloured Doppler-echocardiography the left-to-right shunt could directly be visualized, as well as a diastolic right-to-left shunt. By calculation of pressure gradient using adjusted continuous wave Doppler, estimation of right ventricular pressure was possible. The results demonstrated that colour Doppler in addition to two-dimensional echocardiography has an important diagnostic role in patients with complications of myocardial infarction.