SENSE技术在急性心梗磁共振成像中的应用价值

目的　通过快速MR心脏电影及灌注成像评价急性心肌梗死组织的心肌运动及血流灌注特点 ,研究敏感编码技术在快速心脏磁共振成像中的应用价值。方法　结扎犬冠状动脉左前降支建立急性心梗模型。结合SENSE技术 6只犬分别行快速多层面多相位屏气电影扫描、快速MR心肌灌注及延迟扫描观察梗死心肌MRI特点。结果　心脏电影成像可显示犬前壁心梗区室壁运动异常 ,MR灌注成像表现为局部灌注缺损区 ,延迟扫描表现为梗死区高信号。使用SENSE技术扫描速度提高 1倍 ,且图像质量无明显变化。结论　快速MR电影及灌注成像有助于评价心肌运动及血流灌注 ,诊断急性梗死心肌。SENSE技术可提高心脏成像的时间分辨率 ,且在扫描时间不变时提高空间分辨率 ,减少运动及敏感伪影性 ,是一种行之有效的提高MRI速度的技术方法 ,在心脏成像中具有非常重要的应用价值。     

磁共振心肌灌注成像急性心肌梗死的实验研究

目的 研究猪急性心肌梗死的首过灌注和延迟时相MRI特点.方法 猪心肌梗死模型12只,均进行快速梯度回波序列(FGREET)首过灌注扫描及反转恢复梯度回波序列(MDE)延迟时相扫描.扫描后处死,分析心肌首过灌注和延迟时相特点,并与病理检查对照.结果 9例(75%)首过灌注时梗死心肌表现为灌注减低,其信号强度显著低于周围心肌,10例(83.33%)延迟期梗死心肌表现为延迟强化,而正常心肌信号强度下降,低于梗死心肌.结论 MR心肌灌注成像可有效检测急性心肌梗死的梗死心肌以及其程度和范围.     

急性心肌梗死MR心肌灌注成像实验及临床应用研究

目的采用MR首过灌注成像评价急性心肌梗死心肌组织血流灌注特点及治疗效果。方法急性心肌梗死模型犬9条,对照组犬4条;心肌梗死患者16例,正常对照组8例。采用磁化准备梯度回波（turboFLASH）序列行MR首过灌注及延迟成像扫描,绘制左心室各壁心肌信号强度-时间曲线,分析病变心肌信号强度-时间曲线特点。结果心肌梗死模型犬及未溶栓治疗组心肌首过呈低强化,延迟扫描信号强度高于正常心肌,曲线上升时间、上升斜率、峰值时间和对比增强率明显低于正常心肌。心肌梗死溶栓再灌注组首过及延迟均强化,延迟扫描时病变心肌信号强度高于正常心肌,信号强度-时间曲线仅曲线上升时间延长。心肌梗死模型犬和未溶栓治疗组病变心肌峰值信号强度较正常心肌明显降低,分别为正常心肌的(44.8±13.0)%和(54.5±12.0)%,溶栓再灌注组病变心肌峰值信号强度可达正常心肌的(90.8±13.0)%。结论turboFLASHMR心肌首过灌注成像有助于评价心肌血流灌注及溶栓疗效。     

基于双源CT双能量成像的犬无复流心肌活性实验研究

_目的：通过双源 CT（DSCT）心肌灌注扫描观察心肌缺血无复流动物模型的 CT 表现,初步探讨双能量心肌灌注扫描在评估无复流心肌中的应用价值。方法：通过球囊堵塞（60～90 min）加微粒明胶海绵栓塞犬前降支中远段,建立犬心肌缺血无复流模型（n＝6）,采用 DSCT 进行首过及3、5、10、15 min 多期延迟心肌灌注扫描,观察梗死区 CT 表现,完成检查后取犬心脏标本行氯化三苯基四氮唑（2,3,5-TTC）染色及 HE 染色,与 DSCT 检查结果进行对照。结果：2只犬在介入手术过程中死亡,4只犬完成模型建立。扫描过程中犬平均心率为135 bpm。DSCT 扫描均可见心肌梗死区 CT 值较正常心肌减低,首过及多期延迟扫描呈固定灌注减低表现,TTC 染色显示梗死区范围与 DSCT 所见相符,HE 染色梗死中心区和边缘区均可见心肌坏死。在不同能量的 DSCT 图像中,100 kV 灌注图像对心肌密度区分能力最强,140 kV 灌注图像噪声最低,而双能量融合灌注图像则在实现密度差异的前提下保证了较低的噪声。结论：DSCT 可以较好地在快心率状态下显示心肌,心肌灌注扫描显示固定灌注减低可能与心肌完全坏死有关。     

犬急性心肌梗死磁共振心肌灌注及电影成像实验研究

目的　采用MR快速序列研究急性心肌梗死的首过灌注特点及心功能改变。材料与方法　犬心肌梗死模型 9只 ,均进行T1WI磁化准备梯度回波序列 (TurboFLASH)首过灌注扫描及MR电影成像 (cine MR) ,完成检查后处死 ,分析心肌首过灌注特点及局部心功能变化 ,并与病理检查比较。结果　首过灌注时梗死心肌表现为灌注缺损 ,信号强度 时间曲线上升延缓 ,曲线斜率和峰值信号强度分别为 0 .0 2 5± 0 .0 2 0和 0 .84± 0 .2 7,较正常心肌(0 .13± 0 .0 80和 2 .0 2± 0 .99,P <0 .0 0 0 1)明显下降 ,峰值时间和曲线上升时间分别为 37.78± 11.90s和 32 .70±14 .0 9s,较正常心肌 (17.14± 6 .0 6s和 14 .2 8± 5 .14s,P <0 .0 0 0 1)明显延长。延迟期正常心肌信号强度下降 ,而梗死心肌仍呈上升趋势。首过灌注中灌注缺损面积与TTC染色一致。梗死节段室壁运动及室壁厚度异常。结论　MR首过灌注成像可反映病变心肌组织血流灌注信息 ,cine MR能测定节段室壁功能。结合首过灌注和心功能分析 ,可对梗死心肌在形态学和功能学两方面进行定性、定量分析 ,有助于评价梗死心肌活力     

容积CT心肌灌注成像进展及其临床应用

CT心肌灌注通过心肌内对比剂的浓度直接反映心肌灌注情况,与MRI、单光子发射体层成像(SPECT)等心肌灌注技术一致性良好.CT心肌灌注扫描方法分为单次心肌灌注扫描和动态心肌灌注扫描,通过定性、半定量和定量分析可对心肌缺血进行临床研究和诊断,药物负荷试验、延迟扫描还能区分梗死心肌和缺血心肌.随着256层、320层等动态容积CT的出现,CT在合理剂量下同时对冠状动脉狭窄、心肌灌注及心脏功能进行定性和定量评价成为现实.     

急性心肌梗塞MR灌注成像和SPECT对照研究

目的 探讨MR灌注成像和SPECT检测存活心肌的价值.方法 对30例临床诊断为急性心肌梗塞的患者(共计510个心肌节段),进行MR心肌灌注扫描检查,包括MR心肌灌注首过时相及MR心肌灌注延迟扫描.将MR扫描结果与单光子发射计算机体层显像(SPECT)结果进行对照,所有病例均行X线冠状动脉造影检查证实.结果 MR心肌灌注首过时相扫描发现198个节段呈低灌注缺血改变,312个节段灌注正常;MR心肌灌注延迟扫描发现56个节段造影剂潴留呈梗死改变,454个节段为活性心肌.X线冠状动脉造影检查显示49支冠状动脉主干或其主要分支狭窄.SPECT检出的梗死节段比MR心肌灌注扫描检出的节段少,二者的差异具有统计学意义.结论 MR心肌灌注扫描对存活心肌的诊断、预后评估具有重要意义.     

增强MRI评价急性心肌梗塞后再灌注的实验研究

目的：通过动物模型的Gd－DTPA增强MRI检查并与病理对照，以评价急性心肌梗塞后再灌注的MRI表现及其诊断价值。材料和方法：复制犬的急性心肌梗塞后再灌注（12只）和非再灌注模型（8只），进行Gd－DTPA增强MRI的动态扫描，同时对犬心做不同染色的病理检查。将增强MRI扫描结果与病理检查结果进行对比，并通过MRI机内测量功能进行梗塞区心肌的信号变化特点分析。结果：由于急性心肌梗塞后再灌注和非再灌注的病理表现不一样，其增强MRI表现亦不一样。前者表现为均匀一致的强化，动态扫描也不能区分中央和周围的信号强度差别；后者则在增强早期呈不均匀的强化，其中周围区的强化要比中央区明显。动态扫描显示在增强后30分钟两区的信号强度趋于一致。结论：增强后MRI可以显示和鉴别急性心肌梗塞后梗塞心肌有无发生再灌注。     

梗死心肌的MRI评价及病理对照实验研究

目的　通过MR影像与病理对照的方法明确心肌梗死后 7～ 10dMRI延迟强化区与梗死心肌的关系 ,以期为MRI评价心肌活性提供病理依据。方法　利用 6只猪无再灌注和再灌注的心肌梗死模型 ,行短轴面MR心肌延迟强化扫描。扫描结束后将心脏离体 ,沿短轴面将心脏切成断面行氯化三苯基四氮唑 (TTC)染色。比较心肌梗死区和正常对照区的延迟强化信号强度的差异 ;比较相应层面的MRI延迟强化区和TTC染色所示梗死区的关系。结果　在心肌梗死的 7～ 10d ,无论有无再灌注 ,MR延迟强化扫描均可见心肌梗死区信号较正常对照区明显升高 ,无再灌注组梗死区信号( 2 0 81± 6 49)是正常对照区 ( 2 68± 1 10 )的 7 76倍 (t =11 68,P <0 0 1) ,再灌注组梗死区信号( 14 2 8± 1 64)是正常对照区 ( 1 44± 0 52 )的 9 92倍 (t =3 1 69,P <0 0 1) ;无再灌注组的延迟强化区[占同层面左室面积的百分率为 ( 15 49± 6 0 7) % ]与梗死心肌 [( 14 95± 7 3 6) % ]一致 (t =-0 78,P>0 0 5) ,再灌注组的延迟强化区 [( 12 52± 5 93 ) % ]包括梗死区 [( 11 13± 5 81) % ]和梗死周围区 ,过度估计梗死心肌范围约 12 47% (t =-14 48,P <0 0 1)。结论　在心肌梗死的 7～ 10d ,MR延迟强化扫描可较准确地反映梗死心肌的范围     

急性心肌梗死多层螺旋CT心肌灌注和冠状动脉造影的实验研究

目的　应用多层螺旋CT(MSCT)心肌灌注研究急性心肌缺血和梗死的灌注特点 ,探索MSCT冠状动脉造影对冠状动脉阻断的显示情况。方法　健康杂种犬 9只 ,于左冠状动脉前降支结扎前及结扎后 30min、和 1、2、4、6、8h不同时间分别行MSCT心肌灌注扫描 ,分析心肌在不同时期的灌注特点 ,并与病理检查结果对照。同时于左冠状动脉前降支结扎前及结扎后行MSCT冠状动脉造影 ,观察冠状动脉阻断的情况。结果　犬心肌正常灌注量为 (6 9 3± 13 9)ml·10 0 g-1·min-1、达峰值时间为 (12 8± 2 1)s。左冠状动脉前降支结扎 30min后MSCT心肌灌注表现为灌注量减低 ,为(2 5 2± 3 4 )ml·10 0 g -1·min-1,时间 密度曲线低平 ,延迟 10min扫描左冠状动脉前降支供血区心肌密度为 (6 7 1± 11 4 )HU ,与正常心肌密度 (44 9± 2 2 0 )HU比较差异无显著性意义 (P >0 .0 5 )。左冠状动脉前降支结扎 4h后 ,局部心肌呈明显延迟增强 ,为 (82 1± 15 2 )HU。 9只犬MSCT冠状动脉造影均显示结扎处左冠状动脉前降支中断。结论　MSCT心肌灌注结合冠状动脉造影可以判断心肌缺血和梗死 ,同时显示冠状动脉的阻塞状况。     

磁共振成像诊断陈旧性心肌梗塞的初步评价

目的：探讨ＭＲＩ在评价陈旧性心肌梗塞的形态和功能中的应用价值。材料和方法：对７例陈旧性心肌梗塞进行ＭＲＩ检查，观察心脏形态学变化、心室壁运动、二尖瓣和主动脉瓣开闭功能，测量左室功能。结果：左室壁限局性变薄６例，其中３例在变薄的左室壁邻近部位见血流信号异常增高，左室壁节段性运动减弱，１例室壁瘤形成。左室射血分数降低。１例见二尖瓣有轻度返流。增强扫描（２例）显示梗塞心肌与正常心肌的增强有明显差异。结论：ＭＲＩ能为临床提供心肌的局部和整体功能、梗塞心肌的信号改变、心脏的瓣膜功能及心肌灌注等信息     

Mouse myocardial first‐pass perfusion MR imaging

A first‐pass myocardial perfusion sequence for mouse cardiac MRI is presented. A segmented ECG‐triggered acquisition combined with parallel imaging acceleration was used to capture the first pass of a Gd‐DTPA bolus through the mouse heart with a temporal resolution of 300–400 msec. The method was applied in healthy mice (N = 5) and in mice with permanent occlusion of the left coronary artery (N = 6). Baseline semiquantitative perfusion values of healthy myocardium showed excellent reproducibility. Infarct regions revealed a significant decrease in the semiquantitative myocardial perfusion values (0.05 ± 0.02) compared to remote myocardium (0.20 ± 0.04). Myocardial areas of decreased perfusion correlated well to infarct areas identified on the delayed‐enhancement scans. This protocol is a valuable addition to the mouse cardiac MRI toolbox for preclinical studies of ischemic heart disease. Magn Reson Med, 2010. © 2010 Wiley‐Liss, Inc.     

Granulocyte accumulation in ischemic/reperfused myocardium: Assessment with a technetium-99m-labeled antigranulocyte monoclonal antibody in the dog

This study tested the usefulness of technetium-99m-labeled antigranulocyte monoclonal antibody BW250/183 (AGMAb) for identifying granulocyte accumulation in ischemic/reperfused canine myocardium. In dogs with 90 minutes coronary artery occlusion and 180 minutes reperfusion (n = 8), ischemic/reperfused myocardial samples demonstrated 8.5 +/- 2.4 times more Tc-99m-AGMAb accumulation than nonischemic samples. Dogs given Tc-99m-labeled nonspecific human immunoglobulin instead of Tc-99m-AGMAb (n = 3) had about half as much accumulation (4.5 +/- 1.6, P < .05). Ex vivo myocardial imaging of Tc-99m-AGMAb demonstrated marked uptake in infarcted regions identified by absent triphenyl tetrazolium chloride staining. The amount of uptake was inversely related to the severity of ischemia (determined by radioactive microspheres) and directly correlated with tissue myeloperoxidase activity, a specific marker of granulocyte accumulation. No increase in Tc-99m-AGMAb uptake occurred in dogs with 90 minutes ischemia and no reperfusion (n = 3) or 15 minutes ischemia and 180 minutes reperfusion (n = 2). In conclusion, Tc-99m-AGMAb is taken up in reperfused infarcted myocardium by both nonspecific and specific mechanisms. Because the amount of uptake reflects myocardial granulocyte accumulation, Tc-99m-AGMAb combined with nuclear imaging techniques may be useful for studying inflammatory processes in the heart in experimental animal models and human beings.     

Gd(ABE-DTTA)-enhanced cardiac MRI for the diagnosis of ischemic events in the heart

PURPOSE: To demonstrate that contrast-enhanced MRI (ceMRI) with the aid of Gd(ABE-DTTA) is able to detect ischemic events in the heart in a canine ischemia/reperfusion (30/40 minutes) model. MATERIALS AND METHODS: ECG-gated, T1-weighted MR image sets (four to five slices each) with three-minute time resolution were collected in transiently LAD-occluded dogs. Following the acquisition of control image sets, ischemia was started by occluding the LAD. Either Gd(ABE-DTTA) (N = 6) or Gd(DTPA) (N = 6) was injected, and imaging was continued for 30 minutes of ischemia and 40 minutes of reperfusion. The contrast agent (CA)-induced MRI signal intensity enhancement (SIE) and contrast were monitored. Microspheres measured myocardial perfusion (MP) to verify areas of ischemia and reperfusion. RESULTS: SIEs of 86% +/- 3% and 97% +/- 3% in nonischemic, and 25% +/- 5% and 29% +/- 8% in ischemic regions were found within three minutes of onset of ischemia with Gd(ABE-DTTA) and Gd(DTPA), respectively. For the rest of the 30 minutes of ischemia, with Gd(ABE-DTTA) SIE of 60% +/- 3% and 25% +/- 5% persisted in the nonischemic and ischemic regions, respectively. With Gd(DTPA), however, SIE in the nonischemic areas decreased rapidly after the first three minutes of ischemia, while SIE in the ischemic areas increased, abolishing contrast. Thus, there was a persistent contrast with Gd(ABE-DTTA) and a short-lived contrast with Gd(DTPA) during ischemia. Furthermore, with Gd(ABE-DTTA) some contrast was still visible in the early reperfusion period. CONCLUSION: Gd(ABE-DTTA) in an ischemia/reperfusion model induces a persistent MRI contrast between regions of normal and ischemic myocardium, and verifies reperfusion. Therefore, it can be used to detect myocardial ischemic events.     

Measurement of the distribution volume of gadopentetate dimeglumine at echo-planar MR imaging to quantify myocardial infarction: comparison with 99mTc-DTPA autoradiography in rats.

PURPOSE: To measure the fractional distribution volume of gadopentetate dimeglumine in normal and reperfused infarcted myocardium at magnetic resonance (MR) imaging by using the fractional distribution volume of technetium 99m-diethylenetriaminepentaacetic acid (DTPA) as an independent reference. MATERIALS AND METHODS: Rats were subjected to 1 hour of coronary artery occlusion and 1 hour of reperfusion before inversion-recovery echo-planar imaging or autoradiography. Regional change in relaxation rate (delta R1) ratios for myocardium over blood were compared with radioactivity ratios for myocardium over blood after the injection of 99mTc-DTPA. RESULTS: Both delta R1 and radioactivity ratios demonstrated equilibrium distribution and hence represent partition coefficients (lambda). The fractional distribution volumes were greater in infarcted myocardium (0.90 +/- 0.05 for gadopentetate dimeglumine and 0.89 +/- 0.04 for 99mTc-DTPA) than in normal myocardium (0.23 +/- 0.02 for gadopentetate dimeglumine and 0.16 +/- 0.01 for 99mTc-DTPA). Area at risk at autoradiography was not significantly different from that at histomorphometry. The infarction size defined by using triphenyltetrazolium chloride was 13% +/- 4 smaller than that defined by using autoradiography. CONCLUSION: The fractional distribution volumes of gadopentetate dimeglumine and 99mTc-DTPA are similar and indicate extracellular distribution in normal myocardium and intracellular as well as extracellular distribution in reperfused infarction. Because the failure of cells to exclude these agents is indicative of necrosis, contrast medium-enhanced MR imaging may be useful to quantify myocardial infarction.     

Granulocyte accumulation in ischemic/reperfused myocardium: Assessment with a technetium-99m—labeled antigranulocyte monoclonal antibody in the dog

This study tested the usefulness of technetium-99m—labeled antigranulocyte monoclonal antibody BW250/183 (AGMAb) for identifying granulocyte accumulation in ischemic/reperfused canine myocardium. In dogs with 90 minutes coronary artery occlusion and 180 minutes reperfusion (n = 8), ischemic/reperfused myocardial samples demonstrated 8.5 ± 2.4 times more Tc-99m—AGMAb accumulation than nonischemic samples. Dogs given Tc-99m—labeled nonspecific human immunoglobulin instead of Tc-99m—AGMAb (n = 3) had about half as much accumulation (4.5 ± 1.6, P < .05). Ex vivo myocardial imaging of Tc-99m—AGMAb demonstrated marked uptake in infarcted regions identified by absent triphenyl tetrazolium chloride staining. The amount of uptake was inversely related to the severity of ischemia (determined by radioactive microspheres) and directly correlated with tissue myeloperoxidase activity, a specific marker of granulocyte accumulation. No increase in Tc-99m—AGMAb uptake occurred in dogs with 90 minutes ischemia and no reperfusion (n = 3) or 15 minutes ischemia and 180 minutes reperfusion (n = 2). In conclusion, Tc-99m—AGMAb is taken up in reperfused infarcted myocardium by both nonspecific and specific mechanisms. Because the amount of uptake reflects myocardial granulocyte accumulation, Tc-99m—AGMAb combined with nuclear imaging techniques may be useful for studying inflammatory processes in the heart in experimental animal models and human beings.     

Use of gadolinium-DTPA as a myocardial perfusion agent: potential applications and limitations for magnetic resonance imaging

To establish the effect of the paramagnetic contrast agent gadolinium diethylenetriaminepentaacetic acid ([Gd]DTPA) on myocardial magnetic resonance relaxation parameters T1 and T2, and its relationship to myocardial perfusion, we administered [Gd] DTPA 0.2 mM/kg to two groups of dogs. Group I had severe, resting myocardial ischemia induced by coronary occlusion, followed in 2 min by [Gd]DTPA infusion and heart excision 1 min later. Group II had a variable reduction in blood flow. In Group II the coronary vasodilator dipyridamole was infused to enhance blood flow to the normal myocardium before [Gd]DTPA was given. In Group I [Gd]DTPA caused a significant difference in T1 between the normal and severely ischemic zones; changes in T1 correlated with the severity of myocardial ischemia. Although vasodilatation delivered more Gd-DTPA to the normal myocardium in Group II, the lack of further decrease in T1 suggested that it was cleared more rapidly. Thus, [Gd]DTPA permits the detection and characterization of severe, resting myocardial ischemia by magnetic resonance techniques. Using the experimental techniques described in this study, less severe flow differences caused by vasodilatation and resultant hyperemia are not detected.     

Head‐to‐head comparison between delayed enhancement and percent infarct mapping for assessment of myocardial infarct size in a canine model

Purpose

To compare a novel method, percent‐infarct‐mapping (PIM), with conventional delayed enhancement (DE) of contrast for accurate myocardial viability assessment. Contrary to signal intensity (SI), the longitudinal relaxation‐rate enhancement (ΔR1) is an intrinsic parameter linearly proportional to the concentration of contrast agent (CA). Determining ΔR1 voxel‐by‐voxel, after administering an infarct‐avid CA, allows determination of per‐voxel percentage of infarcted tissue. The feasibility of generating PIM is demonstrated in canine reperfused infarction using an infarct‐avid, persistent‐CA (PCA), (Gd)(ABE‐DTTA). PIM is compared to the DE method using Gd(DTPA), and both to triphenyltetrazolium chloride (TTC) staining histochemistry.

Materials and Methods

In six dogs, 48 hours following closed‐chest, 180‐minute coronary occlusion, DE imaging was carried out. PCA was administered immediately thereafter. Pixel‐by‐pixel R1 maps of the entire left ventricle (LV) were generated 48 hours after PCA using inversion‐recovery with multiple inversion times. R1, ΔR1, and percent‐infarct values were calculated voxel‐by‐voxel.

Results

Significant correlations (P < 0.01, R ≥ 0.8) were obtained for percent‐infarct‐per‐slice (PIS) determined by DE or PIM vs. those from corresponding TTC‐stained slices. Compared to TTC, DE overestimated PIS by 32 ± 18%. PIM underestimated PIS by 2.5 ± 4.9%. Infarction fraction overestimation was 29 ± 6% of LV by DE, but only 1.0 ± 2.3% by PIM. Errors with PIM were significantly smaller than those with DE. Infarct area determined by signal intensity was similarly overestimated whether using Gd(DTPA) or Gd(ABE‐DTTA).

Conclusion

The ΔR1‐based PIM method is highly reproducible and more accurate than DE for quantifying myocardial viability in vivo. J. Magn. Reson. Imaging 2008;28:1386–1392. © 2008 Wiley‐Liss, Inc.     

Left ventricular postmyocardial infarction remodeling studied by combining MR-tagging with delayed MR contrast enhancement

OBJECTIVES: We sought to monitor the evolution of noninfarcted and infarcted myocardium function in the process of left ventricular (LV) remodeling after a reperfused myocardial infarction. MATERIAL AND METHODS: Pigs (n = 8) were subjected to reperfused infarction. Magnetic resonance imaging (MRI) was performed at 3 days and 8 weeks after infarction. Regional circumferential shortening (Ecc) and principal strain L1 in the infarcted, peri-infarcted, and remote myocardium were evaluated by tagged cine MRI combined with matched late enhancement data (Gadolinium-DOTA-enhanced IR-GRE) Global LV function was evaluated by cine MRI. Animals were euthanized after the second imaging session and tissue samples from the different myocardial regions were obtained for histopathologic study. RESULTS: There was a significant deterioration in Ecc between the 3-day and 8-week studies in the peri-infarcted myocardium at apex (-9.9% +/- 4.5% to -6.5 +/- 3.9; P = 0.046) whereas it remained stable for all other regions at all levels. A trend toward improvement in Ecc existed in the infarcted myocardium when infarction transmurality was less than 50% of the LV wall (-7.5% +/- 0.8% to -12.2% +/- 2.9% P = 0.06). Ecc in infarcted myocardium was significantly inferior (P < 0.002) to that in remote and peri-infarcted myocardium at the apical level (2.7% +/- 2.6% vs. -14.4% +/- 3.3% and -9.9% +/- 4.5%, respectively). Global LV function substantially deteriorated after infarction and was associated with a significant LV dilation. CONCLUSION: These results confirm the hypothesis that scarred myocardium imposes additional functional burden to the peri-infarcted myocardium.     

Blood pool contrast agent CMD-A2-Gd-DOTA-enhanced MR imaging of infarcted myocardium in pigs.

The purpose of this study was to assess the ability of the new blood pool contrast agent meglumine-carboxymethyldextran-ethylenediamino-gadoterate (CMD-A2-Gd-DOTA) to depict acute occlusive myocardial infarction (AMI). First-pass gradient-echo and delayed spin-echo magnetic resonance imaging (MRI) was performed 5 days after induction of AMI in a pig model. MRI was correlated with pathology. First-pass imaging with CMD-A2-Gd-DOTA allowed detection of infarcted myocardium in all pigs (n = 7). The infarction was recognized as a black spot on MRI as well as on a parametric image. The signal intensity (SI) amplitudes of normal versus infarcted myocardium were 80.55 +/- 18.61 versus 8.48 +/- 15.50 on MRI and 81.62 +/- 18.50 versus 1.61 +/- 3.73 on the parametric image (both P values < 0.001. The contrast ratio between normal and infarcted myocardium was not significantly improved on spin-echo MRI, suggesting largely intact vascular integrity outside the occluded area. CMD-A2-Gd-DOTA is useful for depicting occlusive myocardial infarction by first-pass MRI. Spin-echo imaging is promising in assessing vascular integrity. J. Magn. Reson. Imaging 1999;10:170-177.