Cardiac magnetic resonance imaging: infarct size is an independent predictor of mortality in patients with coronary artery disease

Background

Cardiac magnetic resonance imaging (CMR) can accurately determine infarct size. Prior studies using indirect methods to assess infarct size have shown that patients with larger myocardial infarctions have a worse prognosis than those with smaller myocardial infarctions.

Objectives

This study assessed the prognostic significance of infarct size determined by CMR.

Methods

Cine and contrast CMR were performed in 100 patients with coronary artery disease (CAD) undergoing routine cardiac evaluation. Infarct size was determined by planimetry. We used Cox proportional hazards regression analyses (stepwise forward selection approach) to evaluate the risk of all-cause death associated with traditional cardiovascular risk factors, symptoms of heart failure, medication use, left ventricular ejection fraction, left ventricular mass, angiographic severity of CAD and extent of infarct size determined by CMR.

Results

Ninety-one patients had evidence of myocardial infarction by CMR. Mean follow-up was 4.8±1.6 years after CMR, during which time 30 patients died. The significant multivariable predictors of all-cause mortality were extent of myocardial infarction by CMR, extent of left ventricular systolic dysfunction, symptoms of heart failure, and diabetes mellitus (P<.05). The presence of infarct greater than or equal to 24% of left ventricular mass and left ventricular ejection fraction less than or equal to 30% were the most optimal cut-off points for the prediction of death with bivariate adjusted hazard ratios of 2.11 (95% confidence interval 1.02-4.38) and 4.06 (95% confidence interval 1.73-9.54), respectively.

Conclusions

The extent of myocardial infarction determined by CMR is an independent predictor of death in patients with CAD.     

Intraventricular dispersion and temporal delay of early left ventricular filling after acute myocardial infarction. Assessment by magnetic resonance velocity mapping

This article aims to describe early left ventricular diastolic inflow using magnetic resonance velocity mapping in patients with recent acute myocardial infarction and in normal volunteers. Magnetic resonance velocity mapping was performed in a long axis plane through the hearts of 46 patients with recent, first time acute myocardial infarction and 43 age-matched normal volunteers. The peak velocities at six levels of the early diastolic inflow stream were recorded. A velocity index was calculated as the peak velocity in each position relative to the peak velocity at the mitral leaflet tips. Also, the temporal delay of velocity propagation was computed. Velocity index 4 cm downstream of mitral leaflet tips was lower in the acute myocardial infarction group (0.42 (0.17)) (mean (SD)) compared to controls (0.59 (0.25)) (p < 0.001). Temporal delay in the same position was longer in the acute myocardial infarction group (62 (67) ms) than in controls (32 (39) ms) (p < 0.02). Blood flow patterns in patients after acute myocardial infarction were characterized by increased dispersion of velocities and increased temporal delay of velocity propagation, probably reflecting impaired active left ventricular relaxation. Intraventricular flow measurements constitute a promising new technique for non-invasive assessment of left ventricular diastolic function.     

Magnetic resonance imaging dynamic contrast enhancement (DCE) characteristics of healed myocardial infarction differ from viable myocardium

Purpose

To determine whether healed myocardial infarction alters dynamic contrast-enhancement (DCE) curve shapes as well as late gadolinium-enhancement (LGE).

Materials and methods

Twenty patients with chronic myocardial infarction underwent MR imaging at 1.5 T with blood and myocardial T1 measurements before and after contrast administration for forty minutes. Viable and infarcted myocardial partition coefficients were calculated using multipoint slope methods for ten different DCE sampling intervals and windows. Partition coefficients and coefficients of determination were compared with paired statistical tests to assess the linearity of DCE curve shapes over the 40 min time period.

Results

Calculated partition coefficients did not vary significantly between methods (p = 0.325) for viable myocardium but did differ for infarcted myocardium (p < 0.001), indicating a difference in infarcted DCE. There was a significant difference between viable and infarcted myocardial partition coefficients estimates for all methods with the exception of methods that included measurements during the first 10 min after contrast agent administration.

Conclusion

Myocardial partition coefficients calculated from a slope calculation vary in healed myocardial infarction based on the selection of samples due to non-linear DCE curve shapes. Partition coefficient calculations are insensitive to data sampling effects in viable myocardium due to linear DCE curve shapes.     

冠状动脉系统高阶滑模自适应混沌同步设计

针对冠状动脉系统混沌同步问题, 系统模型受到有界但未知的不确定干扰条件下, 利用几何齐次性理论和积分滑模面设计高阶滑模自适应控制器, 使响应系统在有限时间内跟踪驱动系统, 该方法无需提前预知扰动边界. 采用Lyapunov理论对闭环系统进行分析并证明该控制器保证该系统能够在有限时间内镇定, 从仿真实验结果可以看出所设计的控制器在不确定干扰的情况下系统具有良好鲁棒性和未知参数的自适应性, 为能够有效治疗心肌梗死等冠状动脉疾病提供了一定的理论依据.     

Quantification of myocardial viability distribution with Gd(DTPA) bolus-enhanced, signal intensity-based percent infarct mapping

Introduction

A substantial, common shortcoming of the currently used semiautomated techniques for the quantification of myocardial infarct with delayed enhancement magnetic resonance imaging is the assumption that the whole myocardial slab that corresponds to the hyperenhanced tomographic area is 100% nonviable. This assumption is, however, incorrect. To resolve this conflict, we have recently proposed the signal intensity percent-infarct mapping method and validated it in an ex vivo, canine experiment. The purpose of the current study has been the validation of the signal intensity percent-infarct mapping method in vivo, using a porcine model of reperfused myocardial infarct.

Methods

In swines (n=6), reperfused myocardial infarct was generated occluding for 90 min by an angioplasty balloon either the left anterior descending or the left circumflex coronary artery. To obtain DE images, Gd(DTPA) enhanced inversion-recovery fast gradient-echo acquisitions were carried out on day 28 after myocardial infarction. Scanning started 15 min after intravenous injection of 0.2 mmol/kg Gd(DTPA). At the end of the MRI session, the animal was sacrificed and 2,3,5-triphenyltetrazolium chloride staining was used to validate the existence and to determine the accurate size of the myocardial infarct. Tissue samples were taken and stained with hematoxylin-eosin and Masson's trichrome for histological assessment of the infarct and the periinfarct zone. The signal intensity percent-infarct mapping data were compared with corresponding data from the delayed enhancement images analyzed with SI_remote+2S.D. thresholding, and with corresponding triphenyltetrazolium-chloride staining data using Friedman's repeated measure analysis of variance on ranks.

Results

The infarct volume determined by the triphenyltetrazolium chloride, SI_remote+2S.D. and signal intensity percent-infarct mapping methods was 3.04 ml [2.74, 3.45], 13.62 ml [9.06, 18.45] and 4.27 ml [3.45, 6.33], respectively. Median infarct volume determined by SI_remote+2S.D. significantly differed from that determined by triphenyltetrazolium chloride (P<.05). The Bland-Altman overall bias was 12.49% of the volume of the left ventricle. Median infarct volume determined by signal intensity percent-infarct mapping, however, did not differ significantly (NS) from that obtained by triphenyltetrazolium chloride. Signal intensity percent-infarct mapping yielded only a 1.99% Bland-Altman overall bias of the left ventricular volume.

Conclusions

This in vivo study in the porcine reperfused myocardial infarct model demonstrates that signal intensity percent-infarct mapping is a highly accurate method for the determination of the extent of myocardial infarct. MRI images for signal intensity percent-infarct mapping are obtained with the pulse sequence of conventional delayed enhancement imaging and are acquired within clinically acceptable scanning time. This makes signal intensity percent-infarct mapping a practical method for clinical implementation.     

结合生物力学模型重建左心室位移场

左心室心肌最为发达,心肌收缩产生的高压将动脉血泵入全身,集中体现了心脏的泵血能力.定量分析左心室收缩运动是诊断心血管疾病（如心肌梗死）的重要途径.本文采用描述左心室心肌材质的生物力学模型重建左心室位移场.该力学模型作为插值项,与心脏电影磁共振图像的观测位移场共同纳入贝叶斯估计框架,并采用有限元法求解位移场方程.实验比较了左心室射血无力组（46例）与正常组（55例）的左心室功能参数,发现两组在径向和圆周方向的位移、速度、应变和应变率都具有非常显著的差异（p < 0.001）,这证明本文方法能够有效区别左心室运动正常与否.实验结果还与CVI软件测量的左心室功能参数具有较高的相关性,说明本文方法有望辅助心血管疾病的临床诊断.     

Synchronization of low-frequency oscillations in the cardiovascular system: Application to medical diagnostics and treatment

We investigate synchronization between the low-frequency oscillations of heart rate and blood pressure having in humans a basic frequency close to 0.1?Hz. A quantitative estimation of this synchronization based on calculation of relative time of phase synchronization of oscillations is proposed. We show that assessment of synchronization between the considered oscillations can be useful for selecting an optimal dose of beta-blocker treatment in patients after acute myocardial infarction. It is found out that low value of synchronization between the low-frequency rhythms in heart rate and blood pressure at the first week after acute myocardial infarction is a sensitive marker of high risk of mortality during the subsequent 5 years.     

Ultrasmall superparamagnetic particles of iron oxide (USPIO) MR imaging of infarcted myocardium in pigs

The purpose of this study is to assess the potential value of ultrasmall superparamagnetic iron oxide (USPIO) for the detection of acute myocardial infarction by magnetic resonance (MR) imaging. Spin-echo magnetic resonance imaging of the heart was performed before, immediately after, and approximately 35 and 90 min after 30 μmol Fe/kg of USPIO administration in seven pigs with surgically induced myocardial infarction. Gradient-echo sequences were used to identify contraction abnormalities at the site of infarction. Myocardial signal intensities were measured using region-of-interest analysis in normal and infarcted myocardium. In addition, liver and lung signal intensities were measured. Pathologic correlation was performed after sacrificing the animals. The infarct area was located with wall-motion analysis. The site of infarction was confirmed at pathologic examination. The signal-intensity ratio between infarcted and normal myocardium was not significantly changed after USPIO administration at equilibrium stages (immediately after injection p = 0.64, at 35 min p = 0.32, at 90 min p = 0.73). The signal intensity of the liver decreased significantly after contrast administration (p < 0.05). For the lung, the change in signal intensity after USPIO administration was not significant. This pig model is well suited to study wall motion abnormalities after induction of acute myocardial infarction. USPIO-enhanced magnetic resonance imaging does not improve the visualization of acute myocardial infarction at equilibrium stage.     

Magnetic resonance imaging in patients with unstable angina: comparison with acute myocardial infarction and normals

The role of magnetic resonance imaging in characterizing normal, ischemic and infarcted segments of myocardium was examined in 8 patients with unstable angina, 11 patients with acute myocardial infarction, and 7 patients with stable angina. Eleven normal volunteers were imaged for comparison. Myocardial segments in short axis magnetic resonance images were classified as normal or abnormal on the basis of perfusion changes observed in thallium-201 images in 22 patients and according to the electrocariographic localization of infarction in 4 patients. T2 relaxation time was measured in 57 myocardial segments with abnormal perfusion (24 with reversible and 33 with irreversible perfusion changes) and in 25 normally perfused segments. T2 measurements in normally perfused segments of patients with acute myocardial infarction, unstable angina and stable angina were within normal range derived from T2 measurements in 48 myocardial segments of 11 normal volunteers (42 +/- 10 ms). T2 in abnormal myocardial segments of patients with stable angina also was not significantly different from normal. T2 of abnormal segments in patients with unstable angina (64 +/- 14 in reversibly ischemic and 67 +/- 21 in the irreversibly ischemic segments) was prolonged when compared to normal (p less than 0.0001) and was not significantly different from T2 in abnormal segments of patients with acute myocardial infarction (62 +/- 18 for reversibly and 66 +/- 11 for irreversibly ischemic segments). The data indicate that T2 prolongation is not specific for acute myocardial infarction and may be observed in abnormally perfused segments of patients with unstable angina.(ABSTRACT TRUNCATED AT 250 WORDS)     

超宽谱微波急性辐照对大鼠外周血血象的影响

 采用90 kV/m低剂量和180 kV/m高剂量超宽谱微波全身一次辐照大鼠10 min，于照后5个时相点取静脉血进行血常规参数测定。结果发现：低剂量微波辐照后0 h WBC总数就开始升高；高剂量微波辐照后0 h WBC总数明显升高，辐照后12和24 h，WBC总数下降，在188 h时WBC总数又显著升高。RBC,HGB,HCT和RDW-CV在两个剂量辐照后24 h内升高，至辐照后188 h，降至正常水平。红细胞的MCV,MCH在两个剂量的微波辐照后无显著变化。低剂量微波辐照后3,12,24 h，MCHC明显低于正常对照值，高剂量微波辐照后仅在照后24 h内MCHC明显低于正常对照值。在两个剂量辐照后,血小板总数显著高于正常对照值。辐照后24 h和188 h PDW均显著低于正常对照值；MPV,P-LCR在两个剂量辐照后188 h显著低于正常对照值。实验结果表明:低剂量和高剂量的微波辐照均可造成机体类似急性炎症性反应，对红细胞形态和功能影响较小，可使骨髓生成和释放红细胞及血小板增加。     

Left ventricular aneurysmectomy after myocardial infarction following detection of left ventricular thrombosis by magnetic resonance imaging

A 54-year-old man with a history of myocardial infarction presented with recurrent transient ischemic attacks 7 yr after the acute event. The emboli originated from a left ventricular thrombus despite adequate oral anticoagulant therapy. The thrombus was best detected with magnetic resonance imaging and had to be removed by surgery.     

Leakage and water exchange characterization of gadofosveset in the myocardium

Purpose

To determine the compartmentalization of the blood pool agent gadofosveset and the effect of its transient binding to albumin on the quantification of steady-state fractional myocardial blood volume (fMBV).

Methods

Myocardial vascular fraction measurements were simulated assuming the limiting cases (slow or fast) of two-compartment water exchange for different contrast agent injection concentrations, binding fractions, bound and free relaxivities, and true cardiac vascular fractions.fMBV was measured in five healthy volunteers (4 males, 1 female, average age 33) at 1.5 T after administration of five injections of gadofosveset. The measurements in the volunteers were retrospectively compared to measurements of fMBV after three serial injections of the ultra-small, paramagnetic iron oxide (USPIO) blood pool agent ferumoxytol in an experimental animal. The true fMBV and exchange rate of water protons in both human and animal data sets was determined by chi square minimization.

Results

Simulations showed an error in the measurement of fMBV due to partial binding of gadofosveset of less than 30%. Measured fMBV values over-estimate simulation predictions, and approach cardiac extracellular volume (22%), which suggests that the intravascular assumption may not be appropriate for the myocardium, although it may apply to more distal perfusion beds. In comparison, fMBV measured with ferumoxytol (5%, with slow water proton exchange across vascular wall) agree with published values of myocardial vascular fraction. Further comparison between myocardium relaxation rates induced by gadofosveset and by other extracellular and intravascular contrast agents showed that gadofosveset behaves like an extracellular contrast agent.

Conclusions

The distribution of the volunteer data indicates that a three-compartment model, with slow water exchange of gadofosveset and water protons between the vascular and interstitial compartments, and fast water exchange between the interstitium and the myocytes, is appropriate. The ferumoxytol measurements indicate that this USPIO is an intravascular contrast agent that can be used to quantify myocardial blood volume, with the appropriate correction for water exchange using a two-compartment water exchange model.     

Assessment of acute myocardial infarction in man with magnetic resonance imaging and the use of a new paramagnetic contrast agent gadolinium-bopta

To assess the feasibility of and characterize the new paramagnetic contrast agent gadolinium-BOPTA/dimeglumine (Gd-BOPTA) to detect acute myocardial infarctions with MR imaging, 24 patients (53.3 ± 8.3 yr) were examined 9.3 ± 3.6 days after a first myocardial infarction. Short-axis T₁-weighted and T₂-weighted MR imaging was performed at three slice levels. T₁-weighted images were obtained before, immediately after, 15, 30, and 45 min after injection. Patients received either 0.05 or 0.1 mmol/kg body weight Gd-BOPTA. Images were qualitatively and quantitatively analyzed. Two patients showed no signs of infarction on T₂-weighted images as opposed to contrast-enhanced T₁-weighted images. Contrast-to-noise ratio was not affected by the dosage level. Signal intensity (SI) of normal to infarcted myocardium was significantly improved by both dosages (p < .0005) but a dosage of 0.05 mmol/kg produced significantly higher SI inf/norm (1.42 ± 0.07 vs. 1.34 ± 0.06, respectively, p = .015). SI of normal and infarcted myocardium enhanced immediately after administration of 0.05 mmol/kg (29.3 ± 5.1% and 53.8 ± 9.6% respectively), which decreased thereafter to 5.3 ± 4.8% and 40.2 ± 8.5% respectively, at 45 min (p < .002 for normal myocardium). SI enhancement immediately after 0.1 mmol/kg Gd-BOPTA showed no decrease within the first 45 min. Gd-BOPTA enables the detection of myocardial infarction. Optimal infarct delineation is achieved from 15 to 45 min after administration of 0.05 mmol/kg body weight Gd-BOPTA. Gd-BOPTA at 0.05 mmol/kg does improve image quality as measured by contrast-to-noise ratio and SI enhancement as compared to 0.10 mmol/kg.     

低剂量连续辐射引起的小鼠免疫系统的变化

为了评估低剂量X射线连续辐射对BALB/c小鼠健康机体免疫系统的影响, 实验采用X射线全身连续照射BALB/c小鼠, 照射第一天剂量为0.07 Gy, 剂量率0.2 Gy/min, 之后每天照射0.08 Gy, 共照射12 d, 累积剂量1.03 Gy, 照射后24和48 h取血、胸腺和脾脏。 流式细胞仪检测免疫细胞周期和凋亡的变化, 胸腺和脾脏指数用重量法获取。 实验结果表明, 小鼠胸腺细胞的周期在照射后24 h被阻滞在G2/M期; 外周血淋巴和胸腺细胞周期48 h被阻滞在 G0/G1期, 细胞凋亡比例在照射后两个时间点都显著增加; 脾脏淋巴细胞周期24 h被阻滞在 G0/G1期, 48 h被阻滞在 S期, 细胞凋亡比例在24和48 h显著减少; 脾脏指数在照射后48 h显著减少。 故低剂量X射线连续全身照射BALB/c小鼠可激活免疫细胞不同的周期监测点, 引起免疫细胞凋亡比例发生变化, 造成一定的辐射损伤, 且这种影响随着免疫器官的不同而不同。 For estimating the effect of low doses X ray continual irradiation to immunity system of mouse, BALB/c mice were continually irradiated to 1.03 Gy by X rays at a dose rate of 0.2 Gy/min in 13 d. At 24 or 48 h after irradiation, the immunocyte cycle and apoptosis were determined by flow cytometry, and the thymus and spleen weights were measured too. The results showed that the cycle of thymocyte were arrested in G2/M at 24 h, the number of peripheral blood lymphocytes and thymocytes in G0/G1 phase at 48 h was up and the percentage of apoptosis had a significance increase in both of time points; the cycle of spleen lymphocytes was delayed in G0/G1 at 24 h, in S phase at 48 h, the apoptosis had a significance decrase at 24 and 48 h; spleen index declined significantly at 48 h. The results suggested that low doses continual X ray whole body irradiation could activate different cell cycle checkpoints, and result in some changes of apoptosis and some damages to immunocytes. The continual X ray irradiation affects the organs differently, it might provide experiment basis for radioprotection.     

Restoration of low resolution metabolic images with a priori anatomic information: 23Na MRI in myocardial infarction

A new iterative extrapolation image reconstruction algorithm is presented, which enhances low resolution metabolic magnetic resonance images (MRI) with information about the bounds of signal sources obtained from a priori anatomic proton ((1)H) MRI. The algorithm ameliorates partial volume and ringing artefacts, leaving unchanged local metabolic heterogeneity that is present in the original dataset but not evident at (1)H MRI. Therefore, it is ideally suited to metabolic studies of ischemia, infarction and other diseases where the extent of the abnormality at (1)H MRI is uncertain. The performance of the algorithm is assessed by simulations, MRI of phantoms, and by surface coil 23Na MRI studies of canine myocardial infarction on a clinical scanner where the injury was not evident at (1)H MRI. The algorithm includes corrections for transverse field inhomogeneity, and for the leakage of intense signals into regions of interest such as 23Na MRI signals from ventricular blood ringing into the myocardium. The simulations showed that the algorithm reduced ringing artefacts by 15%, was stable at low SNR ( approximately 7), but is sensitive to the positioning of the (1)H MRI boundaries. The 23Na MRI showed hyperenhancement of regions identified as infarcted at post-mortem histological staining. The areas of hyperenhancement were measured by five independent observers in four 23Na images of infarction reconstructed with and without the algorithm. The infarct areas were correlated with areas determined by post-mortem histological staining with coefficient 0.85 for the enhanced images, compared to 0.58 with the conventional images. The scatter in the amplitude and in the area measurements of ischemia-associated hyper-enhancement in 23Na MRI was reduced by the algorithm by 1.6-fold and by at least 3-fold, respectively, demonstrating its ability to substantially improve quantification of the extent and intensity of metabolic changes in injured tissue that is not evident by (1)H MRI.     

Localization of ischemia in canine hearts using tagged rotated long axis MR images,endocardial surface stretch and wall thickening

Tagged magnetic resonance imaging allows the noninvasive measurement of regional systolic myocardial deformations and helps localize ischemic regions in the left ventricle (LV). The objective of this study was to evaluate the potential accuracy of localizing ischemic regions in the LV using endocardial and epicardial data obtained from tagged rotated long axis images. Nine canine hearts with acute ischemia induced by coronary artery ligation were imaged along four long axis planes rotated around the LV long axis, at end diastole and end systole. Each plane was tagged by four parallel lines perpendicular to the LV long axis. Tracing the endocardial and epicardial intersection points of the tag lines, 24 myocardial cuboids were reconstructed for each LV at end diastole and end systole. Endocardial surface stretch and transmural systolic thickening were calculated for each cuboid. The functional data were compared to perfusion data obtained from postmortem monastral blue staining of the heart. The ability of each functional index to discriminate between ischemic and non-ischemic regions was assessed using the “t”-statistic. The potential accuracy in localizing ischemia was evaluated by studying the corresponding sensitivity-specificity curves. The results demonstrate that adequate discrimination and localization can be obtained with both functional indices. However, endocardial surface stretch is advantageous as it uses only endocardial data and can save 50% of the post-processing time.     

Characterization of mitochondria isolated from normal and ischemic hearts in rats utilizing atomic force microscopy

Mitochondria play critical roles in both the life and the death of cardiac myocytes. Various factors, such as the loss of ATP synthesis and increase of ATP hydrolysis, impairment in ionic homeostasis, formation of reactive oxygen species (ROS), and release of proapoptotic proteins are related to the generation of irreversible damage. It has been proposed that the release of cytochrome c is caused by a swelling of the mitochondrial matrix triggered by the apoptotic stimuli. However, there is a controversy about whether or not the mitochondria, indeed, swell during apoptosis. The major advantages of atomic force microscopy (AFM) over conventional optical and electron microscopes for bio-imaging include the fact that no special coating and vacuum are required and imaging can be done in all environments--air, vacuum or aqueous conditions. In addition, AFM force-distance curve measurements have become a fundamental tool in the fields of surface chemistry, biochemistry, and material science. In this study, we used AFM to observe the morphological and property changes in heart mitochondria that were isolated from a rat myocardial infarction model. From the shape parameters of the mitochondria in the AFM topographic image, it seemed that myocardial infarction caused the mitochondrial swelling. Also, the results of force-distance measurements showed that the adhesion force of heart mitochondria was significantly decreased by myocardial in infarction. Therefore, we suggested that myocardial infarction might be the cause of mitochondrial swelling and the changes in outer membrane of heart mitochondria.     

Absence of biological damage from prolonged exposure to intravascular ultrasound: a swine model

Ultrasound (US) has been used in IMS II (intravascular US) and CLOTBUST (transcranial US) clinical trials for thrombolysis. During the treatment, in addition to the targeted thrombus, other biological components, such as blood and vessel walls are subjected to long durations of US exposure. In this study we explored evidence of biological damage due to mechanical forces or thermal effects of US exposure at the frequency, intensity and duration employed for thrombolysis treatment. Biological effects were investigated by exposing swine ilio-femoral arteries bilaterally to an intravascular US generating catheter and a conventional catheter. A total of 12 animals each underwent 8h of exposure to intravascular pulsed US with a frequency of 2.2MHz and spatial peak time average intensity (I(SPTA)) of 6W/cm(2) per transducer (a total of six transducers per catheter) while the ultrasonic device surface temperature was maintained at 43 degrees C. The animals were euthanized either 24+/-3h or 28+/-3 days post treatment. A range of physiological and hematological parameters were evaluated pre-, post-, and during US exposure. The vascular diameter was determined pre- and post-US exposure using angiograms. Following euthanasia, each animal underwent a gross pathological examination, and the treated vessels and an unexposed vessel were excised for comparative histopathological evaluation. No evidence of biological damage was found at the end of 8h exposure to intravascular US.     

Intracardiac lipid accumulation, lipoatrophy of muscle cells and expansion of myocardial infarction in type 2 diabetic patients

The overall mortality of diabetic patients after myocardial infarction is 3-4 times higher than non-diabetics. The cellular mechanisms underlying such a poor clinical prognosis remain incompletely understood. Recent reports suggest that lipotoxicity associated with impaired liporegulation is among the leading factors in the pathogenesis of type 2 diabetes. The goal of this study was to investigate whether excess lipid accumulation specifically in heart muscle cells contributes to the expansion of myocardial infarction in type 2 diabetic patients. Comparative structural analysis of cardiac tissue was performed on autopsy samples from the infracted hearts of diabetic and non-diabetic individuals with special reference to the expansion of the infarction, degenerative changes, lipoatrophy, cell death, and replacement fibrosis. We found that progressive accumulation of lipids in cardiac myocytes was accompanied by considerable loss of myofibrils and was frequently observed in the heart tissue of type 2 diabetic patients. This indicates that disassembly of the contractile apparatus in the cells infiltrated with lipids weakens their capability for functional activity. Analysis of degenerative changes in the diabetic tissue has shown that lipid-laden cardiac myocytes were more susceptible to necrotic and apoptotic cells death leading to expansion of the infarction and the development of progressive focal replacement fibrosis both in the perinecrotic zone and in the areas located far from the site of injury. Our data show that lipoatrophy and loss of muscle cells during the post-infarction period aggravate the functional impairment in the diabetic heart and limits its adaptive capacity for compensatory remodeling. This suggests that lipotoxic myocardial injury associated with defects of lipid metabolism in type 2 diabetes predisposes its evolution toward congestive heart failure and is an important factor contributing to a high mortality following infarction.     

分光光度法测定家兔体内铁和锰的代谢

为探讨补铁和补锰药物的代谢情况,我们对家兔灌胃中剂量金施尔康多维元素片,每小时对家兔取血,利用邻二氮菲分光光度法测定血样中铁与锰的含量。结果显示:7h铁在家兔血液中含量达到峰值37.86μg·mL-1,10h基本代谢完毕,恢复至正常值28.72μg·mL-1;5h锰在家兔血液中含量达到峰值1.31μg·mL-1,但代谢缓慢,16h后代谢完毕,恢复至正常值0.008μg·mL-1。本实验可为科学补铁、补锰提供一定依据。