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Infarcted Myocardium (infarcted + myocardium)
Selected AbstractsTissue edema does not change gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA)-enhanced T1 relaxation times of viable myocardium,,JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 6 2005Gang Li MD Abstract Purpose To determine whether tissue edema changes gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA)-enhanced T1 relaxation times of the viable myocardium. Materials and Methods A total of 16 isolated pig hearts were divided into four groups (N = 4/group) and perfused in a Langendorff apparatus. Gd-DTPA was injected into the aortic perfusion line. Tissue edema was then induced by two hours of simultaneous arterial/venous perfusion (SAVP). Myocardial water content and T1 relaxation times were monitored throughout SAVP. The volumes of the extracellular and intracellular compartments were assessed using 31P MRS-detectable markers, phenylphosphonic acid (PPA) and dimethyl methylphosphonate (DMMP). Results Tissue water content in both viable and infarcted myocardium increased significantly during two-hour SAVP. However, Gd-DTPA-enhanced T1 relaxation times of the viable myocardium remained relatively unchanged. Infarcted myocardium, on the other hand, exhibited significant T1 shortening during SAVP. Furthermore, SAVP resulted in significant expansions of both extracellular and intracellular compartments, but the ratio of the volumes of the two compartments remained relatively constant. Conclusion Tissue edema in the viable myocardium does not increase the relative distribution volume of the contrast agent. As a result, edema does not change Gd-DTPA-enhanced T1 relaxation times of the viable myocardium. J. Magn. Reson. Imaging 2005;21:744,751. Published 2005 Wiley-Liss, Inc. [source] Irradiated cultured apoptotic peripheral blood mononuclear cells regenerate infarcted myocardiumEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 6 2009H. J. Ankersmit Abstract Background, Acute myocardial infarction (AMI) is followed by post AMI cardiac remodelling, often leading to congestive heart failure. Homing of c-kit+ endothelial progenitor cells (EPC) has been thought to be the optimal source for regenerating infarcted myocardium. Methods, Immune function of viable peripheral blood mononuclear cells (PBMC) was evaluated after co-culture with irradiated apoptotic PBMC (IA-PBMC) in vitro. Viable PBMC, IA-PBMC and culture supernatants (SN) thereof were obtained after 24 h. Reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay were utilized to quantify interleukin-8 (IL-8), vascular endothelial growth factor, matrix metalloproteinase-9 (MMP9) in PBMC, SN and SN exposed fibroblasts. Cell suspensions of viable- and IA-PBMC were infused in an experimental rat AMI model. Immunohistological analysis was performed to detect inflammatory and pro-angiogenic cells within 72 h post-infarction. Functional data and determination of infarction size were quantified by echocardiography and Elastica van Gieson staining. Results, The IA-PBMC attenuated immune reactivity and resulted in secretion of pro-angiogenic IL-8 and MMP9 in vitro. Fibroblasts exposed to viable and IA-PBMC derived SN caused RNA increment of IL-8 and MMP9. AMI rats that were infused with IA-PBMC cell suspension evidenced enhanced homing of endothelial progenitor cells within 72 h as compared to control (medium alone, viable-PBMC). Echocardiography showed a significant reduction in infarction size and improvement in post AMI remodelling as evidenced by an attenuated loss of ejection fraction. Conclusion, These data indicate that infusion of IA-PBMC cell suspension in experimental AMI circumvented inflammation, caused preferential homing of regenerative EPC and replaced infarcted myocardium. [source] Early homing of adult mesenchymal stem cells in normal and infarcted isolated beating heartsJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 2 2008Claudia Penna Abstract Little is known on the early homing features of transplanted mesenchymal stem cells (MSCs). We used the isolated rat heart model to study the homing of MSCs injected in the ventricular wall of a beating heart. In this model all types of cells and matrix elements with their interactions are represented, while external interferences by endothelial/neutrophil interaction and neurohormonal factors are excluded. We studied the morphology and marker expression of MSCs implanted in normal hearts and in the border-zone of infarcted myocardium. Early morphological adaptation of MSC homing differs between normal and infarcted hearts over the first 6 hrs after transplantation. In normal hearts, MSCs migrate very early through the interstitial milieu and begin to show morphological changes. Yet, in infarcted hearts MSCs remain in the site of injection forming clusters of round-shaped cells in the border-zone of the infarcted area. Both in normal and infarcted hearts, immuno-histochemistry and confocal imaging showed that, besides the proliferative marker proliferating cell nuclear agent (PCNA), some transplanted cells early express myoblastic maker GATA-4, and some of them show a VWF immunopositivity. Moreover, a few hours after injection connexin-43 is well evident between cardiomy-ocytes and injected cells. This study indicates for the first time that the isolated beating heart is a good model to study early features of MSC homing without external interferences. The results show (i) that MSCs start to change marker expression few hours after injection into a beating heart and (ii) that infarcted myocardium influences transplanted MSC morphology and mobility within the heart. [source] Comparison of various kinds of bone marrow stem cells for the repair of infarcted myocardium: Single clonally purified non-hematopoietic mesenchymal stem cells serve as a superior source,JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 4 2006Shaoheng Zhang Abstract A variety of adult stem cells have been used to transplant into the infarcted (MI) heart, however, comparative studies are lacking to show more suitable source of cells for transplantation. We have identified a single non-hematopoietic mesenchymal stem cell subpopulation (snMSCs) isolated from human bone marrow and clonally purified, that over 99% of them expressed MSC marker proteins and cardiomyocyte marker proteins when induction in vitro. We also compared the effects of the snMSCs with unpurified MSC (uMSCs), mononuclear cells (BMMNCs), or peripheral blood mononuclear cells (PBMNCs) on myocardial repair after induction of MI in rats. Ninety days later, we observed a better cardiac function assessed by ejection fraction, fraction of shortening and lung wet/dry weight ratios, less remodeling of left ventricle (LV), lower collagen density in the LV, and more vessels in the ischemic wall in the snMSCs transplantation group than in other cell-transplanted groups. Furthermore, the transplanted cells expressing cardiomyocyte specific proteins or vascular endothelial cell marker proteins were more in the snMSCs group than in other ones. We conclude that transplantation with single clonally purified MSCs seems to be more beneficial to the cardiac repair than with other stem cells after MI. J. Cell. Biochem. 99: 1132,1147, 2006. © 2006 Wiley-Liss, Inc. [source] Time course of 23Na signal intensity after myocardial infarction in humansMAGNETIC RESONANCE IN MEDICINE, Issue 3 2004Joern J.W. Sandstede Abstract Experimental studies demonstrated persistently increased 23Na content in nonviable myocardium post-myocardial infarction (MI). We hypothesized that nonviable myocardium in humans would show elevated 23Na content at all stages of infarct development, and therefore could be imaged with 23Na MRI. Ten patients were examined on days 4, 14, and 90 after infarction, and five of these patients participated in a 12-month follow-up. Double angulated short-axis cardiac 23Na images were obtained with the use of a 23Na surface coil and an ECG-triggered, 3D gradient-echo sequence. 1H T2 -weighted imaging (N = 9) was performed on days 4, 14, and 90. Wall motion was assessed by cine MRI, and the infarct size was determined by late enhancement on day 90. The 23Na signal intensity (SI) of infarcted myocardium was expressed as the percentage increase over 23Na SI of noninfarcted myocardium. All of the patients showed an area of elevated SI on 23Na and 1H T2 -weighted images that correlated with wall motion abnormalities and late enhancement. 23Na SI was highest on day 4. It then decreased until day 90, but remained elevated (39% ± 18%, 31% ± 17%, 28% ± 13% on days 4, 14, and 90, respectively, P = 0.001). No further decrease was found 1 year after infarction (25% ± 7%, P = 0.89 vs. day 90). 1H T2 -weighted SI decreased between days 4 and 14, but on day 90 only six of nine patients had a residual elevated SI. Thus, 23Na SI is elevated in nonviable infarction at all time points following MI, and 23Na MRI may become a suitable technique for imaging nonviable myocardium in humans. Magn Reson Med 52:545,551, 2004. © 2004 Wiley-Liss, Inc. [source] Complementary displacement-encoded MRI for contrast-enhanced infarct detection and quantification of myocardial function in miceMAGNETIC RESONANCE IN MEDICINE, Issue 4 2004Wesley D. Gilson Abstract MRI is emerging as an important modality for assessing myocardial function in transgenic and knockout mouse models of cardiovascular disease, including myocardial infarction (MI). Displacement encoding with stimulated echoes (DENSE) measures myocardial motion at high spatial resolution using phase-reconstructed images. The current DENSE technique uses inversion recovery (IR) to suppress T1 -relaxation artifacts; however, IR is ill-suited for contrast-enhanced infarct imaging in the heart, where multiple T1 values are observed. We have developed a modified DENSE method employing complementary acquisitions for T1 -independent artifact suppression. With this technique, displacement and strain are measured in phase-reconstructed images, and contrast-enhanced regions of infarction are depicted in perfectly coregistered magnitude-reconstructed images. The displacement measurements and T1 -weighted image contrast were validated with the use of a rotating phantom. Modified DENSE was performed in mice (N = 9) before and after MI. Circumferential (Ecc) and radial (Err) strain were measured, and contrast-enhanced infarcted myocardium was detected by DENSE. At baseline, Ecc was ,0.16 ± 0.01 and Err was 0.39 ± 0.07. After MI, Ecc was 0.04 ± 0.02 and Err was 0.03 ± 0.04 in infarcted regions, whereas Ecc was ,0.12 ± 0.02 and Err was 0.38 ± 0.09 in noninfarcted regions. In vivo Ecc as determined by DENSE correlated well with Ecc obtained by conventional tag analysis (R = 0.90). Magn Reson Med 51:744,752, 2004. © 2004 Wiley-Liss, Inc. [source] Bone marrow stem cells regenerate infarcted myocardiumPEDIATRIC TRANSPLANTATION, Issue 2003Donald Orlic Abstract: Heart disease is the leading cause of death in the United States for both men and women. Nearly 50% of all cardiovascular deaths result from coronary artery disease. Occlusion of the left coronary artery leads to ischemia, infarction, necrosis of the affected myocardial tissue followed by scar formation and loss of function. Although myocytes in the surviving myocardium undergo hypertrophy and cell division occurs in the border area of the dead tissue, myocardial infarcts do not regenerate and eventually result in the death of the individual. Numerous attempts have been made to repair damaged myocardium in animal models and in humans. Bone marrow stem cells (BMSC) retain the ability throughout adult life to self-renew and differentiate into cells of all blood lineages. These adult BMSC have recently been shown to have the capacity to differentiate into multiple specific cell types in tissues other than bone marrow. Our research is focused on the capacity of BMSC to form new cardiac myocytes and coronary vessels following an induced myocardial infarct in adult mice. In this paper we will review the data we have previously published from studies on the regenerative capacity of BMSC in acute ischemic myocardial injury. In one experiment donor BMSC were injected directly into the healthy myocardium adjacent to the injured area of the left ventricle. In the second experiment, mice were treated with cytokines to mobilize their BMSC into the circulation on the theory that the stem cells would traffic to the myocardial infarct. In both experimental protocols, the BMSC gave rise to new cardiac myocytes and coronary blood vessels. This BMSC-derived myocardial regeneration resulted in improved cardiac function and survival. [source] Lack of Impact of Myocardial Ischemia on the Signal-Averaged ECG Assessment by Time-Domain AnalysisANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2002Michael A. E. Schneider M.D. Background: Late potentials represent an arrhythmogenic substrate in chronically infarcted myocardium. It is hypothesized that acute transient ischemia enhances anisotropic electrical ventricular activation and facilitates reentry mechanisms. Study aim was the prospective assessment of the impact of dipyridamole-induced myocardial ischemia on the signal-averaged ECG. Methods: Dipyridamole stress thallium-201 SPECT imaging was utilized to avoid noise contamination of the signal-averaged ECG from exercise and to document evidence and localization of myocardial ischemia or persistent perfusion defects in 68 patients with suspected coronary artery disease. Before and during dipyridamole-induced vasodilatation serial signal-averaged ECG was performed to evaluate the influence of transient ischemia on the occurrence of late potentials. Results: There was a significant difference between heart rate at rest and heart rate under dipyridamole influence in patients with inducible ischemia (70 ± 13 vs. 87 ± 13; P < 0.0001) in contrast to patients without dipyridamole-induced ischemia (74 ± 20 vs. 80 ± 16; n.s.). The number of averaged beats and achieved noise level was comparable between both groups. Thirty-three of 68 patients (49%) revealed dipyridamole-induced ischemia; however, no changes of the SAECG parameters, such as QRS, RMS, LAS at 25,250 and 40,250 Hz bandpass filtering in the leads X, Y, Z and vector magnitude, respectively, were observed as a result of ischemia. Conclusion: These results suggest that transient myocardial ischemia does not affect the signal-averaged ECG. Clinically, the signal-averaged ECG analysis seems not to be helpful in identifying patients with silent ischemia. A.N.E. 2002;7(3):191,197 [source] Promigratory Activity of Oxytocin on Umbilical Cord Blood-Derived Mesenchymal Stem CellsARTIFICIAL ORGANS, Issue 6 2010Yong Sook Kim Abstract Recent studies show that oxytocin has various effects on cellular behaviors. Oxytocin is reported to stimulate cardiomyogenesis of embryonic stem cells and endothelial cell proliferation. Mesenchymal stem cells (MSCs) are widely used for cardiac repair, and we elucidated the effect of oxytocin on umbilical cord derived-MSCs (UCB-MSCs). UCB-MSCs were pretreated with oxytocin (100 nM) and washed with saline prior to experiments. To evaluate their angiogenic potential and migration activity, tube formation assay and Boyden chamber assay were performed. For in vivo study, ischemia-reperfusion was induced in rats, and UCB-MSCs with or without oxytocin pretreatment were injected into the infarcted myocardium to evaluate the engraftment of injected cells. Histological and hemodynamic studies were performed. Oxytocin-treated UCB-MSCs showed a decrease in tube formation but a drastic increase in transwell migration activity. The transcription level of matrix metalloproteinase (MMP)-2 was increased in oxytocin-treated UCB-MSCs. Knock-down of MMP-2 by use of siRNA restored the tube formation, while reducing transmigration activity. In rats injected with oxytocin-treated UCB-MSCs, cardiac fibrosis and CD68 infiltration in the peri-infarct zone were reduced, whereas cell engraftment and connexin43 expression were greater than in rats injected with untreated UCB-MSCs. By contrast, angiogenesis did not differ significantly between the two groups. Cardiac contractility was higher in the group injected with oxytocin-treated UCB-MSCs than in the group injected with phosphate-buffered saline alone. Collectively, oxytocin is an effective priming reagent for stem cells for application to damaged heart tissue. [source] | ||||||||||