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Myocardial Cells (myocardial + cell)
Selected AbstractsSide-to-side linking of myocardial cells in hypertrophic cardiomyopathy: Whole heart microscopic observation with tangential sectionsPATHOLOGY INTERNATIONAL, Issue 11 2005Hirotake Masuda By cross-section or longitudinal section, it is difficult to investigate longitudinal features of myocardial cells in the whole heart. Here, introducing the use of tangential sections to obtain longitudinal aspect of myocardial cells in any part of myocardium, the authors evaluated myocardium in the left ventricle in 10 normal hearts and four hearts with hypertrophic cardiomyopathy (HCM). Tangential sections were obtained by peeling the superficial layer of myocardium. After peeling the whole surface, secondary deep layer was peeled. These procedures were repeated more than five times through the wall. Intercalated discs (ICD) were observed immunohistochemically with anti-N-cadherin and antidesmoplakin. In normal hearts, myocardial cells were cut longitudinally and ran parallel in tangential sections. They linked end-to-end with simple and regular ICD with average lengths of 120,130 µm and average sarcomere numbers of 56,65. In HCM hearts, many myocardial cells were cut almost longitudinally running approximately parallel in tangential sections. Myocardial cells frequently showed side-to-side linking characterized by skewed ICD, indistinct ICD counterparts, and longitudinally arranged ICD. Two young HCM hearts had circle-shaped ICD and vacuole-like structures highlighted by immunostaining for N-cadherin, which were actually extracellular structures comparable with irregular side-to-side linking. It is considered that side-to-side linking of myocardial cells is a characteristic microscopic feature in HCM rather than myocardial disarray. [source] Role of progenitor endothelial cells in cardiovascular disease and upcoming therapiesCATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 4 2007Atsuhiko Kawamoto MD Abstract The field of cell-based transplantation has expanded considerably and is poised to become an established cardiovascular therapy in the near future. In this review, we will focus on endothelial progenitor cells (EPCs), which are immature cells capable of differentiating into mature endothelial cells. EPCs share many surface marker antigens such as CD34, AC133, Flk-1, etc. with hematopoietic stem cells (HSCs) and the major source of EPCs as well as HSCs is the bone marrow (BM). BM-derived EPCs are mobilized into peripheral blood and recruited to the foci of pathophysiological neovascularization and reendothelialization, thereby contributing to vascular regeneration. Severe EPC dysfunction is an indicator of poor prognosis and severe endothelial dysfunction. Indeed, number of circulating EPCs and their migratory activity are reduced in patients with diabetes, coronary artery disease (CAD), or subjects with multiple coronary risk factors. Effective neovascularization induced by EPC transplantation for hindlimb, myocardial, and cerebral ischemia has been demonstrated in many preclinical studies, and early clinical trials of EPC transplantation in chronic and acute CAD indicate safety and feasibility of myocardial cell-based therapies. For therapeutic reendothelialization in patients undergoing percutaneous coronary intervention, CD34 antibody-coated stents have been used clinically to capture circulating EPCs at the injury sites and enhance reendothelialization and safety of stents. Further development in cell processing technology for efficient isolation, expansion, mobilization, recruitment, and transplantation of EPCs into target tissues are underway and expected to be tested in clinical trials in the near future. © 2007 Wiley-Liss, Inc. [source] Left Ventricular Non Compaction in ChildrenCONGENITAL HEART DISEASE, Issue 5 2010Sara H. Weisz MD ABSTRACT Left ventricular non compaction (LVNC) is a myocardial disease characterized by a hypertrabeculated myocardium. The hypertrabeculations in the left ventricular wall define deep recesses communicating with the left ventricular chamber where blood penetrates with increased risk of blood clots in the meshwork of the prominent trabeculations. The left ventricular apex and the free wall are particularly affected. During in utero ventriculogenesis, myocardial blood supply is initially linked to the presence of sinusoids, in which blood penetrates and diffuses nutriments and oxygen to myocardial cells. Progressively, with the development of the heart and the increase of cells demand of blood, coronary arteries system develops. This step is associated with myocardial modification that leads to compaction of hypertrabeculated myocardial net. Probably, the premature interruption of this process leads to ventricular noncompaction. Many studies have been conducted in adults with hypertrabeculated myocardium. To date, data regarding childhood LVNC are sparse. The aim of this review is to summarize the clinical and preclinical knowledge about LVNC in children. [source] Human Histopathology of Electroanatomic Mapping After Cooled-Tip Radiofrequency Ablation to Treat Ventricular Tachycardia in Remote Myocardial InfarctionJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2005THOMAS DENEKE M.D. Introduction: Catheter ablation of ventricular tachycardia (VT) in remote myocardial infarction (MI) often requires excessive mapping procedures. Documentation of the electrical substrate via electrogram amplitude may help to identify regions of altered myocardium resembling exit areas of reentrant VTs. Methods and Results: A patient with multiple symptomatic monomorphic VTs (biventricular ICD, remote MI) underwent electroanatomic substrate mapping (CARTOÔ) for VT ablation. Regions of scar (bipolar electrogram amplitudes ,0.5 mV), normal myocardium (,1.5 mV), and "altered" myocardium (0.5,1.5 mV) were identified. Ablation was directed to regions with "altered" myocardium based on pace map correlation. After ablation the clinical VT did not reoccur. The patient died due to worsening of heart failure 7 days afterward. During postmortal evaluation specified sites of electroanatomic mapping were correlated to histopathological findings. Annotated scar areas were documented to consist of areas with massive fibrosis (,80% of mural composition). Ablations were found to span through regions with intermediate fibrosis (21,79%) mapped as "altered" myocardium. Ablation produced transmural coagulation necrosis of mesh-like fibrotic tissue with interspersed remnants of myocardial cells up to a maximum depth of 7.0 mm. Subendocardial intramural bleedings were universal findings 7 days after ablation. Conclusions: Electroanatomic substrate mapping for VT ablation sufficiently identified regions of scar and normal myocardium. Regions with bipolar electrogram amplitudes between 0.5 and 1.5 mV were found to correlate to areas of "intermediate" fibrosis (21,79%) with only remnant strands of myocardial cells and were identified as target region for ablation. Cooled-tip endocardial radiofrequency ablation lead to transmural coagulation necrosis up to a depth of 7.0 mm. [source] Antiplatelet Therapy: Anti-Ischemic Benefits versus Bleeding RiskJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 2008C. MICHAEL GIBSON M.D., F.A.C.C. Balance between efficacy and safety is a major concern in therapeutic interventions of patients with acute coronary syndromes. Identifying and managing the risks that may negatively affect this balance can potentially minimize the incidence of morbidity and/or mortality among patients with acute coronary syndromes. Unstable angina and non-ST-elevation myocardial infarction are potentially life-threatening disorders and a major cause of hospitalization and emergency medical care. At the time of presentation, the use of algorithms that provide reasonable assessment of a patient's risk of cardiovascular events, such as the Thrombolysis in Myocardial Infarction risk score, can help clinicians identify which patients will most likely benefit from a specific strategy. The ultimate goal of treatment for non-ST-elevation myocardial infarction is to reduce short- and long-term morbidity and mortality, as well as salvage myocardial cells and cardiac function. Pharmacologic intervention with antiplatelet and/or antithrombotic agents has proven to be effective in achieving this goal in numerous outcome studies. However, clinicians must balance anti-ischemic efficacy with the need to minimize the risk of serious bleeding complications (e.g., hemorrhage). Issues related to safety include timing of the dose, duration of infusion, drug compatibility, errors in estimating a patient's weight and/or age, failure to adjust the dosage based upon renal function, and errors in drug preparation. [source] Side-to-side linking of myocardial cells in hypertrophic cardiomyopathy: Whole heart microscopic observation with tangential sectionsPATHOLOGY INTERNATIONAL, Issue 11 2005Hirotake Masuda By cross-section or longitudinal section, it is difficult to investigate longitudinal features of myocardial cells in the whole heart. Here, introducing the use of tangential sections to obtain longitudinal aspect of myocardial cells in any part of myocardium, the authors evaluated myocardium in the left ventricle in 10 normal hearts and four hearts with hypertrophic cardiomyopathy (HCM). Tangential sections were obtained by peeling the superficial layer of myocardium. After peeling the whole surface, secondary deep layer was peeled. These procedures were repeated more than five times through the wall. Intercalated discs (ICD) were observed immunohistochemically with anti-N-cadherin and antidesmoplakin. In normal hearts, myocardial cells were cut longitudinally and ran parallel in tangential sections. They linked end-to-end with simple and regular ICD with average lengths of 120,130 µm and average sarcomere numbers of 56,65. In HCM hearts, many myocardial cells were cut almost longitudinally running approximately parallel in tangential sections. Myocardial cells frequently showed side-to-side linking characterized by skewed ICD, indistinct ICD counterparts, and longitudinally arranged ICD. Two young HCM hearts had circle-shaped ICD and vacuole-like structures highlighted by immunostaining for N-cadherin, which were actually extracellular structures comparable with irregular side-to-side linking. It is considered that side-to-side linking of myocardial cells is a characteristic microscopic feature in HCM rather than myocardial disarray. [source] The water extract of Omija protects H9c2 cardiomyoblast cells from hydrogen peroxide through prevention of mitochondrial dysfunction and activation of caspases pathwayPHYTOTHERAPY RESEARCH, Issue 1 2007Channy Park Abstract The water extract of Omija (Omija) has been used traditionally in the treatment of ischemic damage of the heart and brain tissues. However, little is known about the mechanism by which it rescues myocardial cells from oxidative stress. This study was designed to investigate the protective mechanisms of Omija on H2O2 -induced cytotoxicity in H9c2 cardiomyoblast cells. Treatment with H2O2 resulted in the death of H9c2 cells, characterized by apparent apoptotic features, including fragmentation of the nucleus and an increase in the sub-G0/G1 fraction of the cell cycle. However, Omija markedly suppressed the apoptotic characteristics of H9c2 cells induced by H2O2. In addition, Omija suppressed the features of mitochondrial dysfunction, including changes in the mitochondrial membrane potential and cytosolic release of cytochrome c in H2O2 -treated cells. Treatment with Omija further inhibited the catalytic activation of caspase-9 and caspase-3 and induction of Fas by H2O2. Taken together, these data indicate that the water extract of Omija protects H9c2 cardiomyoblast cells from oxidative stress of H2O2 through inhibition of mitochondrial dysfunction and activation of intrinsic caspase cascades, including caspase-3 and caspase-9. Copyright © 2006 John Wiley & Sons, Ltd. [source] POINT: A Prescription to Decrease Left Ventricular FunctionPREVENTIVE CARDIOLOGY, Issue 4 2009Myrvin H. Ellestad MD The Courage Trial, published in 2007, has significantly reduced the incidence of treating stable angina with angioplasty. The investigators randomized 2297 patients with documented cardiac ischemia to conservative or invasive therapy and concluded that there was no difference in major events during a follow-up of 2.5 to 7 years and that the urge to open the narrowed artery was unjustified. Over the years it has been well documented by myocardial biopsy that repeated ischemic episodes result in replacement of myocardial cells by fibrous tissue, loss of mitochondria, and deterioration of left ventricular function. Ischemic episodes often occur in the absence of angina so that it is impossible to determine whether the therapy is reducing the magnitude or duration of the process. Also, in their study, 32% of the conservatively treated patients crossed over to invasive. The evidence indicated that conservative treatment may result in a progressive decrease in left ventricular function. [source] Three-dimensional architecture of the left ventricular myocardiumTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 6 2006Paul P. Lunkenheimer Abstract Concepts for ventricular function tend to assume that the majority of the myocardial cells are aligned with their long axes parallel to the epicardial ventricular surface. We aimed to validate the existence of aggregates of myocardial cells orientated with their long axis intruding obliquely between the ventricular epicardial and endocardial surfaces and to quantitate their amount and angulation. To compensate for the changing angle of the long axis of the myocytes relative to the equatorial plane of the ventricles with varying depths within the ventricular walls, the so-called helical angle, we used pairs of cylindrical knives of different diameters to punch semicircular slices from the left ventricular wall of pigs, the slices extending from the epicardium to the endocardium. The slices were pinned flat, fixed in formaldehyde, embedded in paraffin, sectioned, stained with azan or hematoxilin and eosin, and analyzed by a new semiautomatic procedure. We made use of new techniques in informatics to determine the number and angulation of the aggregates of myocardial cells cut in their long axis. The alignment of the myocytes cut longitudinally varied markedly between the epicardium and the endocardium. Populations of myocytes, arranged in strands, diverge by varying angles from the epicardial surface. When paired knives of decreasing diameter were used to cut the slices, the inclination of the diagonal created by the arrays increases, while the lengths of the array of cells cut axially decreases. The visualization of the size, shape, and alignment of the myocytic arrays at any side of the ventricular wall is determined by the radius of the knives used, the range of helical angles subtended by the alignment of the myocytes throughout the thickness of the wall, and their angulation relative to the epicardial surface. Far from the majority of the ventricular myocytes being aligned at angles more or less tangential to the epicardial lining, we found that three-fifths of the myocardial cells had their long axes diverging at angles between 7.5 and 37.5° from an alignment parallel to the epicardium. This arrangement, with the individual myocytes supported by connective tissue, might control the cyclic rearrangement of the myocardial fibers. This could serve as an important control of both ventricular mural thickening and intracavitary shape. Anat Rec Part A 288A:565,578, 2006. © 2006 Wiley-Liss, Inc. [source] Prominent expression of lysyl oxidase during mouse embryonic cardiovascular developmentTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 2 2003Takeshi Tsuda Abstract By mRNA differential display in mouse hearts, lysyl oxidase (Lox), a key enzyme catalyzing cross-links in elastin and collagens, was found to be up-regulated between embryonic days 11 (E11) and 13 (E13). This was confirmed by semiquantitative RT-PCR. We analyzed its spatio-temporal expression pattern by in situ hybridization in regard to the development of myocardial cells, endocardial cushion tissue, aortic arch vessels, and epicardium. Anat Rec Part A 270A:93,96, 2003. © 2003 Wiley-Liss, Inc. [source] Anaesthetic implications of arrhythmogenic right ventricular dysplasia/cardiomyopathyANAESTHESIA, Issue 1 2009A. K. Alexoudis Summary Arrhythmogenic right ventricular dysplasia, also called right ventricular cardiomyopathy, is a genetically determined heart muscle disease, characterised by life-threatening ventricular arrhythmias in apparently healthy young people. The primary myocardial pathology is that the myocardium of the right ventricular free wall is replaced by fibrous or fibrofatty tissue, with scattered residual myocardial cells. Right ventricular function is abnormal and in severe cases is associated with global right ventricular dilation and overt biventricular heart failure. Although still relatively rare, arrhythmogenic right ventricular cardiomyopathy is a well recognised cause of sudden unexpected peri-operative death. In this review, we describe the basic characteristics of this disease, emphasising the diagnosis and we offer some suggestions for the anaesthetic management of these patients in the peri-operative period. [source] Anti-apoptotic effect of benidipine, a long-lasting vasodilating calcium antagonist, in ischaemic/reperfused myocardial cellsBRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2001Feng Gao Ischaemia/reperfusion causes intracellular calcium overloading in cardiac cells. Administration of calcium antagonists reduces myocardial infarct size. Recent in vitro studies have demonstrated that calcium plays a critical role in the signal transduction pathway leading to apoptosis. However, whether or not calcium antagonists may reduce myocardial apoptosis induced by ischaemia-reperfusion, and thus decrease myocardial infarction, has not been directly investigated. The present study investigated the effects of benidipine, an L-type calcium channel blocker, on myocardial infarct size, apoptosis, necrosis and cardiac functional recovery in rabbits subjected to myocardial ischaemia/reperfusion (MI/R, 45 min/240 min). Ten minutes prior to coronary occlusion, rabbits were treated with vehicle or benidipine (10 ,g kg,1 or 3 ,g kg,1, i.v.). In the vehicle-treated group, MI/R caused cardiomyocyte apoptosis as evidenced by DNA ladder formation and TUNEL positive nuclear staining (12.2±1.1%). Treatment with 10 ,g kg,1 benidipine lowered blood pressure, decreased myocardial apoptosis (6.2±0.8%, P<0.01 vs vehicle) and necrosis, reduced infarct size (20±2.3% vs 49±2.6%, P<0.01), and improved cardiac functional recovery after reperfusion. Administering benidipine at 3 ,g kg,1, a dose at which no haemodynamic effect was observed, also exerted significant anti-apoptosis effects, which were not significantly different from those observed with higher dose benidipine treatment. However, treatment with this low dose benidipine failed to reduce myocardial necrosis. These results demonstrate that benidipine, a calcium antagonist, exerts significant anti-apoptosis effects, which are independent of haemodynamic changes. Administration of benidipine at a higher dose produced favourable haemodynamic effects and provided additional protection against myocardial necrotic injury and further improved cardiac functional recovery. British Journal of Pharmacology (2001) 132, 869,878; doi:10.1038/sj.bjp.0703881 [source] | ||||||||||||||||||||||