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Left Ventricular Wall (leave + ventricular_wall)

Distribution by Scientific Domains
Medical Sciences85%

Terms modified by Left Ventricular Wall

  • leave ventricular wall thickness
    		•

    Selected Abstracts

    Left Ventricular Non Compaction in Children

    CONGENITAL HEART DISEASE, Issue 5 2010
    Sara 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]

    Laplacian Electrograms and the Interpretation of Complex Ventricular Activation Patterns During Ventricular Fibrillation

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2000
    PH.D., RUBEN CORONEL M.D.
    Laplacian Electrograms and Ventricular Fihrillation. Introduction. During ventricular fibrillation (VF) interpretation of a local electrogram and determination of the local activation moment are hampered by remote activity or intervening repolarization waves. Successful defibrillation depends on critical timing of the shock relative to local activation. We tested the applicabillity of Laplacian electrograms for detection of the moment of local activation during VF. Methods and Results. From isolated perfased porcine infact heart, 247 local unipolar electrograms were recorded simultaneously (13 × 19 matrix, interelectrode distance 0.3 mm) from the left ventricular wall during sinus rhythm, following pacing or during VF, Activation maps were constructed based on local unipolar electrograms, and Laplacian electrograms were calculated from local electrograms ane its eight neighbors. The Laplacian electrogram displayed a sharp R/S complex with local activation iodicted by the moment of zero crossing without interference from remote activity or repolarization waves. Its amplitude increased with decreasing interelectrode distance, Following epicardial stimulation, Laplacian amplitude was significantly larger than during complexes with different morphology. Collision of wavefronts was associated with entirely positive Laplacian waveforms; "focal" appearancce of acitivity was associated with an entirely negative waveform. Activation block in the activation maps was correlated with the appearance of substanined episodes of negativity or positivity in the Laplacian electrogram (depending on the location of the recording site relative to the line of block). Conclusion. Laplacian electrograms allow detection of the moment of local activation without interference from remote activity or repolarization, especially during complex arrhythmias. The technique applied toe automatic sensing devices, such its the internal defibrillator, may optimize defibrtilation success. (J Cardiovasc Electrophysiol, Vol. 11, pp. 1119-1128, October 2000) [source]

    Catheter-Based Transendocardial Myocardial Gene Transfer

    JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 1 2002
    CHRISTER SYLVÉNM.D. Ph.D.
    Background and Aim: Local modulation of myocardial function by gene transfer or cell depositions constitutes a potential method of cardiac treatment. This study tested the morphology of myocardial plasmid gene transfer by catheter-based transendocardial injection (NOGA). Methods: Left ventricular morphology and electrical and mechanical characteristics were mapped in three dimensions. In two pigs, 0.10 mL oftoluidine blue was injected at ten sites. In seven pigs, seven to ten injections of 0.10 mL saline containing 0.10 mg pCMV-LacZ expressing the enzyme ,-galactosidase and 0.10 mg phVEGF-A165 were given. The pigs were sacrificed after 3 days and gene expression was determined. Results: Macroscopically on the endocardial surface, all identified spots were located in the target area. However, along the transmyocardial axis, injections with color and plasmid were located randomly throughout the left ventricular wall from the endocardium to the epicardium. In each detected spot, gene expression of ,-galactosidase was observed in an approximate myocardial volume of 5 × 5 × 5 mm. Microscopically, the transfected cells were located typically at the tip of the injection scar. As a rule, 10 to 20 transfected cells were located at the end of the injection scar. In sections where expression of both transcripts was observed, 42% of the cells expressed both ,-galactosidase and vascular endothelial growth factors (VEGF), 32% only ,-galactosidase, and 26% only VEGF. Conclusions: Myocardial gene transfer following magnetic guidance can be located precisely on the left ventricular inner surface. Within the myocardium, gene expression is local around the distal tip of the injection scar and is located randomly at every level of depth of the left ventricular wall. [source]

    Three-dimensional diffusion tensor microscopy of fixed mouse hearts

    MAGNETIC RESONANCE IN MEDICINE, Issue 3 2004
    Yi Jiang
    Abstract The relative utility of 3D, microscopic resolution assessments of fixed mouse myocardial structure via diffusion tensor imaging is demonstrated in this study. Isotropic 100-,m resolution fiber orientation mapping within 5.5° accuracy was achieved in 9.1 hr scan time. Preliminary characterization of the diffusion tensor primary eigenvector reveals a smooth and largely linear angular rotation across the left ventricular wall. Moreover, a higher level of structural hierarchy is evident from the organized secondary and tertiary eigenvector fields. These findings are consistent with the known myocardial fiber and laminar structures reported in the literature and suggest an essential role of diffusion tensor microscopy in developing quantitative atlases for studying the structure,function relationships of mouse hearts. Magn Reson Med 52:453,460, 2004. © 2004 Wiley-Liss, Inc. [source]

    In vivo study of microcirculation in canine myocardium using the IVIM method,

    MAGNETIC RESONANCE IN MEDICINE, Issue 3 2003
    Virginie Callot
    Abstract The intravoxel incoherent motion (IVIM) method was implemented in closed-chest dogs to obtain measurements on microcirculation in the left ventricular wall in vivo. Specifically, it enabled us to measure the mean microflow velocity (400 ± 40 ,m/s) and the vascular volume fraction (VVF) (11.1% ± 2.2%), and observe the directional preference of capillary orientation. The apparent diffusion coefficients (ADCs) of water along and perpendicular to myofibers were also measured. With vasodilatation by adenosine infusion, a 25% increase in the VVF and a 7% increase in the mean microflow velocity were observed, while no change in the ADC was detected. A 28.5% decrease of the ADC was observed postmortem. Magn Reson Med 50:531,540, 2003. Published 2003 Wiley-Liss, Inc. [source]

    Three-dimensional architecture of the left ventricular myocardium

    THE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 6 2006
    Paul 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]

    Nicorandil Improves Myocardial High-Energy Phosphates In Postinfarction Porcine Hearts

    CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 8 2002
    Yo Murakami
    SUMMARY 1.,Nicorandil is a potent vasodilator combining the effects of a nitrate with an ATP-sensitive potassium channel (KATP) opener. Because the postinfarct remodelled heart has increased vulnerability to subendocardial hypoperfusion, it is possible that the vasodilator effects of nicorandil could cause transmural redistribution of blood flow away from the subendocardium. Alternatively, the KATP channel opening effects of nicorandil could exert a beneficial effect on mitochondrial respiration. Consequently, the present study was performed to examine the effect of nicorandil on energy metabolism in the postinfarct heart. 2.,Studies were performed in swine in which myocardial infarction produced by proximal left circumflex coronary artery ligation had resulted in left ventricular remodeling. [31P] nuclear magnetic resonance spectroscopy (MRS) was used to examine the myocardial energy supply/demand relationship across the left ventricular wall while the transmural distribution of blood flow was examined with radioactive microspheres. Data were obtained during baseline conditions and during infusion of nicorandil (100 ,g, i.v., followed an infusion of 25 ,g/kg per min). 3.,Nicorandil caused coronary vasodilation with a preferential increase in subepicardial flow; however, subendocardial flow also increased significantly. Nicorandil had no significant effect on the rate,pressure product or myocardial oxygen consumption. The ratio of phosphocreatine (PCr)/ATP determined with MRS was abnormally depressed in remodelled hearts (2.01 ± 0.11, 1.85 ± 0.10 and 1.59 ± 0.11 for subepicardium, midwall and subendocardium, respectively) compared with normal (2.22 ± 0.11, 2.01 ± 0.15 and 1.80 ± 0.09, respectively). Nicorandil had no effect on the high-energy phosphate content of normal hearts. However, nicorandil increased the PCr/ATP ratio in the subendocardium of remodelled hearts from 1.59 ± 0.11 to 1.87 ± 0.10 (P < 0.05). 4.,Although nicorandil caused modest redistribution of blood flow away from the subendocardium of the postinfarct left ventricle, this was associated with an increase of the PCr/ATP ratio towards normal. These results suggest that nicorandil exerts a beneficial effect on energy metabolism in the subendocardium of the postinfarct remodelled left ventricle. [source]