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Myocardium

The myocardium is the muscular middle layer of the heart wall that is responsible for the pumping action of the heart.
It is composed of cardiac muscle tissue and is essential for the efficient circulation of blood throughout the body.
Understanding the structure and function of the myocardium is crucial for the study and treatment of various cardiovascular diseases, such as heart failure, myocardial infarction, and arrhythmias.
Researchers can utilize PubCompare.ai's AI-driven protocol comparision to streamline their myocardium research, enhancing reproducibility and acuracy to achieve more reliable results.

Most cited protocols related to «Myocardium»

A limitation of the previous Task Force Criteria was the reliance on subjective criteria for assessing ventricular structure and function and for evaluation of myocardial histology. In this modification of the Task Force Criteria, quantitative criteria are proposed and abnormalities are defined based on comparison with normal subject data. (Table 1) The data from 108 probands with newly diagnosed ARVC/D, age 12 years or older, who were enrolled in the National Institutes of Health supported Multidisciplinary Study of Right Ventricular Dysplasia,43 (link) were compared with that of normal subjects. (See appendix) The criteria were selected on the basis of analysis of sensitivity and specificity from ROC curves. For analysis of each test (i.e. echocardiogram, MRI etc.) proband data was excluded if that test was crucial for the diagnosis of the individual patient. This was done to eliminate bias in estimating the sensitivity and specificity of that particular test. In general, when determining the sensitivity and specificity of a new screening test it is recommended that none of the screening test elements are used in making the primary diagnosis; this principle also holds when establishing diagnostic criteria.
Publication 2010
Arrhythmogenic Right Ventricular Dysplasia Congenital Abnormality Diagnosis Echocardiography Heart Ventricle Myocardium Patients Reliance resin cement
In comparing the survival distributions of two or more groups (for example, new therapy vs standard of care), Kaplan-Meier estimation1 and the log-rank test2 are the basic statistical methods of analyses. These are non-parametric methods in that no mathematical form of the survival distributions is assumed. If an investigator is interested in quantifying or investigating the effects of known covariates (e.g., age or race) or predictor variables (e.g., blood pressure), regression models are utilized. As in the conventional linear regression models, survival regression models allow for the quantification of the effect on survival of a set of predictors, the interaction of two predictors, or the effect of a new predictor above and beyond other covariates.
Among the available survival regression models, the Cox proportional hazards model developed by Sir David Cox3 has seen great use in epidemiological and medical studies, and the field of nuclear cardiology is no exception. What follows are some examples of Cox models being used in nuclear cardiology. Xu et al4 (link) looked at how myocardial scarring (assessed with positron emission tomography [PET] or single photon emission computed tomography [SPECT]) and other demographic and medical history factors predicted mortality in patients with advanced heart failure who received cardiac resynchronization therapy. Bourque et al5 (link) looked at how left ventricular ejection fraction (LVEF, assessed with angiography) and nuclear summed rest score (SRS, assessed with SPECT) interacted to change the risk of mortality. Hachamovitch and Berman6 (link) looked at the incremental prognostic value of myocardial perfusion SPECT (MPS) parameters in the prediction of sudden cardiac death. Nakata et al7 (link) looked at how the heart-to-mediastinum ratio (assessed with metaiodobenzylguanidine [MIBG] imaging) predicted cardiac death.
Survival models other than the Cox model have been used in nuclear cardiology as well. For example, in a study of diagnosis strategies for quantifying myocardial perfusion with SPECT, Duvall et al8 (link) utilized a log-normal survival model, a member of the parametric family of regression survival models, since initial data exploration revealed that the proportional hazards assumption of the Cox model was invalid. While this is an excellent example of when to utilize other survival models, it has been more common to see such data presented in conjunction with a Cox model analysis. In earlier studies of MPS-derived predictors of cardiac events, Hachamovitch et al9 (link) used Cox models to identify significant predictors and parametric models, specifically the accelerated failure time (AFT) model, to make estimates of the time to certain percentiles of survival. An identical analysis strategy was used by the research group comprised of Cuocolo, Acampa, Petretta, Daniele et al10 (link)–13 (link) in their research of the impact of various SPECT-derived predictors on the occurrence of cardiac events.
Publication 2014
3-Iodobenzylguanidine Angiography Blood Pressure Cardiac Death Cardiac Events Cardiac Resynchronization Therapy Cardiovascular System Family Member Heart Heart Failure Mediastinum Myocardium Patients Perfusion Positron-Emission Tomography Sudden Cardiac Death Tests, Diagnostic Therapeutics Tomography, Emission-Computed, Single-Photon Ventricular Ejection Fraction
Single and double, fluorescent and non-fluorescent, in situ hybridization and immunohistochemical stainings were performed using standard protocols. To analyze the ltbp3 loss of function phenotype, we injected anti-sense ltbp3 morpholinos into one-cell stage WT and transgenic embryos. For genetic lineage tracing, a transgenic driver strain expressing Cre recombinase in ltbp3+ cells and four Cre-responsive “color switching” reporter strains were generated using standard methods. The driver strain was crossed individually to each of the reporter strains and their double transgenic progenies were analyzed for ZsYellow protein fluorescence using confocal microscopy. To follow the migration of zebrafish SHF cells, a tracking dye was injected into the ZsYellow+, AmCyan region of Tg(nkx2.5::ZsYello); Tg(cmlc2::CSY) embryos at 24hpf, the embryos were imaged immediately, and then again at 48 and/or 72hpf. A transgenic strain carrying a cDNA encoding a constitutively active human TGFβ type I receptor (caALK5) under control of the zebrafish heat shock promoter was generated and used to rescue the myocardial defect in ltbp3 morphant embryos.
Full Methods and any associated references are available in the online version of the paper at www.natre.com/nature
Publication 2011
Animals, Transgenic Cells Cre recombinase Cultured Cells DNA, Complementary Embryo Fluorescence Fluorescent in Situ Hybridization Heat-Shock Response Homo sapiens Microscopy, Confocal Migration, Cell Morpholinos Myocardium Phenotype Proteins Receptor, Transforming Growth Factor-beta Type I Staining Strains Zebrafish

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Publication 2008
Antihypertensive Agents Body Size Body Surface Area Dental Caries Diabetes Mellitus Diastole Endocardium Epistropheus Glucose Heart Heart Ventricle High Blood Pressures Hypoglycemic Agents Left Ventricles Males Myocardium Obesity Papillary Muscles Woman
10 normal volunteers (7 men; age 35 ± 7 years, normal ECGs without history of cardiac diseases or symptoms) underwent CMR imaging at 1.5T and 3T on the same day. Following standard planning, end-expiration basal, mid-cavity and apical short-axis images using MOLLI and ShMOLLI were collected. Images for specific TI were collected using exactly the same SSFP readouts for both methods to allow direct comparisons, typically: TR/TE = 2.14/1.07 ms, flip angle = 35°, FOV = 340 × 255 mm, matrix = 192 × 144, 107 phase encoding steps, interpolated voxel size = 0.9 × 0.9 × 8 mm, GRAPPA = 2 with 24 reference lines, cardiac delay time TD = 500 ms; 206 ms acquisition time for single image. A single slice, which was judged to have the "best quality" at the time of scanning, was repeated twice at the end of the protocol to assess short-term intra-scan variability of the T1 measurements; this was not performed in the first pilot case. Offline post-processing involved manual tracing of endo- and epi-cardial contours for analysis of the T1 measurements in myocardial segments 1 to 16 of the American Heart Association (AHA) 17-segment model [16 (link)] using in-house software.
Publication 2010
Cardia Dental Caries Electrocardiogram Endometriosis Epistropheus Heart Heart Diseases Myocardium Normal Volunteers Radionuclide Imaging

Most recents protocols related to «Myocardium»

Example 10

Oncomice®, obtained through an in-house breeding program, were anesthetized intramuscularly with 0.1 mL of ketamine/acepromazine (1.8 mL saline, 1.0 mL ketamine, and 0.2 mL acepromazine) prior to dosing and tissue sampling. Individual mice were then injected via the tail vein with an imaging agent of the present invention (0.5-2.0 mCi/kg in 0.1 mL). Mice were euthanized and biodistribution performed at 1 h post-injection. Selected tissues were removed, weighed, and counted on a gamma counter. Results are expressed as the percentage of injected dose per gram tissue (mean±SEM; Table 3).

TABLE 3
Summary of imaging agent distribution in the Oncomouse ®
Imaging Agent Distribution
(% ID/g)
tissue246
blood1.07 ± 0.0600.41 ± 0.0990.88 ± 0.061
heart0.95 ± 0.0650.36 ± 0.0640.69 ± 0.073
lung0.97 ± 0.1210.45 ± 0.0711.69 ± 0.382
liver13.1 ± 2.1723.6 ± 5.1911.3 ± 1.73
spleen0.69 ± 0.0850.34 ± 0.0570.81 ± 0.021
kidney20.6 ± 3.2514.8 ± 1.796.66 ± 1.46
bone2.02 ± 0.3201.28 ± 0.2002.86 ± 0.124
muscle0.50 ± 0.0730.17 ± 0.0430.44 ± 0.049
urine71.87.67 ± 5.007.21 ± 6.71
tumor0.95 ± 0.1031.12 ± 0.2040.73 ± 0.026

Patent 2024
Acepromazine Bones Gamma Rays Hematologic Neoplasms Hematuria Ketamine Kidney Liver Lung Mus Myocardium Neoplasms Saline Solution Spleen Tail Tissues Urine Veins
Not available on PMC !

Example 4

A cohort of patients with a recent history of myocardial infarction are administered an effective amount of the imaging agent of the invention, images of each patient's left atrium are obtained and the uptake of the imaging agent is quantified. The patients also undergo a resting flurpiridaz F 18 myocardial perfusion study and the summed rest score determined for each patient. Logisitic regression analysis is performed to produce an equation expressing the likelihood of future AF as a function of summed rest score and quantified imaging agent uptake.

Patent 2024
Atrial Fibrillation Atrium, Left Matrix Metalloproteinases Myocardial Infarction Myocardium Patients Perfusion

Example 10

LacZ and Luciferase Modified RNA Cardiac Transfection and Translation in a Citrate Saline Buffer

As depicted, 75 μg of LacZ encoding modified RNA with cardiac injections was transfected and translated in approximately 10% of the left ventricle (FIGS. 11A, 11B, 11C, and 11D). RNA in situ hybridization for luciferase modified RNA revealed staining expression in the myocardium at the site of injection (FIGS. 11E and 11F) and correlative luciferase protein expression shown via immunohistochemical analysis in the serial section (FIG. 11G).

Patent 2024
Buffers Citrate Heart In Situ Hybridization LacZ Genes Left Ventricles Luciferases Myocardium Polypeptides Proteins Saline Solution Transfection Vascular Endothelial Growth Factors
The MW parameters for ventricular systole were derived by entering the timings of the mitral valve closure and aortic valve closure (defined from the Doppler trace at the aortic valve). Global systolic constructive work (GSCW) was defined as the MW during shortening in systole, and global systolic wasted work (GSWW) was defined as the MW during lengthening in systole. The MW parameters specific for IVR were calculated through deduction: MCWIVR (myocardial constructive work during IVR, the myocardial work performed for lengthening during IVR) = GCW—GSCW; MWWIVR (myocardial wasted work during IVR, the myocardial work performed for shortening during IVR) = GWW—GSWW. The total myocardial work during IVR (MWIVR) was obtained from the sum of MCWIVR and MWWIVR. Myocardial work efficiency during IVR (MWEIVR) was calculated, as follows: MCWIVR / (MCWIVR + MWWIVR) × 100%. The MWIVR parameters were normalized by dividing these by the corresponding IVRT.
Publication 2023
Heart Ventricle Mitral Valve Myocardium Systole Valves, Aortic
In the EchoPAC software, the MW parameters were obtained through the pressure-strain loop (PSL) area module constructed from the curves for noninvasively estimated LV pressures and LV strains. The peak LV systolic pressure was assumed to be equal to the brachial cuff systolic BP measured during the echocardiographic study. This noninvasive method was validated by various research teams [1 (link), 3 (link), 4 (link), 21 , 22 (link)]. The myocardial work was calculated as the integral of power between mitral valve closure and mitral valve opening. The timings for the valvular events were defined on Doppler spectrums before entering the automated function imaging (AFI). The global work index (GWI) was defined as the total MW within the PSL area, from mitral valve closure to mitral valve opening. Global constructive work (GCW) was defined as the MW performed for shortening during ventricular systole and lengthening during IVR. Global wasted work (GWW) was defined as the MW performed for lengthening during ventricular systole and shortening during IVR. Global work efficiency (GWE) was calculated as the percentage of myocardial constructive work in the total MW (GCW / [GCW + GWW] × 100).
Publication 2023
Echocardiography Heart Ventricle Mitral Valve Myocardium Pressure Strains Systole Systolic Pressure

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More about "Myocardium"

The myocardium, also known as the cardiac muscle or heart muscle, is the thick middle layer of the heart wall that is responsible for the pumping action of the heart.
It is composed of specialized cardiac muscle tissue, which is essential for the efficient circulation of blood throughout the body.
Understanding the structure and function of the myocardium is crucial for the study and treatment of various cardiovascular diseases, such as heart failure, myocardial infarction, and arrhythmias.
Researchers can utilize PubCompare.ai's AI-driven protocol comparison to streamline their myocardial research, enhancing reproducibility and accuracy to achieve more reliable results.
PubCompare.ai's intelligent protocol analysis can help users find the best protocols and products from literature, pre-prints, and patents, optimizing the research process.
When studying the myocardium, researchers may use various tools and techniques, such as TRIzol reagent for RNA extraction, Image-Pro Plus 6.0 for image analysis, Cvi42 for cardiovascular imaging, MATLAB for data processing, TRIzol for tissue homogenization, Gadovist for contrast-enhanced cardiac MRI, the In Situ Cell Death Detection Kit for apoptosis analysis, and FBS (fetal bovine serum) for cell culture.
Additionally, techniques like TTC (triphenyltetrazolium chloride) staining may be employed to assess myocardial infarction, and Magnetom Avanto MRI scanners can be used for noninvasive imaging of the myocardium.
By incorporating these tools and techniques, along with the insights provided by PubCompare.ai's AI-driven protocol comparison, researchers can streamline their myocardial research, enhance reproducibility, and achieve more reliable and accruate results in the study and treatment of cardiovascular diseases.