Search

Representative day 28 long-axis ultrasound images (top), 3D surface strains (middle), and bullseye strain maps (bottom) of the remodeled LVs for all five mice in the I/R group. The akinetic myocardium is marked in dashed yellow lines, and the strain estimated infarct size is outlined in solid black line. Sternal artifact is shaded in gray with black dashed border. Scalebar: 1mm.

Representative day 28 long-axis ultrasound images (top), 3D surface strains (middle), and bullseye strain maps (bottom) of the remodeled LVs for all five mice in the PL group. The akinetic myocardium is marked in dashed yellow lines, the strain estimated infarct boundary is outlined in solid black line, and the wall-thinned infarct boundary is marked in dotted white line. Sternal artifact is shaded in gray with black dashed border. Scalebar: 1mm.

Representative day-28 maximum principal 3D strains are presented along the entire thickness of the LV wall for each surgical group. Yellow and blue regions correspond to areas of high and low strains respectively. A: anterior, S: septal, L: lateral; B: base. Scalebar: 1mm.

Bullseye maps of the maximum principal 3D Green-Lagrange strain (EI) for all 15 mice at baseline. Consistent high strain values throughout the LV myocardium across all animals highlight the reproducibility of the 3D strain technique.

Representative day 28 long-axis ultrasound images (top), 3D surface strains (middle), and bullseye strain maps (bottom) of the remodeled LVs for all five mice in the I/R group. The akinetic myocardium is marked in dashed yellow lines, and the strain estimated infarct size is outlined in solid black line. Sternal artifact is shaded in gray with black dashed border. Scalebar: 1mm.

Representative day-28 maximum principal 3D strains are presented along the entire thickness of the LV wall for each surgical group. Yellow and blue regions correspond to areas of high and low strains respectively. A: anterior, S: septal, L: lateral; B: base. Scalebar: 1mm.

Supplemental Material, DS1_TPX_10.1177_0192623319838491 for Epithelial–mesenchymal Transition Phenotypes in Vertebral Metastases of Lung Cancer by Alexandra M. Dieterly, Gozde Uzunalli, Chinyere M. Kemet, Arvin H. Soepriatna, Craig J. Goergen and L. Tiffany Lyle in Toxicologic Pathology

Bullseye maps of the maximum principal 3D Green-Lagrange strain (EI) for all 15 mice at baseline. Consistent high strain values throughout the LV myocardium across all animals highlight the reproducibility of the 3D strain technique.

Comparison of maximum principal strains estimated with 3D Direct Deformation Estimation (DDE, solid lines) and Vic2D (dashed lines). Short-axis ultrasound strain data along the anterior (red) and posterior (blue) myocardial walls are shown at baseline and at day 28 post-permanent ligation. Although both 3D-DDE and Vic2D demonstrated significantly lower strain values along the infarcted, anterior myocardium post-surgery, the 3D-DDE method more appropriately tracked changes in myocardial strain, as strain values returned to 0 at the end of the cardiac cycle.

Heart failure is a leading cause of death in the United States, and cardiac thrombus, a common morbidity associated with heart failure, significantly increases a patient’s risk of embolic events. The objective of this project is to characterize left-ventricular (LV) thrombus development using high frequency ultrasound imaging in a murine model. C57BL/6J wild-type mice (n=6) were injected intraperitoneally with iron dextran five times a week for six weeks to increase oxidative stress in the heart. Granulocyte-colony stimulating factor (G-CSF) was subcutaneously injected daily during the second week to initiate stem cell migration and stimulate endothelial cell activation, thus increasing the hypercoagulability state of the blood. A high-frequency, small animal ultrasound system (Vevo2100, VisualSonics FUJIFILM Inc.) and a 40 MHz central frequency transducer were used to track LV thrombus progression and evaluate LV function weekly. Four out of six mice developed thrombus, but no significant differences in LV performance were observed when compared to mice that did not form a thrombus. Further investigation is necessary to study the role of attenuated heart function on thrombus formation. Future work will incorporate a murine model of myocardial infarction to investigate if a severely compromised heart increases the risk of or accelerates LV thrombus formation. This study will aid in identifying patients who are predisposed to thrombus formation following a heart attack, leading to more effective prevention and treatment methods.