Transcranial myogenic motor-evoked potentials after transient spinal cord ischemia predicts neurologic outcome in rabbits

AbstractObjectiveMyogenic transcranial motor-evoked potentials (tc-MEPs) were applied to monitor spinal cord ischemia in the repairs of thoracoabdominal aortic aneurysms . We investigated whether tc-MEPs after spinal cord ischemia/reperfusion could be used to predict neurologic outcome in leporine model.MethodsTc-MEPs were measured at 30-second intervals before, during, and after spinal cord ischemia (SCI) induced by balloon occlusion of the infrarenal aorta. Twenty rabbits were divided into five groups. Four groups (n = 4 animals in each group) had transient ischemia induced for 10, 15, 20, or 30 minutes. In fifth group, the terminal aorta at the aortic bifurcation was occluded for 30 minutes. All animals were evaluated neurologically 48 hours later, and their spinal cords were removed for histologic examination.ResultsThe tc-MEPs in each SCI group rapidly disappeared after SCI. After reperfusion, the recovery of tc-MEPs amplitude was inversely correlated to duration of SCI. Tc-MEPs amplitude at one hour after reperfusion was correlated with both neurologic score and number of neuron cells in the spinal cord 48 hours later. Logistic regression analysis demonstrated that the neurologic deficits differed significantly between animals with tc-MEPs amplitude of less than 75% of the baseline and those with an amplitude of more than 75%.ConclusionsThe amplitude of tc-MEPs after ischemia /reperfusion of the spinal cord showed a high correlation with durations of SCI, with neurologic deficits, and with pathologic findings of the spinal cord. Tc-MEPs, therefore, could be used to predict neurologic outcome. In particular, tc-MEPs whose amplitude recovered by less than 75% indicated a risk of paraplegia

Structural properties in ruptured mitral chordae tendineae measured by synchrotron-based X-ray phase computed tomography

The link between the structural properties and the rupturing of chordae tendineae in the mitral valve complex is still unclear. Synchrotron-radiation-based X-ray phase computed tomography (SR-XPCT) imaging is an innovative way to quantitatively analyze three-dimensional morphology. XPCT has been employed in this study to evaluate the chordae tendineae from patients with mitral regurgitation and to analyze structural changes in the ruptured chordae tendineae in patients with this condition. Six ruptured mitral chordae tendineae were obtained during surgical repairs for mitral regurgitation and were fixed with formalin. In addition, 12 healthy chordae tendineae were obtained from autopsies. Employing XPCT (effective pixel size, 3.5 µm; density resolution, 1 mg cm−3), the density of the chordae tendineae in each sample was measured. The specimens were subsequently analyzed pathologically. The mean age was 70.2 ± 3.0 in the rupture group and 67.2 ± 14.1 years old in the control group (p = 0.4927). All scans of chorda tendineae with SR-XPCT were performed successfully. The mean densities were 1.029 ± 0.004 in the rupture group and 1.085 ± 0.015 g cm−3 in the control group (p < 0.0001). Density based on SR-XPCT in the ruptured mitral chordae tendineae was significantly lower compared with the healthy chorda tendinea. Histological examination revealed a change in the components of the connective tissues in ruptured chorda tendinea, in accordance with the low density measured by SR-XPCT. SR-XPCT made it possible to measure tissue density in mitral chordae tendineae. Low density in mitral chordae tendineae is associated with a greater fragility in ruptured mitral chordae tendineae

Structural properties in ruptured mitral chordae tendineae measured by synchrotron-based X-ray phase computed tomography

The link between the structural properties and the rupturing of chordae tendineae in the mitral valve complex is still unclear. Synchrotron-radiation-based X-ray phase computed tomography (SR-XPCT) imaging is an innovative way to quantitatively analyze three-dimensional morphology. XPCT has been employed in this study to evaluate the chordae tendineae from patients with mitral regurgitation and to analyze structural changes in the ruptured chordae tendineae in patients with this condition. Six ruptured mitral chordae tendineae were obtained during surgical repairs for mitral regurgitation and were fixed with formalin. In addition, 12 healthy chordae tendineae were obtained from autopsies. Employing XPCT (effective pixel size, 3.5 µm; density resolution, 1 mg cm⁻³), the density of the chordae tendineae in each sample was measured. The specimens were subsequently analyzed pathologically. The mean age was 70.2 ± 3.0 in the rupture group and 67.2 ±14.1 years old in the control group (p = 0.4927). All scans of chorda tendineae with SR-XPCT were performed successfully. The mean densities were 1.029 ±0.004 in the rupture group and 1.085 ± 0.015 g cm⁻³ in the control group (p < 0.0001). Density based on SR-XPCT in the ruptured mitral chordae tendineae was significantly lower compared with the healthy chorda tendinea. Histological examination revealed a change in the components of the connective tissues in ruptured chorda tendinea, in accordance with the low density measured by SR-XPCT. SR-XPCT made it possible to measure tissue density in mitral chordae tendineae. Low density in mitral chordae tendineae is associated with a greater fragility in ruptured mitral chordae tendineae

Mechanism of sac expansion without evident endoleak analyzed with X ray phase-contrast tomography

Objective: Synchrotron radiation-based X ray phase-contrast tomography (XPCT) was used in this study to evaluate abdominal aorta specimens from patients with sac expansion without evidence of an endoleak (endotension) following endovascular aortic repair (EVAR) for an abdominal aortic aneurysm (AAA). The aim of this study was to analyze the morphologic structure of the aortic wall in patients with this condition and to establish the cause of the endotension. Methods: Human aortic specimens of the abdominal aorta were obtained during open repair, fixed with formalin, and analyzed among three groups. Group A was specimens from open abdominal aortic aneurysm repairs (n = 7). Group E was specimens from sac expansion without an evident endoleak after EVAR (n = 7). Group N was specimens from non-aneurysmal “normal” cadaveric abdominal aortas (n = 5). Using XPCT (effective voxel size, 12.5 μm; density resolution, 1 mg/cm3), we measured the density of the tunica media (TM) in six regions of each sample. Then, any changes to the elastic lamina and the vasa vasorum were analyzed pathologically. The specimens were immunohistochemically examined with anti-CD31 and vascular endothelial growth factor antibodies. Results: The time from EVAR to open aortic repair was 64.2 ± 7.2 months. There were significant differences in the thickness of the TM among three groups: 0.98 ± 0.03 mm in Group N; 0.31 ± 0.01 mm in Group A; and 0.15 ± 0.03 mm in Group E (P < .005). There were significant differences in the TM density among the groups: 1.087 ± 0.004 g/cm3 in Group N; 1.070 ± 0.001 g/cm3 in Group A; and 1.062 ± 0.007 g/cm3 in Group E (P < .005). Differences in the thickness and density of the TM correlated with the thickness of the elastic lamina; in Group N, uniform high-density elastic fibers were observed in the TM. By contrast, a thinning of the elastic lamina in the TM was observed in Group A. A marked thinness and loss of elastic fibers was observed in Group E. CD31 immunostaining revealed that the vasa vasorum was localized in the adventitia and inside the outer third of the TM in Group N, and in the middle of the TM in Group A. In Group E, the vasa vasorum advanced up to the intima with vascular endothelial growth factor-positive cells in the intimal section. Conclusions: XPCT could be used to demonstrate the densitometric property of the aortic aneurysmal wall after EVAR. We confirmed that the deformation process that occurs in the sac expansion after EVAR without evidence of an endoleak could be explained by hypoxia in the aortic wall. : Clinical Relevance: The pathophysiology of the sac expansion without evidence of an endoleak (endotension) following EVAR remains an enigma. Several theories have been proposed regarding the cause of endotension, including the presence of blood flow below the sensitivity limits of current imaging modalities, pressure transmission through a thrombus or endograft fabric, and the presence of microleak or ultrafiltration. We demonstrated the marked thinning of the elastic lamella and neovascularization in the TM and the intima and proposed that the insertion of a stent graft into an aortic aneurysm may worsen the hypoxic conditions of the aneurysmal wall