Echocardiographic assessment of embryonic and fetal mouse heart development: a focus on haemodynamics and morphology.
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ABSTRACT:
SUBMITTER: Hahurij ND
PROVIDER: S-EPMC3951091 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundRecently, it was reported that the adult X. tropicalis heart can regenerate in a nearly scar-free manner after injury via apical resection. Thus, a cardiac regeneration model in adult X. tropicalis provides a powerful tool for recapitulating a perfect regeneration phenomenon, elucidating the underlying molecular mechanisms of cardiac regeneration in an adult heart, and developing an interventional strategy for the improvement in the regeneration of an adult heart, which may be more applicable in mammals than in species with a lower degree of evolution. However, a noninvasive and rapid real-time method that can observe and measure the long-term dynamic change in the regenerated heart in living organisms to monitor and assess the regeneration and repair status in this model has not yet been established.ResultsIn the present study, the methodology of echocardiographic assessment to characterize the morphology, anatomic structure and cardiac function of injured X. tropicalis hearts established by apex resection was established. The findings of this study demonstrated for the first time that small animal echocardiographic analysis can be used to assess the regeneration of X. tropicalis damaged heart in a scar-free perfect regeneration or nonperfect regeneration with adhesion manner via recovery of morphology and cardiac function.ConclusionsSmall animal echocardiography is a reliable, noninvasive and rapid real-time method for observing and assessing the long-term dynamic changes in the regeneration of injured X. tropicalis hearts.
| S-EPMC9926761 | biostudies-literature
Project description:Intracardiac haemodynamics is crucial for normal cardiogenesis, with recent evidence showing valvulogenesis is haemodynamically dependent and inextricably linked with shear stress. Although valve anomalies have been associated with genetic mutations, often the cause is unknown. However, altered haemodynamics have been suggested as a pathogenic contributor to bicuspid aortic valve disease. Conversely, how abnormal haemodynamics impacts mitral valve development is still poorly understood. In order to analyse altered blood flow, the outflow tract of the chick heart was constricted using a ligature to increase cardiac pressure overload. Outflow tract-banding was performed at HH21, with harvesting at crucial valve development stages (HH26, HH29 and HH35). Although normal valve morphology was found in HH26 outflow tract banded hearts, smaller and dysmorphic mitral valve primordia were seen upon altered haemodynamics in histological and stereological analysis at HH29 and HH35. A decrease in apoptosis, and aberrant expression of a shear stress responsive gene and extracellular matrix markers in the endocardial cushions were seen in the chick HH29 outflow tract banded hearts. In addition, dysregulation of extracellular matrix (ECM) proteins fibrillin-2, type III collagen and tenascin were further demonstrated in more mature primordial mitral valve leaflets at HH35, with a concomitant decrease of ECM cross-linking enzyme, transglutaminase-2. These data provide compelling evidence that normal haemodynamics are a prerequisite for normal mitral valve morphogenesis, and abnormal blood flow could be a contributing factor in mitral valve defects, with differentiation as a possible underlying mechanism.
| S-EPMC5529288 | biostudies-literature
Project description:BackgroundThis study sought to explore the clinical application value of fetal heart quantification (HQ) technology in the evaluation of fetal heart morphology in hypertensive disorders of pregnancy (HDP).MethodsFetal HQ software was used to quantitatively analyze the 4-chamber global sphericity index (GSI) and 24-segment sphericity index (SI) and Z scores of 53 normal fetal hearts (the normal group) and 26 fetal hearts with gestational hypertension (the case group). The normal Z value range was set at -2 to 2.ResultsThere was a statistically significant difference between the 1-16 and 20-24 segments of the left and right ventricles in the normal group (P<0.05), but there was no statistically significant difference between the 17-19 segments (P>0.05). There was no statistically significant difference in the fetal GSI between the 2 groups (P>0.05). There was no statistically significant difference in the SI of the 24 segments of the fetal left ventricle between the 2 groups (P>0.05). There was no statistically significant difference in the SI between the 1-20 segments of the right ventricle between the 2 groups (P>0.05), but there was a statistically significant difference in the SI between the 21-24 segments (P<0.05). There was no statistically significant difference in the incorrect ratio of the Z value of the GSI between the 2 groups (P>0.05). There was no statistically significant difference in the abnormal rate of the Z value of the SI in each segment of the fetal left ventricle between the 2 groups (P>0.05). There was a significant difference in the abnormal rate of the Z value of the SI in each segment of the fetal right ventricle between the 2 groups (P<0.05).ConclusionsFetal HQ technology can be used in the quantitative analysis of cardiac morphology in gestational hypertension, and provides a new method for fetal cardiac morphology analysis.
| S-EPMC9732594 | biostudies-literature
Project description:AimsPTMC produces significant changes in mitral valve morphology as improvement in leaflets mobility. The determinants of such improvement have not been assessed before.Methods and resultsThe study included 291 symptomatic patients with mitral stenosis undergoing PTMC. Post-PTMC subvalvular splitting area was a determinant of post-PTMC excursion in both the anterior (B 0.16, 95% CI 0.03 to 0.30, p < 0.05) and the posterior (B 0.12, 95% CI 0.01 to 0.24, p < 0.05) leaflets. Another determinant was the post-PTMC transmitral pressure gradient for anterior (B -0.02, 95% CI -0.04 to -0.005, p < 0.01) and posterior (B -0.01, 95% CI -0.04 to -0.005, p < 0.05) leaflets excursion. The relationship between post-PTMC MVA and leaflet excursion was non-linear "S curve". There was a steep increase of both anterior (p, 0.02) and posterior (p, 0.03) leaflets excursion with increased MVA till the MVA reached a value of about 1.5 cm2; after which both linear and S curves became nearly parallel.ConclusionThe improvement in leaflets excursion after PTMC is determined by several morphologic and hemodynamic changes produced in the valve. The increase in MVA improves mobility within limit; after which any further increase in MVA is not associated by a significant improvement in mobility in both leaflets.
| S-EPMC2248162 | biostudies-literature
Project description:Background4D flow magnetic resonance imaging (4D flow MRI) can assess and measure the complex flow patterns of the right ventricle (RV) in congenital heart diseases, but its limited availability makes the broad application of intracardiac flow assessment challenging. Color Doppler imaging velocity reconstruction from conventional echocardiography is an emerging alternative, but its validity against 4D flow MRI needs to be established.ObjectiveTo compare intracardiac flow parameters measured by color Doppler velocity reconstruction (DoVeR) against parameters measured from 4D flow MRI.MethodsWe analyzed 20 subjects, including 7 normal RVs and 13 abnormal RVs (10 with repaired Tetralogy of Fallot, and 3 with atrial-level shunts). Intracardiac flow parameters such as relative pressure difference, vortex strength, total kinetic energy, and viscous energy loss were quantified using DoVeR and 4D flow MRI. The agreement between the two methods was determined by comparing the spatial fields and quantifying the cross-correlation and normalized difference between time-series measurements.ResultsThe hemodynamic parameters obtained from DoVeR and 4D flow MRI showed similar flow characteristics and spatial distributions. The time evolutions of the parameters were also in good agreement between the two methods. The median correlation coefficient between the time-series of any parameter was between 0.87 and 0.92, and the median L2-norm deviation was between 10% to 14%.ConclusionsOur study shows that DoVeR is a reliable alternative to 4D flow MRI for quantifying intracardiac hemodynamic parameters in the RV.
| S-EPMC10947680 | biostudies-literature
Project description:BACKGROUND:Mouse models of heart disease are extensively employed. The echocardiographic characterization of contractile function is usually focused on systolic function with fewer studies assessing diastolic function. Furthermore, the applicability of diverse echocardiographic parameters of diastolic function that are commonly used in humans has not been extensively evaluated in different pathophysiological models in mice. METHODS AND RESULTS:We used high resolution echocardiography to evaluate parameters of diastolic function in mouse models of chronic pressure overload (aortic constriction), volume overload (aorto-caval shunt), heart failure with preserved ejection fraction (HFpEF; DOCA-salt hypertension), and acute sarcoplasmic reticulum dysfunction induced by thapsigargin - all known to exhibit diastolic dysfunction. Left atrial area increased in all three chronic models while mitral E/A was difficult to quantify at high heart rates. Isovolumic relaxation time (IVRT) and Doppler E/E' increased significantly and the peak longitudinal strain rate during early filling (peak reverse longitudinal strain rate) decreased significantly after aortic constriction, with the changes being proportional to the magnitude of hypertrophy. In the HFpEF model, reverse longitudinal strain rate decreased significantly but changes in IVRT and E/E' were non-significant, consistent with less severe dysfunction. With volume overload, there was a significant increase in reverse longitudinal strain rate and decrease in IVRT, indicating a restrictive physiology. Acute thapsigargin treatment caused significant prolongation of IVRT and decrease in reverse longitudinal strain rate. CONCLUSION:These results indicate that the combined measurement of left atrial area plus reverse longitudinal strain rate and/or IVRT provide an excellent overall assessment of diastolic function in the diseased mouse heart, allowing distinction between different types of pathophysiology.
| S-EPMC5807035 | biostudies-literature
Project description:Due to the cyclic function of the human heart, pressure and flow in the circulation are pulsatile rather than continuous. Addressing pulsatile haemodynamics starts with the most convenient measurement, brachial pulse pressure, which is widely available, related to development and treatment of heart failure (HF), but often confounded in patients with established HF. The next level of analysis consists of central (rather than brachial) pressures and, more importantly, of wave reflections. The latter are closely related to left ventricular late systolic afterload, ventricular remodelling, diastolic dysfunction, exercise capacity, and, in the long-term, the risk of new-onset HF. Wave reflection may also represent a suitable therapeutic target. Treatments for HF with preserved and reduced ejection fraction, based on a reduction of wave reflection, are emerging. A full understanding of ventricular-arterial coupling, however, requires dedicated analysis of time-resolved pressure and flow signals, which can be readily accomplished with contemporary non-invasive imaging and modelling techniques. This review provides a summary of our current understanding of pulsatile haemodynamics in HF.
| S-EPMC6234849 | biostudies-literature
Project description:Several in vitro models have been developed to recapitulate mouse embryogenesis solely from embryonic stem cells (ESCs). Despite mimicking many aspects of early development, they fail to capture the interactions between embryonic and extraembryonic tissues. To overcome this difficulty, we have developed a mouse ESC-based in vitro model that reconstitutes the pluripotent ESC lineage and the two extraembryonic lineages of the post-implantation embryo by transcription-factor-mediated induction. This unified model recapitulates developmental events from embryonic day 5.5 to 8.5, including gastrulation; formation of the anterior-posterior axis, brain, and a beating heart structure; and the development of extraembryonic tissues, including yolk sac and chorion. Comparing single-cell RNA sequencing from individual structures with time-matched natural embryos identified remarkably similar transcriptional programs across lineages but also showed when and where the model diverges from the natural program. Our findings demonstrate an extraordinary plasticity of ESCs to self-organize and generate a whole-embryo-like structure.
| S-EPMC9648694 | biostudies-literature
Project description:BackgroundIntrauterine growth restriction (IUGR) leads to cardiac dysfunction and adverse remodeling of the fetal heart, as well as a higher risk of postnatal cardiovascular diseases. The rat model of IUGR, via uterine artery ligation, is a popular model but its cardiac sequelae is not well investigated. Here, we performed an echocardiographic evaluation of its cardiac function to determine how well it can represent the disease in humans.MethodsUnilateral uterine artery ligation was performed at embryonic day 17 (E17) and echocardiography was performed at E19 and E20.ResultsGrowth-restricted fetuses were significantly smaller and lighter, and had an higher placenta-to-fetus weight ratio. Growth-restricted fetal hearts had reduced wall thickness-to-diameter ratio, indicating left ventricular (LV) dilatation, and they had elevated trans-mitral and trans-tricuspid E/A ratios and reduced left and right ventricular fractional shortening (FS), suggesting systolic and diastolic dysfunction. These were similar to human IUGR fetuses. However, growth-restricted rat fetuses did not demonstrate head-sparing effect, displayed a lower LV myocardial performance index, and ventricular outflow velocities were not significantly reduced, which were dissimilar to human IUGR fetuses.ConclusionsDespite the differences, our results suggest that this IUGR model has significant cardiac dysfunction, and could be a suitable model for studying IUGR cardiovascular physiology.ImpactAnimal models of IUGR are useful, but their fetal cardiac function is not well studied, and it is unclear if they can represent human IUGR fetuses. We performed an echocardiographic assessment of the heart function of a fetal rat model of IUGR, created via maternal uterine artery ligation. Similar to humans, the model displayed LV dilatation, elevated E/A ratios, and reduced FS. Different from humans, the model displayed reduced MPI, and no significant outflow velocity reduction. Despite differences with humans, this rat model still displayed cardiac dysfunction and is suitable for studying IUGR cardiovascular physiology.
| S-EPMC8566221 | biostudies-literature
Project description:Neurodevelopmental impairments are the most common extracardiac morbidities among patients with complex congenital heart disease (CHD) across the lifespan. Robust clinical research in this area has revealed several cardiac, medical, and social factors that can contribute to neurodevelopmental outcome in the context of CHD. Studies using brain magnetic resonance imaging (MRI) have been instrumental in identifying quantitative and qualitative difference in brain structure and maturation in this patient population. Full-term newborns with complex CHD are known to have abnormal microstructural and metabolic brain development with patterns similar to those seen in premature infants at approximately 34 to 36 weeks' gestation. With the advent of fetal brain MRI, these brain abnormalities are now documented as they begin in utero, as early as the third trimester. Importantly, disturbed brain development in utero is now known to be independently associated with neurodevelopmental outcome in early childhood, making the prenatal period an important timeframe for potential interventions. Advances in fetal brain MRI provide a robust imaging tool to use in future neuroprotective clinical trials. The causes of abnormal fetal brain development are multifactorial and include cardiovascular physiology, genetic abnormalities, placental impairment, and other environmental and social factors. This review provides an overview of current knowledge of brain development in the context of CHD, common prenatal imaging tools to evaluate the developing fetal brain in CHD, and known risk factors contributing to brain immaturity.
| S-EPMC9905309 | biostudies-literature