whole heart
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Herz ◽  
2022 ◽  
Author(s):  
Uzair Ansari ◽  
Sonja Janssen ◽  
Stefan Baumann ◽  
Martin Borggrefe ◽  
Stephan Waldeck ◽  
...  

Abstract Background We investigated the feasibility of evaluating coronary arteries with a contrast-enhanced (CE) self-navigated sparse isotropic 3D whole heart T1-weighted magnetic resonance imaging (MRI) study sequence. Methods A total of 22 consecutive patients underwent coronary angiography and/or cardiac computed tomography (CT) including cardiac MRI. The image quality was evaluated on a 3-point Likert scale. Inter-reader variability for image quality was analyzed with Cohen’s kappa for the main coronary segments (left circumflex [LCX], left anterior descending [LAD], right coronary artery [RCA]) and the left main trunk (LMT). Results Inter-reader agreement for image quality of the coronary tree ranged from substantial to perfect, with a Cohen’s kappa of 0.722 (RCAmid) to 1 (LCXprox). The LMT had the best image quality. Image quality of the proximal vessel segments differed significantly from the mid- and distal segments (RCAprox vs. RCAdist, p < 0.05). The LCX segments showed no significant difference in image quality along the vessel length (LCXprox vs. LCXdist, p = n.s.). The mean acquisition time for the study sequence was 553 s (±46 s). Conclusion Coronary imaging with a sparse 3D whole-heart sequence is feasible in a reasonable amount of time producing good-quality imaging. Image quality was poorer in distal coronary segments and along the entire course of the LCX.


Author(s):  
Alina Schneider ◽  
Gastao Cruz ◽  
Camila Munoz ◽  
Reza Hajhosseiny ◽  
Thomas Kuestner ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Jochen Brenneisen ◽  
Anna Daub ◽  
Tobias Gerach ◽  
Ekaterina Kovacheva ◽  
Larissa Huetter ◽  
...  

Background: The human heart is a masterpiece of the highest complexity coordinating multi-physics aspects on a multi-scale range. Thus, modeling the cardiac function in silico to reproduce physiological characteristics and diseases remains challenging. Especially the complex simulation of the blood's hemodynamics and its interaction with the myocardial tissue requires a high accuracy of the underlying computational models and solvers. These demanding aspects make whole-heart fully-coupled simulations computationally highly expensive and call for simpler but still accurate models. While the mechanical deformation during the heart cycle drives the blood flow, less is known about the feedback of the blood flow onto the myocardial tissue.Methods and Results: To solve the fluid-structure interaction problem, we suggest a cycle-to-cycle coupling of the structural deformation and the fluid dynamics. In a first step, the displacement of the endocardial wall in the mechanical simulation serves as a unidirectional boundary condition for the fluid simulation. After a complete heart cycle of fluid simulation, a spatially resolved pressure factor (PF) is extracted and returned to the next iteration of the solid mechanical simulation, closing the loop of the iterative coupling procedure. All simulations were performed on an individualized whole heart geometry. The effect of the sequential coupling was assessed by global measures such as the change in deformation and—as an example of diagnostically relevant information—the particle residence time. The mechanical displacement was up to 2 mm after the first iteration. In the second iteration, the deviation was in the sub-millimeter range, implying that already one iteration of the proposed cycle-to-cycle coupling is sufficient to converge to a coupled limit cycle.Conclusion: Cycle-to-cycle coupling between cardiac mechanics and fluid dynamics can be a promising approach to account for fluid-structure interaction with low computational effort. In an individualized healthy whole-heart model, one iteration sufficed to obtain converged and physiologically plausible results.


2021 ◽  
Vol 12 ◽  
Author(s):  
Robin Moss ◽  
Eike Moritz Wülfers ◽  
Steffen Schuler ◽  
Axel Loewe ◽  
Gunnar Seemann

The ECG is one of the most commonly used non-invasive tools to gain insights into the electrical functioning of the heart. It has been crucial as a foundation in the creation and validation of in silico models describing the underlying electrophysiological processes. However, so far, the contraction of the heart and its influences on the ECG have mainly been overlooked in in silico models. As the heart contracts and moves, so do the electrical sources within the heart responsible for the signal on the body surface, thus potentially altering the ECG. To illuminate these aspects, we developed a human 4-chamber electro-mechanically coupled whole heart in silico model and embedded it within a torso model. Our model faithfully reproduces measured 12-lead ECG traces, circulatory characteristics, as well as physiological ventricular rotation and atrioventricular valve plane displacement. We compare our dynamic model to three non-deforming ones in terms of standard clinically used ECG leads (Einthoven and Wilson) and body surface potential maps (BSPM). The non-deforming models consider the heart at its ventricular end-diastatic, end-diastolic and end-systolic states. The standard leads show negligible differences during P-Wave and QRS-Complex, yet during T-Wave the leads closest to the heart show prominent differences in amplitude. When looking at the BSPM, there are no notable differences during the P-Wave, but effects of cardiac motion can be observed already during the QRS-Complex, increasing further during the T-Wave. We conclude that for the modeling of activation (P-Wave/QRS-Complex), the associated effort of simulating a complete electro-mechanical approach is not worth the computational cost. But when looking at ventricular repolarization (T-Wave) in standard leads as well as BSPM, there are areas where the signal can be influenced by cardiac motion of the heart to an extent that should not be ignored.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Ramsey Omari ◽  
Charles Curtis ◽  
Nichole Burket ◽  
Michael Weisman ◽  
Xiaofeng Chen ◽  
...  

Motivation:  Receiving radiation to the heart has been recognized as a risk factor for the development of major adverse cardiovascular events (MACEs) for many years. However, recent data suggests that radiation dosing to substructures of the heart serve as a better surrogate for evaluating the risk of developing a MACE than whole heart radiation dose. Recent papers suggest that dosing to the left anterior descending artery (LAD) can be used as a robust marker for cardiotoxicity risk; however, this association lacks corroborative data and is currently not incorporated into clinically routine care.  Problem:  In this paper we seek to investigate the relationship between radiation dose to the LAD and risk of developing a MACE in lung cancer patients treated with curative intent radiation.  Approach:  Chart review to confirm the presence of MACE events was performed in patients who were identified based on elevated troponin values to potentially have had a MACE after receiving their last dose of radiation therapy. Patients who had multiple courses of radiation therapy separated in time (>60 days) that received greater than 0.2 Gy whole heart dose during their subsequent courses before having a MACE were excluded. Selected patients were then stratified based on presence cardiovascular co-morbidities. Contours of patient’s LADs were made after patient selection, and will be verified by an expert (e.g., cardiologist or thoracic radiologist).  Results:  Dose to the LAD will be calculated and an assessment of the correlation between radiation dose and risk of having a MACE will be made. Analysis will assess the cardiac event rate at various times as well as time to MACE.  Implications:  This paper can help set a quantifiable standard with which radiation oncologists can use to minimize their patient’s risk of developing a MACE by minimizing radiation dosing to specific cardiac substructures while maintaining tumor coverage. 


2021 ◽  
Author(s):  
Fei Xu ◽  
Lingli Lin ◽  
Dihan Li ◽  
Qingqi Hong ◽  
Kunhong Liu ◽  
...  

2021 ◽  
Author(s):  
Hsuan-Cheng Kuo ◽  
Lixia Luo ◽  
Yan Ma ◽  
Nerissa T. Williams ◽  
Lorraine da Silva Campos ◽  
...  

AbstractThoracic radiation therapy can cause endothelial injury in the heart, leading to cardiac dysfunction and heart failure. Although it has been demonstrated that the tumor suppressor p53 functions in endothelial cells to prevent the development of radiation-induced myocardial injury, the key mechanism(s) by which p53 regulates the radiosensitivity of cardiac endothelial cells is not completely understood. Here, we utilized genetically engineered mice that express mutations in p53 transactivation domain 1 (TAD1) (p5325,26) or mutations in p53 TAD1 and TAD2 (p5325,26,53,54) specifically in endothelial cells to study the p53 transcriptional program that protects cardiac endothelial cells from ionizing radiation in vivo. p5325,26,53,54 loses the ability to drive transactivation of p53 target genes after irradiation while p5325,26 can induce transcription of a group of non-canonical p53 target genes, but not the majority of classic radiation-induced p53 targets critical for p53-mediated cell cycle arrest and apoptosis. After 12 Gy whole-heart irradiation, we found that both p5325,26 and p5325,26,53,54 sensitized mice to radiation-induced cardiac injury, in contrast to wild-type p53. Histopathological examination suggested that mutation of TAD1 contributes to myocardial necrosis after whole-heart irradiation, while mutation of both TAD1 and TAD2 abolishes the ability of p53 to prevent radiation-induced heart disease. Taken together, our results show that the transcriptional program downstream of p53 TAD1, which activates the acute DNA damage response after irradiation, is necessary to protect cardiac endothelial cells from radiation injury in vivo.


Author(s):  
Steffen Bruns ◽  
Jelmer M. Wolterink ◽  
Thomas P.W. van den Boogert ◽  
Jurgen H. Runge ◽  
Berto J. Bouma ◽  
...  

Author(s):  
Marwa Ali Gamal El-Deen ◽  
Ahmed Samir Ibrahim ◽  
Emad H. Abdeldayem ◽  
Remon Zaher Elia ◽  
Soha Romeih

Abstract Background Multi-slice computed tomography (MSCT) angiography is the gold standard imaging modality to evaluate the patency of Glenn shunt and the presence of veno–veno collaterals. The goal of this study is to evaluate the ability of two cardiac magnetic resonance imaging (MRI) techniques to assess the patency of Glenn shunt and the presence of veno–veno collaterals compared to MSCT angiography. Results Patients with Glenn shunt had MSCT angiography and cardiac MRI using two techniques: TWIST (Time-resolved angiography With Stochastic Trajectories) and the three-dimensional (3D) post-contrast whole heart techniques. MSCT angiography and cardiac MRI images were post-processed for quantitative and qualitative assessment of Glenn shunt and veno–veno collaterals. Our study included 29 patients (17 male, 59%) with Glenn shunt, the median age was 22 years (range 3–36 years). 3D post-contrast whole heart images give similar results compared to MSCT angiography results in the evaluation of Glenn shunt and veno–veno collaterals, 100% agreement in Glenn shunt visualization and agreement was 86.2% in the detection of veno–veno collaterals with a perfect agreement (kappa = 1) as regards their proximal connection to superior vena cava (SVC). While TWIST showed lower agreement compared to MSCT angiography results, 87.5% agreement in Glenn shunt visualization and agreement was 68.9% in the detection of veno–veno collaterals with poor agreement (kappa = 0.266) as regards their proximal connection to SVC. Conclusions 3D post-contrast whole heart MRI images have similar results as MSCT angiography in the evaluation of superior cavo-pulmonary anastomosis and can be a good and safer alternative to MSCT angiography.


2021 ◽  
Vol 12 ◽  
Author(s):  
Shengqi Yang ◽  
Ran Li ◽  
Jiliang Chen ◽  
Zhen Li ◽  
Zhangqin Huang ◽  
...  

Ca2+ sparks are the elementary Ca2+ release events in cardiomyocytes, altered properties of which lead to impaired Ca2+ handling and finally contribute to cardiac pathology under various diseases. Despite increasing use of machine-learning algorithms in deciphering the content of biological and medical data, Ca2+ spark images and data are yet to be deeply learnt and analyzed. In the present study, we developed a deep residual convolutional neural network method to detect Ca2+ sparks. Compared to traditional detection methods with arbitrarily defined thresholds to distinguish signals from noises, our new method detected more Ca2+ sparks with lower amplitudes but similar spatiotemporal distributions, thereby indicating that our new algorithm detected many very weak events that are usually omitted when using traditional detection methods. Furthermore, we proposed an event-based logistic regression and binary classification model to classify single cardiomyocytes using Ca2+ spark characteristics, which to date have generally been used only for simple statistical analyses and comparison between normal and diseased groups. Using this new detection algorithm and classification model, we succeeded in distinguishing wild type (WT) vs RyR2-R2474S± cardiomyocytes with 100% accuracy, and vehicle vs isoprenaline-insulted WT cardiomyocytes with 95.6% accuracy. The model can be extended to judge whether a small number of cardiomyocytes (and so the whole heart) are under a specific cardiac disease. Thus, this study provides a novel and powerful approach for the research and application of calcium signaling in cardiac diseases.


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