Kedar Aras
University of Utah
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Kedar Aras.
Journal of Electrocardiology | 2016
Kedar Aras; Brett Burton; Darrell Swenson; Robert S. MacLeod
INTRODUCTION Myocardial ischemia is a pathological condition initiated by supply and demand imbalance of the blood to the heart. Previous studies suggest that ischemia originates in the subendocardium, i.e., that nontransmural ischemia is limited to the subendocardium. By contrast, we hypothesized that acute myocardial ischemia is not limited to the subendocardium and sought to document its spatial distribution in an animal preparation. The goal of these experiments was to investigate the spatial organization of ischemia and its relationship to the resulting shifts in ST segment potentials during short episodes of acute ischemia. METHODS We conducted acute ischemia studies in open-chest canines (N=19) and swines (N=10), which entailed creating carefully controlled ischemia using demand, supply or complete occlusion ischemia protocols and recording intramyocardial and epicardial potentials. Elevation of the potentials at 40% of the ST segment between the J-point and the peak of the T-wave (ST40%) provided the metric for local ischemia. The threshold for ischemic ST segment elevations was defined as two standard deviations away from the baseline values. RESULTS The relative frequency of occurrence of acute ischemia was higher in the subendocardium (78% for canines and 94% for swines) and the mid-wall (87% for canines and 97% for swines) in comparison with the subepicardium (30% for canines and 22% for swines). In addition, acute ischemia was seen arising throughout the myocardium (distributed pattern) in 87% of the canine and 94% of the swine episodes. Alternately, acute ischemia was seen originating only in the subendocardium (subendocardial pattern) in 13% of the canine episodes and 6% of the swine episodes (p<0.05). CONCLUSIONS Our findings suggest that the spatial distribution of acute ischemia is a complex phenomenon arising throughout the myocardial wall and is not limited to the subendocardium.
World Congress on Medical Physics and Biomedical Engineering: Image Processing, Biosignal Processing, Modelling and Simulation, Biomechanics | 2009
Darrell Swenson; Jeroen G. Stinstra; Brett Burton; Kedar Aras; L. J. Healy; Robert S. MacLeod
Current computational models of acute ischemia are deficient because of their inability to be validated against experimental data and their lack of geometric realism. Past models of ischemia have been based on geometric primitives or hearts for which no electrical measurements exist. One consequence is that it is necessary to make modeling assumptions that are not supported by measurements or direct validation with experiments. Based on our subject specific simulations and measurements, we hypothesize that assumptions about the nature and scale of the border zone play a significant role in determining the cardiac potential distributions from ischemic sources of injury current. Geometrically accurate models were created from Magnetic Resonance Imaging (MRI) and Diffuser Tensor Imaging (DTI) after an in situ canine ischemia experiment. The ischemic zone was defined based on transmural electrode readings and was used in a static bidomain simulation representing a time point during the ST segment. Varying the width of the border zone in the simulations changed the magnitude and distribution of epicardial depressions and elevations. We also found that a border zone with linear variation of potential from healthy to ischemic regions was not adequate to simulate measured potentials. A more sophisticated border zone that included an explicit region of partial ischemia was necessary to simulate the field gradients seen in experimental data.
Journal of Electrocardiology | 2013
Kedar Aras; Brett Burton; Darrell Swenson; Robert S. MacLeod
INTRODUCTION We hypothesize that electrocardiographic measurements from the intramyocardial space contain more sensitive markers of ischemia than those detectable on the epicardium. The goal of this study was to evaluate different electrical markers for their potential to detect the earliest phases of acute myocardial ischemia. METHODS We conducted acute ischemia studies in open chest animal, by creating finely controlled demand or supply ischemic episodes and recording intramyocardial and epicardial potentials. RESULTS Under the conditions of mild perfusion deficit, acute ischemia induced changes in the T wave that were larger and could be detected earlier on the epicardial surface than ST-segment changes. CONCLUSIONS Our findings indicate that in the setting of very acute ischemia, epicardial T waves have higher sensitivity to mild degrees of acute ischemia than epicardial ST potentials. These results suggest that changes in the T wave shape may augment shifts in ST segments to improve ECG based localization of ischemia.
Journal of Social Structure | 2018
Anton Rodenhauser; Wilson Good; Brian Zenger; Jess D. Tate; Kedar Aras; Brett Burton; Robert S. MacLeod
PFEIFER was specifically designed to process electrocardiographic recordings from electrodes placed on or around the heart or on the body surface. Specific steps included in PFEIFER allow the user to remove some forms of noise, correct for signal drift, and mark specific instants or intervals in time (fiducialize) within all of the time sampled channels. PFEIFER includes many unique features that allow the user to process electrical signals in a consistent and time efficient manner, with additional options for advanced user configurations and input. PFEIFER is structured as a consolidated framework that provides many standard processing pipelines but also has flexibility to allow the user to customize many of the steps. PFEIFER allows the user to import time aligned cardiac electrical signals, semi-automatically determine fiducial markings from those signals, and perform computational tasks that prepare the signals for subsequent display and analysis.
Scientific Reports | 2018
Christopher Gloschat; Kedar Aras; Shubham Gupta; N. Rokhaya Faye; Hanyu Zhang; Roman A. Syunyaev; Roman Pryamonosov; Jack M. Rogers; Matthew W. Kay; Igor R. Efimov
Fluorescence optical imaging techniques have revolutionized the field of cardiac electrophysiology and advanced our understanding of complex electrical activities such as arrhythmias. However, traditional monocular optical mapping systems, despite having high spatial resolution, are restricted to a two-dimensional (2D) field of view. Consequently, tracking complex three-dimensional (3D) electrical waves such as during ventricular fibrillation is challenging as the waves rapidly move in and out of the field of view. This problem has been solved by panoramic imaging which uses multiple cameras to measure the electrical activity from the entire epicardial surface. However, the diverse engineering skill set and substantial resource cost required to design and implement this solution have made it largely inaccessible to the biomedical research community at large. To address this barrier to entry, we present an open source toolkit for building panoramic optical mapping systems which includes the 3D printing of perfusion and imaging hardware, as well as software for data processing and analysis. In this paper, we describe the toolkit and demonstrate it on different mammalian hearts: mouse, rat, and rabbit.
Journal of Electrocardiology | 2018
Brett Burton; Kedar Aras; Wilson Good; Jess D. Tate; Brian Zenger; Robert S. MacLeod
BACKGROUND Computational models of myocardial ischemia often use oversimplified ischemic source representations to simulate epicardial potentials. The purpose of this study was to explore the influence of biophysically justified, subject-specific ischemic zone representations on epicardial potentials. METHODS We developed and implemented an image-based simulation pipeline, using intramural recordings from a canine experimental model to define subject-specific ischemic regions within the heart. Static epicardial potential distributions, reflective of ST segment deviations, were simulated and validated against measured epicardial recordings. RESULTS Simulated epicardial potential distributions showed strong statistical correlation and visual agreement with measured epicardial potentials. Additionally, we identified and described in what way border zone parameters influence epicardial potential distributions during the ST segment. CONCLUSION From image-based simulations of myocardial ischemia, we generated subject-specific ischemic sources that accurately replicated epicardial potential distributions. Such models are essential in understanding the underlying mechanisms of the bioelectric fields that arise during ischemia and are the basis for more sophisticated simulations of body surface ECGs.
Annals of Biomedical Engineering | 2018
Brett Burton; Kedar Aras; Wilson Good; Jess D. Tate; Brian Zenger; Robert S. MacLeod
The biophysical basis for electrocardiographic evaluation of myocardial ischemia stems from the notion that ischemic tissues develop, with relative uniformity, along the endocardial aspects of the heart. These injured regions of subendocardial tissue give rise to intramural currents that lead to ST segment deflections within electrocardiogram (ECG) recordings. The concept of subendocardial ischemic regions is often used in clinical practice, providing a simple and intuitive description of ischemic injury; however, such a model grossly oversimplifies the presentation of ischemic disease—inadvertently leading to errors in ECG-based diagnoses. Furthermore, recent experimental studies have brought into question the subendocardial ischemia paradigm suggesting instead a more distributed pattern of tissue injury. These findings come from experiments and so have both the impact and the limitations of measurements from living organisms. Computer models have often been employed to overcome the constraints of experimental approaches and have a robust history in cardiac simulation. To this end, we have developed a computational simulation framework aimed at elucidating the effects of ischemia on measurable cardiac potentials. To validate our framework, we simulated, visualized, and analyzed 226 experimentally derived acute myocardial ischemic events. Simulation outcomes agreed both qualitatively (feature comparison) and quantitatively (correlation, average error, and significance) with experimentally obtained epicardial measurements, particularly under conditions of elevated ischemic stress. Our simulation framework introduces a novel approach to incorporating subject-specific, geometric models and experimental results that are highly resolved in space and time into computational models. We propose this framework as a means to advance the understanding of the underlying mechanisms of ischemic disease while simultaneously putting in place the computational infrastructure necessary to study and improve ischemia models aimed at reducing diagnostic errors in the clinic.
Circulation-arrhythmia and Electrophysiology | 2017
Kedar Aras; Matthew W. Kay; Igor R. Efimov
See Article by Panitchob et al > As to the fundamental mechanisms of fibrillation we have plenty of theories, but none is universally accepted… we may note in passing that they all center around two ideas … (a) that the impulses arise from centers or pacemakers, or (b) that the condition is caused by re-entry of impulses and the formation of circles of excitation. Each of these views, again, has two groups of exponents … (a) those who believe that a single focus, or excitation ring, occurs, and (b) those who favor the idea that multiple foci, or numerous circus rings, are developed. > > —Carl J. Wiggers, 19401 Ventricular fibrillation (VF) was likely recognized as early as 3500 BCE when the Ebers Papyrus2 described key features of fibrillation as follows: > “If the heart trembles, has little power and sinks, the disease is advancing and death is near.” The modern scientific effort to understand fibrillation did not begin until 1543, when Vesalius3 described worm-like movements in animal hearts during dissection just before they died. Erichsen4 in 1842 documented tumultuous, tremulous, and irregular behavior of ventricles consequent to coronary ligation. Hoffa and Ludwig5 first recorded VF using a kymograph (mechanical wave recorder) in 1850 (Figure, left). Interestingly, Hoffa, who was Ludwig’s pupil at the time, meant to stimulate neurons but accidentally stimulated the myocardium. They showed that irregular contractions of the ventricles could be induced by faradization (electric stimulation) and resulted in cardiac arrest that could not be checked by vagal stimulation. These studies of autonomic control of the heart suggested a neurogenic VF mechanism. Figure. The first recordings of ventricular fibrillation were acquired by Hoffa and Ludwig using a …
Journal of Electrocardiology | 2015
Kedar Aras; Wilson Good; Jess D. Tate; Brett Burton; Dana H. Brooks; Jaume Coll-Font; Olaf Doessel; Walther H. W. Schulze; Danila Potyagaylo; Linwei Wang; Peter M. van Dam; Robert S. MacLeod
computing in cardiology conference | 2014
Jess D. Tate; Thomas Pilcher; Kedar Aras; Brett Burton; Robert S. MacLeod