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Interative Left Atrium Model

Table of Contents

Selected Pics

Micro Reentry ------------------------ Macro Reentry

Spiral Wave Reentry --------------- AFib Like Action

Reentry on Topologically Realistic Model

Project Aims

Our project has several key objectives. Firstly, we aim to utilize N-body techniques to develop an interactive model of the left atrium. This model will allow users to manipulate various parameters in real-time, facilitating the induction and observation of common arrhythmias.

Secondly, we seek to create a training and study tool for electrophysiologists, researchers, and medical students. By accurately simulating left atrial arrhythmias and their treatment using simulated ablations, the model will serve as a valuable educational resource, enhancing understanding and skill development in this critical medical field.

Additionally, the project aims to advance research in electrophysiology by providing a platform for exploring novel treatment strategies and studying arrhythmia mechanisms. This could lead to new insights and innovations in the field, ultimately benefiting patients with cardiac arrhythmias.

In summary, the project's objectives include developing a cutting-edge model for arrhythmia simulation, providing an advanced training tool for medical professionals, and advancing research in electrophysiology.

Background

Heart disease and strokes rank among the leading causes of death globally [1,2]. Supraventricular Tachycardia (SVT) significantly contributes to strokes, heart failure, and, in some cases, acute myocardial infarction [3-5]. Therefore, reducing SVT occurrence is crucial in our efforts to promote healthier lives free of cardiovascular diseases and strokes.

SVT encompasses all cardiac arrhythmias originating above the ventricles. This abnormal heartbeat can disrupt the natural synchronization between the atria and ventricles, causing blood to stagnate in the left atrium (LA) and forming potentially lethal blood clots known as mural thrombi [6]. These clots can dislodge and travel to the brain or coronary arteries, leading to a stroke or heart attack, as seen in individuals with atrial fibrillation (AF) who face a five-fold increased stroke risk [7].

Normally, the sinus node acts as the heart's pacemaker, generating an electrical impulse that dictates the heart's rhythm. Ectopic electrical impulses can disrupt this rhythm, causing the atria to flutter or beat out of sync with the ventricles [8].

While SVT can often be controlled with medication and lifestyle changes, some drugs can be challenging to tolerate, and certain effective medications can have hepatotoxic effects [9]. Catheter ablation, though more invasive, has proven to be the most efficacious and safest method for treating recurring SVT [10-13].

Advancements in radiofrequency (RF) catheter ablation and electro-anatomical mapping have enabled doctors to perform procedures on beating hearts that were once thought impossible [14,15]. However, much remains unknown about the causes of heart arrhythmias and how to treat them using RF catheter ablation [16]. A computer model of the LA, such as the one we have developed, can assist doctors, researchers, and medical students in rapidly and inexpensively testing ideas and observing outcomes.

The LA was chosen for modeling due to its role in complex arrhythmias [17-20]. Our model simulates both electrical and mechanical activity, allowing users to adjust parameters at the muscle level and introduce ectopic events. These tools enable users to induce arrhythmias in the LA that can be eliminated through simulated ablations, all in an interactive simulation setting.

Videos

Video Micro-Reenter: https://youtu.be/llIGgZSiTnE
Video Macro-Reenter: https://youtu.be/3m_7lrOe2cw
Video Spiral Wave-Reentry: https://youtu.be/c-ID603Vm9Q
Video AFib-Like: https://youtu.be/GG6Q7uG8OhQ
Video Realistic Topology: https://www.youtube.com/watch?v=y_ju9k7Y6So

Installation

Hardware Requirements:

  • This simulation requires a CUDA-enabled GPU from Nvidia. Click here for a list of GPUs.
*Note: These are guidelines, not rules CPU GPU RAM
Minimum: AMD/Intel Six-Core Processor Any CUDA-Enabled GPU 16GB DDR4
Recommended: AMD/Intel Eight-Core Processor RTX 3090/Quadro A6000 32GB DDR5

Software Requirements:

Disclosure: This simulation only works on Linux-based distros currently. All development and testing was done in Ubuntu 20.04/22.04

This Repository contains the following:

Linux (Ubuntu/Debian)

Install Nvidia CUDA Toolkit:

sudo apt update
sudo apt install nvidia-cuda-toolkit

Install Mesa Utils:

sudo apt update
sudo apt install mesa-utils

Install gcc and nvcc:

sudo apt update
sudo apt install build-essential

Install GLFW:

sudo apt update
sudo apt install libglfw3-dev libglu1-mesa-dev freeglut3-dev mesa-common-dev

Install X11-related libraries:

sudo apt update
sudo apt install libxinerama-dev libxcursor-dev libxi-dev

Install gedit:

sudo apt update
sudo apt install gedit

Install ffmpeg:

sudo apt update
sudo apt install ffmpeg

Building and Running

Building (Note: this must be done after every code change)

Navigate to the cloned folder and run the following command to build and compile the simulation:

./compile

If it says that you do not have permissions, run the following command and try again.

chmod +x compile

Running

After compiling, run the simulation:

./run

Simulation Setup Files

There are three simulation setup files. 
These files can be adjusted by the user before running a simulation to set up the basic framework of the run.
All units used in the simulation are as follows:
Length is in millimeters (mm)
Time is in milliseconds (ms)
Mass is in grams (g)

BasicSimulationSetup

This file is read at startup and tells the program to either resume the simulation from a previous run or create a new run from the 
frameworks in the nodes and muscles files. It also reads in some basic visualization parameters.

IntermediateSimulationSetup

This file is read at startup and sets base simulation settings, such as beat rate and node and muscle characteristics. 
It also reads in several visualization parameters.  

AdvancedSimulationSetup

This file is read at startup and sets the basic physics of the simulation.

Simulation Runtime Controls

Our model includes a Graphical User Interface (GUI) to allow the user to dynamically adjust various attributes for both the simulation and various characteristics of the left atrium.

Simulation Controls

Primary controls for managing the simulation execution and visual output.

Control Description
Contraction Toggle Enables/disables visual contraction of heart tissue
Draw Front Half Only Renders only the closest half of the model for clarity/performance
Show Nodes Toggle to draw front half/all/no nodes
Record Video Starts/stops recording simulation video
Screenshot Captures still image of current view
Simulation Speed Determines the amount of calculations in between render calls

Mouse Functions

Interactive modes for mouse actions on 3D heart surface.

Mode Description
Mouse Off Turns all mouse functions off
Ablate Mode Block (ablate) the signal from traveling through selected nodes
Ectopic Beat Sets up a recurrent timed pulse (beat) from the selected node
Ectopic Trigger Initiates a single pulse from the selected node
Adjust Area Select/modify muscle characteristics for a group of muscles
Adjust Line Select/modify muscle characteristics for a single muscle
Identify Node Identify the number that corresponds to a specific node

Heartbeat Controls

Panel for management of cardiac rhythms

Control Description
Beat Period (ms) Sets baseline interval between heartbeats
Ectopic Beats View/Adjust current ectopic beats

Utilities

Tools for saving/loading simulation states.

Utility Description
Save Settings Exports simulation parameters to a file for later use
Find Nodes Finds the ID of the top-most and front-most node
Save State Saves complete simulation state for short-term use
Load State Restores simulation from saved state

Changelog

Refer to the changelog for details.

License

  • This code is protected by the MIT License and is free to use for personal and academic use.

Contributing Authors

  • Leah Rogers
  • Mason Bane
  • Kyla Moore
  • Gavin McIntosh
  • Avery Campbell
  • Melanie Little
  • Derek Hopkins
  • Brandon Wyatt
  • Madhur Wyatt
  • Charles Puelz (CoPI)
  • Bryant Wyatt (PI)

Funding Sources

This research was supported by the NVIDIA cooperation’s Applied Research Accelerator Program. Student support was provided by Tarleton State University’s Presidential Excellence in Research Scholars and the Bill and Winnie Wyatt Foundation.

Acknowledgements

We would like to thank Tarleton State University’s Mathematics Department for use of their High-Performance Computing lab for the duration of this project.

References

[1] World Health Organization. (12/9/2020). The top 10 causes of death. World Health Organization. https://www.who.int/news-room/fact-sheets/detail/the top-10-causes-of-death
[2] Virani SS, Alonso A, Aparicio HJ, Benjamin EJ, Bittencourt MS, Callaway CW, Carson AP, Chamberlain AM, Cheng S, Delling FN, Elkind MSV, Evenson KR, Ferguson JF, Gupta DK, Khan SS, Kissela BM, Knutson KL, Lee CD, Lewis TT, Liu J, Loop MS, Lutsey PL, Ma J, Mackey J, Martin SS, Matchar DB, Mussolino ME, Navaneethan SD, Perak AM, Roth GA, Samad Z, Satou GM, Schroeder EB, Shah SH, Shay CM, Stokes A, VanWagner LB, Wang NY, Tsao CW; American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart Disease and Stroke Statistics-2021 Update: A Report From the American Heart Association. Circulation. 2021 Feb 23;143(8):e254-e743. doi: 10.1161/CIR.0000000000000950. Epub 2021 Jan 27. PMID: 33501848.
[3] Brundel BJJM, Ai X, Hills MT, Kuipers MF, Lip GYH, de Groot NMS. Atrial fibrillation. Nature Reviews Disease Primers. 2022;8(1):21–21.
[4] Staerk L, Sherer JA, Ko D, Benjamin EJ, Helm RH. Atrial Fibrillation. Circulation Research. 2017;120(9):1501–1517.
[5] Pellman J, Sheikh F. Atrial fibrillation: mechanisms, therapeutics, and future directions. Comprehensive Physiology. 2015.
[6] Beigel R, Wunderlich NC, Ho SY, Arsanjani R, Siegel RJ. The left atrial appendage: anatomy, function, and noninvasive evaluation. JACC Cardiovasc Imaging. 2014 Dec;7(12):1251-65. doi: 10.1016/j.jcmg.2014.08.009. PMID: 25496544.
[7] Singleton MJ, Imtiaz-Ahmad M, Kamel H, O'Neal WT, Judd SE, Howard VJ, Howard G, Soliman EZ, Bhave PD. Association of Atrial Fibrillation Without Cardiovascular Comorbidities and Stroke Risk: From the REGARDS Study. J Am Heart Assoc. 2020 Jun 16;9(12):e016380. doi: 10.1161/JAHA.120.016380. Epub 2020 Jun 4. PMID: 32495723; PMCID: PMC7429041.
[8] Antzelevitch C, Burashnikov A. Overview of Basic Mechanisms of Cardiac Arrhythmia. 2011.
[9] Long MT, Ko D, Arnold LM, Trinquart L, Sherer JA, Keppel SS, Benjamin EJ, Helm RH. Gastrointestinal and liver diseases and atrial fibrillation: a review of the literature. Therap Adv Gastroenterol. 2019 Apr 2;12:1756284819832237. doi: 10.1177/1756284819832237. PMID: 30984290; PMCID: PMC6448121.
[10] Carlo P, Giuseppe A, Simone S, Filippo G, Gabriele V, Simone G, Gabriele P, Patrizio M, Nicoleta S, Isabelle G, Andreina S, Laura L, Nicola P, Andrea R, Francesco M, et al. A Randomized Trial of Circumferential Pulmonary Vein Ablation Versus Antiarrhythmic Drug Therapy in Paroxysmal Atrial Fibrillation. Journal of the American College of Cardiology. 2006;48(11):2340–2347.
[11] Charitakis E, Metelli S, Karlsson LO, Antoniadis AP, Rizas KD, Liuba I, Almroth H, Hassel Jönsson A, Schwieler J, Tsartsalis D, Sideris S, Dragioti E, Fragakis N, Chaimani A. Comparing efficacy and safety in catheter ablation strategies for atrial fibrillation: a network meta-analysis. BMC Medicine. 2022;20(1):193–193.
[12] Cheng E, Liu C, Yeo I, Markowitz S, George T, Ip J, Kim LK, Lerman BB. Risk of Mortality Following Catheter Ablation of Atrial Fibrillation. Journal of the American College of Cardiology. 2019;74(18):2254–2264.
[13] Mujović N, Marinković M, Lenarczyk R, Tilz R, Potpara TS. Catheter Ablation of Atrial Fibrillation: An Overview for Clinicians. Advances in Therapy. 2017;34(8):1897–1917.
[14] Cappato R, Calkins H, Chen S-A, Davies W, Iesaka Y, Kalman J, Kim Y-H, Klein G, Natale A, Packer D, Skanes A, Ambrogi F, Biganzoli E. Updated Worldwide Survey on the Methods, Efficacy, and Safety of Catheter Ablation for Human Atrial Fibrillation. Circulation: Arrhythmia and Electrophysiology. 2010;3(1):32–38.
[15] Ganesan AN, Shipp NJ, Brooks AG, Kuklik P, Lau DH, Lim HS, Sullivan T, Roberts-Thomson KC, Sanders P. Long-term Outcomes of Catheter Ablation of Atrial Fibrillation: A Systematic Review and Meta-analysis. Journal of the American Heart Association. 2013;2(2).
[16] Quah JX, Dharmaprani D, Lahiri A, Tiver K, Ganesan AN. Reconceptualising Atrial Fibrillation Using Renewal Theory: A Novel Approach to the Assessment of Atrial Fibrillation Dynamics. Arrhythmia & Electrophysiology Review 2021;10(2):77–84. 2021.
[17] Markides V, Schilling RJ. Atrial fibrillation: classification, pathophysiology, mechanisms and drug treatment. Heart. 2003 Aug;89(8):939-43. doi: 10.1136/heart.89.8.939. PMID: 12860883; PMCID: PMC1767799.
[18] Wyndham CRC. Atrial Fibrillation: The Most Common Arrhythmia. Texas Heart Institute Journal. 2000;27(3):257–257.
[19] Cheniti G, Vlachos K, Pambrun T, Hooks D, Frontera A, Takigawa M, Bourier F, Kitamura T, Lam A, Martin C, Dumas-Pommier C, Puyo S, Pillois X, Duchateau J, Klotz N, et al. Atrial Fibrillation Mechanisms and Implications for Catheter Ablation. Frontiers in Physiology. 2018;9.
[20] Gussak G, Pfenniger A, Wren L, Gilani M, Zhang W, Yoo S, Johnson DA, Burrell A, Benefield B, Knight G, Knight BP, Passman R, Goldberger JJ, Aistrup G, Wasserstrom JA, Shiferaw Y, Arora R. Region-specific parasympathetic nerve remodeling in the left atrium contributes to creation of a vulnerable substrate for atrial fibrillation. JCI Insight. 2019 Oct 17;4(20):e130532. doi: 10.1172/jci.insight.130532. PMID: 31503549; PMCID: PMC6824299.

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