scholarly journals B-PO01-015 OPTICAL MAPPING OF INTACT RABBIT HEARTS DURING VENTRICULAR TACHYCARDIA REVEALS INCOMPLETE ROTORS WHICH ARE ORGANIZED AROUND PHASE DEFECT LINES INSTEAD OF PHASE SINGULARITIES

Heart Rhythm ◽  
2021 ◽  
Vol 18 (8) ◽  
pp. S56
Author(s):  
Hans Dierckx ◽  
Louise Arno Jan Quan ◽  
Maarten Vanmarcke Nhan Nguyen ◽  
Elena Talkachova
Keyword(s):  
Ventricular Tachycardia ◽  
Optical Mapping ◽  
Phase Singularities ◽  
Intact Rabbit

Optical mapping of late myocardial infarction in rats

2006 ◽  
Vol 290 (3) ◽  
pp. H1298-H1306 ◽  
Author(s):  
William R. Mills ◽  
Niladri Mal ◽  
Farhad Forudi ◽  
Zoran B. Popovic ◽  
Marc S. Penn ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Tachycardia ◽  
High Resolution ◽  
Action Potentials ◽  
Optical Mapping ◽  
Cellular Heterogeneity ◽  
Artery Ligation ◽  
Conduction Abnormalities ◽  
Mapping Techniques ◽  
Whole Heart

Late myocardial infarction (MI) is associated with ventricular arrhythmias and sudden cardiac death. The exact mechanistic relationship between abnormal cellular electrophysiology, conduction abnormalities, and arrhythmogenesis associated with late MI is not completely understood. We report a novel, rapid dye superfusion technique to enable whole heart, high-resolution optical mapping of late MI. Optical mapping of action potentials was performed in normal rats and rats with anterior MI 7 days after left anterior descending artery ligation. Hearts from normal rats exhibited normal action potentials and impulse conduction. With the use of programmed stimulation to assess arrhythmia inducibility, 29% of hearts with late MI had inducible sustained ventricular tachycardia, compared with 0% in normal rats. A causal relationship between the site of infarction, abnormal action potential conduction (i.e., block and slow conduction), and arrhythmogenesis was observed. Optical mapping techniques can be used to measure high-resolution action potentials in a whole heart model of late MI. This experimental model reproduces many of the electrophysiological characteristics (i.e., conduction slowing, block, and ventricular tachycardia) associated with MI in patients. Importantly, the results of this study can enhance our ability to understand the interplay between cellular heterogeneity, conduction abnormalities, and arrhythmogenesis associated with MI.

scholarly journals Rotor Localization and Phase Mapping of Cardiac Excitation Waves Using Deep Neural Networks

2021 ◽  
Vol 12 ◽  
Author(s):  
Jan Lebert ◽  
Namita Ravi ◽  
Flavio H. Fenton ◽  
Jan Christoph
Keyword(s):  
Neural Network ◽  
Neural Networks ◽  
Optical Mapping ◽  
Simulated Data ◽  
Mapping Data ◽  
Phase Singularities ◽  
Rotor Core ◽  
Phase Mapping ◽  
Spatio Temporal ◽  
Mapping Techniques

The analysis of electrical impulse phenomena in cardiac muscle tissue is important for the diagnosis of heart rhythm disorders and other cardiac pathophysiology. Cardiac mapping techniques acquire local temporal measurements and combine them to visualize the spread of electrophysiological wave phenomena across the heart surface. However, low spatial resolution, sparse measurement locations, noise and other artifacts make it challenging to accurately visualize spatio-temporal activity. For instance, electro-anatomical catheter mapping is severely limited by the sparsity of the measurements, and optical mapping is prone to noise and motion artifacts. In the past, several approaches have been proposed to create more reliable maps from noisy or sparse mapping data. Here, we demonstrate that deep learning can be used to compute phase maps and detect phase singularities in optical mapping videos of ventricular fibrillation, as well as in very noisy, low-resolution and extremely sparse simulated data of reentrant wave chaos mimicking catheter mapping data. The self-supervised deep learning approach is fundamentally different from classical phase mapping techniques. Rather than encoding a phase signal from time-series data, a deep neural network instead learns to directly associate phase maps and the positions of phase singularities with short spatio-temporal sequences of electrical data. We tested several neural network architectures, based on a convolutional neural network (CNN) with an encoding and decoding structure, to predict phase maps or rotor core positions either directly or indirectly via the prediction of phase maps and a subsequent classical calculation of phase singularities. Predictions can be performed across different data, with models being trained on one species and then successfully applied to another, or being trained solely on simulated data and then applied to experimental data. Neural networks provide a promising alternative to conventional phase mapping and rotor core localization methods. Future uses may include the analysis of optical mapping studies in basic cardiovascular research, as well as the mapping of atrial fibrillation in the clinical setting.

Optical mapping of the functional reentrant circuit of ventricular tachycardia in acute myocardial infarction

Heart Rhythm ◽  
2004 ◽  
Vol 1 (4) ◽  
pp. 451-459 ◽  
Author(s):  
Tamana Takahashi ◽  
Pascal van Dessel ◽  
John C. Lopshire ◽  
William J. Groh ◽  
John Miller ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ventricular Tachycardia ◽  
Optical Mapping ◽  
Reentrant Circuit

scholarly journals Role of Reduced Sarco-Endoplasmic Reticulum Ca2+-ATPase Function on Sarcoplasmic Reticulum Ca2+ Alternans in the Intact Rabbit Heart

2021 ◽  
Vol 12 ◽  
Author(s):  
Lianguo Wang ◽  
Rachel C. Myles ◽  
I-Ju Lee ◽  
Donald M. Bers ◽  
Crystal M. Ripplinger
Keyword(s):  
Endoplasmic Reticulum ◽  
Sarcoplasmic Reticulum ◽  
Optical Mapping ◽  
Cyclopiazonic Acid ◽  
Rabbit Heart ◽  
Intracellular Ca ◽  
Cardiac Alternans ◽  
Intact Rabbit ◽  
Rapid Ventricular Pacing ◽  
Serca Inhibition

Sarcoplasmic reticulum (SR) Ca2+ cycling is tightly regulated by ryanodine receptor (RyR) Ca2+ release and sarco-endoplasmic reticulum Ca2+-ATPase (SERCA) Ca2+ uptake during each excitation–contraction coupling cycle. We previously showed that RyR refractoriness plays a key role in the onset of SR Ca2+ alternans in the intact rabbit heart, which contributes to arrhythmogenic action potential duration (APD) alternans. Recent studies have also implicated impaired SERCA function, a key feature of heart failure, in cardiac alternans and arrhythmias. However, the relationship between reduced SERCA function and SR Ca2+ alternans is not well understood. Simultaneous optical mapping of transmembrane potential (Vm) and SR Ca2+ was performed in isolated rabbit hearts (n = 10) using the voltage-sensitive dye RH237 and the low-affinity Ca2+ indicator Fluo-5N-AM. Alternans was induced by rapid ventricular pacing. SERCA was inhibited with cyclopiazonic acid (CPA; 1–10 μM). SERCA inhibition (1, 5, and 10 μM of CPA) resulted in dose-dependent slowing of SR Ca2+ reuptake, with the time constant (tau) increasing from 70.8 ± 3.5 ms at baseline to 85.5 ± 6.6, 129.9 ± 20.7, and 271.3 ± 37.6 ms, respectively (p < 0.05 vs. baseline for all doses). At fast pacing frequencies, CPA significantly increased the magnitude of SR Ca2+ and APD alternans, most strongly at 10 μM (pacing cycle length = 220 ms: SR Ca2+ alternans magnitude: 57.1 ± 4.7 vs. 13.4 ± 8.9 AU; APD alternans magnitude 3.8 ± 1.9 vs. 0.2 ± 0.19 AU; p < 0.05 10 μM of CPA vs. baseline for both). SERCA inhibition also promoted the emergence of spatially discordant alternans. Notably, at all CPA doses, alternation of SR Ca2+ release occurred prior to alternation of diastolic SR Ca2+ load as pacing frequency increased. Simultaneous optical mapping of SR Ca2+ and Vm in the intact rabbit heart revealed that SERCA inhibition exacerbates pacing-induced SR Ca2+ and APD alternans magnitude, particularly at fast pacing frequencies. Importantly, SR Ca2+ release alternans always occurred before the onset of SR Ca2+ load alternans. These findings suggest that even in settings of diminished SERCA function, relative refractoriness of RyR Ca2+ release governs the onset of intracellular Ca2+ alternans.

High-Resolution Optical Mapping of Ventricular Tachycardia in Rats with Chronic Myocardial Infarction

2010 ◽  
Vol 33 (6) ◽  
pp. 687-695 ◽  
Author(s):  
CHUNHUA DING ◽  
LIOR GEPSTEIN ◽  
DUY THAI NGUYEN ◽  
EMILY WILSON ◽  
GEORGE HULLEY ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Tachycardia ◽  
High Resolution ◽  
Optical Mapping ◽  
Chronic Myocardial Infarction

Effects of diacetyl monoxime and cytochalasin D on ventricular fibrillation in swine right ventricles

2001 ◽  
Vol 280 (6) ◽  
pp. H2689-H2696 ◽  
Author(s):  
Moon-Hyoung Lee ◽  
Shien-Fong Lin ◽  
Toshihiko Ohara ◽  
Chikaya Omichi ◽  
Yuji Okuyama ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Ventricular Fibrillation ◽  
Action Potential Duration ◽  
Action Potentials ◽  
Optical Mapping ◽  
Cytochalasin D ◽  
Wave Fronts ◽  
Activation Patterns ◽  
Restitution Curve ◽  
Diacetyl Monoxime

Whether or not the excitation-contraction (E-C) uncoupler diacetyl monoxime (DAM) and cytochalacin D (Cyto D) alter the ventricular fibrillation (VF) activation patterns is unclear. We recorded single cell action potentials and performed optical mapping in isolated perfused swine right ventricles (RV) at different concentrations of DAM and Cyto D. Increasing the concentration of DAM results in progressively shortened action potential duration (APD) measured to 90% repolarization, reduced the slope of the APD restitition curve, decreased Kolmogorov-Sinai entropy, and reduced the number of VF wave fronts. In all RVs, 15–20 mmol/l DAM converted VF to ventricular tachycardia (VT). The VF could be reinduced after the DAM was washed out. In comparison, Cyto D (10–40 μmol/l) has no effects on APD restitution curve or the dynamics of VF. The effects of DAM on VF are associated with a reduced number of wave fronts and dynamic complexities in VF. These results are compatible with the restitution hypothesis of VF and suggest that DAM may be unsuitable as an E-C uncoupler for optical mapping studies of VF in the swine RVs.

scholarly journals Genetic Loss of I K1 Causes Adrenergic-Induced Phase 3 Early Afterdepolariz ations and Polymorphic and Bidirectional Ventricular Tachycardia

2020 ◽  
Vol 13 (9) ◽  
Author(s):  
Louise Reilly ◽  
Francisco J. Alvarado ◽  
Di Lang ◽  
Sara Abozeid ◽  
Hannah Van Ert ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Action Potential ◽  
Cardiac Function ◽  
Ventricular Myocytes ◽  
Optical Mapping ◽  
Adrenergic Stimulation ◽  
Phase 3 ◽  
Early Afterdepolarizations ◽  
Whole Heart

Background: Arrhythmia syndromes associated with KCNJ2 mutations have been described clinically; however, little is known of the underlying arrhythmia mechanism. We create the first patient inspired KCNJ2 transgenic mouse and study effects of this mutation on cardiac function, I K1 , and Ca 2+ handling, to determine the underlying cellular arrhythmic pathogenesis. Methods: A cardiac-specific KCNJ2 -R67Q mouse was generated and bred for heterozygosity (R67Q +/− ). Echocardiography was performed at rest, under anesthesia. In vivo ECG recording and whole heart optical mapping of intact hearts was performed before and after adrenergic stimulation in wild-type (WT) littermate controls and R67Q +/− mice. I K1 measurements, action potential characterization, and intracellular Ca 2+ imaging from isolated ventricular myocytes at baseline and after adrenergic stimulation were performed in WT and R67Q +/− mice. Results: R67Q +/− mice (n=17) showed normal cardiac function, structure, and baseline electrical activity compared with WT (n=10). Following epinephrine and caffeine, only the R67Q +/− mice had bidirectional ventricular tachycardia, ventricular tachycardia, frequent ventricular ectopy, and/or bigeminy and optical mapping demonstrated high prevalence of spontaneous and sustained ventricular arrhythmia. Both R67Q +/− (n=8) and WT myocytes (n=9) demonstrated typical n-shaped I K1 IV relationship; however, following isoproterenol, max outward I K1 increased by ≈20% in WT but decreased by ≈24% in R67Q +/− ( P <0.01). R67Q +/− myocytes (n=5) demonstrated prolonged action potential duration at 90% repolarization and after 10 nmol/L isoproterenol compared with WT (n=7; P <0.05). Ca 2+ transient amplitude, 50% decay rate, and sarcoplasmic reticulum Ca 2+ content were not different between WT (n=18) and R67Q +/− (n=16) myocytes. R67Q +/− myocytes (n=10) under adrenergic stimulation showed frequent spontaneous development of early afterdepolarizations that occurred at phase 3 of action potential repolarization. Conclusions: KCNJ2 mutation R67Q +/− causes adrenergic-dependent loss of I K1 during terminal repolarization and vulnerability to phase 3 early afterdepolarizations. This model clarifies a heretofore unknown arrhythmia mechanism and extends our understanding of treatment implications for patients with KCNJ2 mutation.

Abstract 215: Systemic Inflammation Exacerbates Electrophysiological Remodeling and Arrhythmia Following Myocardial Infarction

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Nicole De Jesus ◽  
Lianguo Wang ◽  
Crystal M Ripplinger
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Tachycardia ◽  
Systemic Inflammation ◽  
Transmembrane Potential ◽  
Optical Mapping ◽  
Fluorescent Sensor ◽  
Prolonged Action ◽  
Fluorescence Reflectance Imaging ◽  
Inflammatory Macrophages ◽  
Perfused Hearts

Introduction: Inflammatory macrophages infiltrate the heart following myocardial infarction (MI) and secrete proteases and cytokines that may contribute to adverse electrophysiological remodeling. Atherosclerosis, the leading cause of MI, is associated with elevated systemic inflammation. Using a novel combination of optical mapping and molecular imaging, we sought to determine if systemic inflammation exacerbates electrophysiological remodeling and arrhythmogenesis. Methods: A protease activatable fluorescent sensor (Prosense680) was injected I.V. 4 days post MI in mice. Optical mapping of transmembrane potential was performed 5 days post MI on Langendorff-perfused hearts to assess electrophysiology. Fluorescence reflectance imaging of Prosense680 was then performed to visualize and quantify inflammatory protease activity. Lipopolysaccharide (LPS:10 μ g/day, n=6) was injected I.P. to promote systemic inflammation or saline as control (SAL, n=7). Results: Inflammation levels were greater in MI+LPS vs MI+SAL hearts (5.626±1.5 vs 1.73±0.25 A.U., p<0.02) and negligible in sham-operated hearts (SH, n=4). MI+LPS hearts had prolonged action potential (AP) duration vs MI+SAL vs SH (62±4.5 vs 56±1.8 vs 45±3.7 ms, p<0.05) and increased AP rise time (5.5±0.5 vs 4.2±0.2 vs 2.9±0.3 ms, p<0.05). A single premature pacing stimulus induced ventricular tachycardia in 67%(4 of 6) of MI+LPS vs 15%(1 of 7) MI+SAL vs 0% (0 of 4) SH, p<0.02. Conclusions: Elevated post-MI inflammation may contribute to electrophysiological remodeling and arrhythmias. These findings have important implications for the etiology of post-MI arrhythmias in humans with systemic inflammation.

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