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.

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

Abstract MP164: Electrophysiologic Conservation of Epicardial Conduction Dynamics After Myocardial Infarction in Newborn Piglets

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Hanjay Wang ◽  
Terrence Pong ◽  
Haley Lucian ◽  
Joy Aparicio-Valenzuela ◽  
Yuko Tada ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
High Resolution ◽  
Electrical Conduction ◽  
Conduction Block ◽  
Cardiac Regeneration ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Newborn Piglets ◽  
High Resolution Mapping ◽  
Resolution Mapping

Introduction: Newborn piglets reportedly exhibit natural heart regeneration after myocardial infarction (MI). However, the electrophysiologic properties of this regenerated muscle have not been examined. We hypothesized that epicardial electrical conduction is preserved after MI in newborn piglets. Methods: Yorkshire-Landrace piglets underwent left anterior descending coronary artery ligation on postnatal day 1 (P1, n=4) or postnatal day 7 (P7, n=7), infarcting the anteroseptal left ventricle through which the Purkinje conduction system passes. After 7 weeks, cardiac magnetic resonance imaging (MRI) was performed with late gadolinium enhancement for fibrosis analysis. Epicardial conduction mapping was performed using custom 3D-printed, 256-channel high-resolution mapping arrays (Fig 1A). Age- and weight-matched healthy pigs served as controls (n=7). Data are expressed as mean±SD. Results: MRI analysis revealed significant differences between the control, P1, and P7 groups in ejection fraction (47.6±3.1% vs 37.6±3.3% vs 30.2±6.6%, p<0.001, Fig 1B) and the degree of transmural anteroseptal LV scar (0.0±0.0% vs 9.1±5.4% vs 15.4±4.2%, p<0.001), respectively. Evidence of infarcted myocardium was identified with high-resolution mapping in the P1 and P7 piglets (black arrows, Fig 1C-F). Epicardial electrical conduction was preserved in control and all P1 pigs (Figs 1C-D), whereas variable conduction block or aberrant propagation were observed in all P7 pigs (Fig 1E-F, p=0.001). Conclusion: P1 piglets exhibited incomplete natural cardiac regeneration after MI but nevertheless demonstrated electrophysiologic conservation of epicardial conduction dynamics.

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

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.

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