Ionic mechanisms of ST segment elevation in electrocardiogram during acute myocardial infarction

Figures

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  Fig. 1. Heart and torso meshes. a Left: heart meshes with the conduction system in the right anterior oblique (RAO) and left anterior oblique (LAO) views. Right: torso mesh. b Effects of hyperkalemia, acidosis, and adenosine triphosphate (ATP) depletion on sodium (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$I_{\text{Na}}$$\end{document}INa), L-type calcium (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$I_{{{\text{Ca}},{\text{L}}}}$$\end{document}ICa,L), rapid delayed rectifier potassium (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$I_{\text{Kr}}$$\end{document}IKr), slow delayed rectifier potassium (\documentclass[12pt]{minimal}…

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  Fig. 2. Electrophysiology under normal condition and subendocardial ischemia. a Cellular electrophysiology: Action potentials (AP) and major ionic currents of the endocardial (endo), mid-myocardial (M), and epicardial (epi) cells. b Time-lapse images showing propagation of excitation in the heart (Excitation), short axis views of the potential distributions in the intracellular space and extracellular space, and the body surface potential map. Numbers indicate the time after the onset of excitation in ms. RV, right ventricle; LV, left ventricle. c 12-lead electrocardiogram. d Cellular electrophysiology under subendocardial ischemia: AP and major ionic currents of the endo, M, and epi cells. e Short axis views of the potential distributions in the intracellular and extracellular spaces during diastole (0 ms) and systole (150 ms) under subendocardial ischemia. Electrical bilayers and their solid angles at the overlying electrodes are shown in the schematics (right column). RV: right ventricle; LV: left ventricle. f 12-lead electrocardiogram. INa, sodium current; IKr, rapid delayed rectifier potassium current; IKs, slow delayed rectifier potassium current; ICaL, L-type calcium current;…

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  Fig. 3. Effects of transmural hyperkalemia and adenosine triphosphate (ATP) depletion on the electrocardiogram (ECG). a Simulated V2 lead ECGs under various concentrations of ATP and potassium are shown. ECGs with similar morphologies are grouped with different colors (mild: light blue; moderate: green; severe: light brown; arrhythmia: dark brown). b 12-lead ECGs of representative cases are shown. Conditions were selected from (a) for normal (black rectangle), mild ischemia (blue rectangle), moderate ischemia (green rectangle), and severe ischemia (red rectangle)

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  Fig. 4. Mechanisms of ST–T changes under ischemic conditions. a The sodium current (INa), L-type calcium current (ICaL), rapid delayed rectifier potassium current (IKr), adenosine triphosphate (ATP)-sensitive potassium current (IKATP), and action potential (AP) are shown under mild, moderate, and severe acute ischemia. During chronic ischemia, cellular activities were completely abolished. In each panel, data from the endocardial region are shown by a black line, the mid-myocardial region by a red line, and the epicardial region by a blue line. b The potential distributions in the intracellular (top row) and extracellular (second row) spaces (at the timing indicated by the blue dot in the below electrocardiogram [ECG]) are shown for mild, moderate, and severe ischemia in the acute and chronic phases. The electrical bilayers and their solid angles at the overlying electrodes are shown in the schematic (third row). The bottom panels show the ECGs (V3 lead) under each condition. The ECG under mild ischemia is compared with the normal ECG (red line). Numbers at the bottom indicate the time after the onset of ventricular activation in milliseconds

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  Fig. 5. Ventricular arrhythmia during transmural ischemia. a V3 lead electrocardiogram (ECG). b Time-lapse images of ventricular activation viewed from the top. The numbers indicate the time after onset in ms. Inset: schematic presentation of the reentrant circuit. Excitation transmitted from the His–Purkinje system (red lines) propagates rapidly in the normal myocardium (green arrow), propagates slowly in the ischemic region (light brown; thin blue arrow), and finally back-propagates to the His–Purkinje system. PMJ: Purkinje–muscle junction

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  Fig. 6. Magnitude of ST elevation and the lead position. a Electrocardiogram of the antero-lateral myocardial infarction. b The area of infarction in the right anterior oblique (RAO) and left anterior oblique (LAO) views. The area of infarction was extended to the lateral wall. The red areas indicate the boundary between the ischemic and non-ischemic myocardium. c Boundaries between the normal and infarcted area (indicated in red) viewed from the V1, V4, and V6 leads. In each panel, the schematic representation of the solid angle is shown on the right side. Non-ischemic areas are indicated by red stripes. Numbers indicate solid angles for the ischemic boundaries