1992 Fiscal Year Final Research Report Summary
Computer simulation of post-ischemic T wave inversion
| Project/Area Number |
02807091
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Division of Cardiology, Showa University Fujigaoka Hospital |
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Principal Investigator |
TSUTSUMI Takeshi Showa Univ.Fujihaoka Hosp. Div. of Cardiol, Instructor, 医学部, 講師 (10119232)
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| Co-Investigator(Kenkyū-buntansha) |
OKAMOTO Yoshio Chiba Technology of Institute, Associate Prof., 電気工学科, 助教授 (20152358)
SEKIYA Soichiro Showa Univ.Fujigaoka Hosp. Div. of Cardiol, Research associate, 医学部, 助手
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| Project Period (FY) |
1990 – 1992
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| Keywords | Computer simulation / Post-ischemic T wave / Transmembrane action potential / Carcium antagonist / Lysophosphatidylcholine / カルシウム拮抗薬 |
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| Research Abstract |
The recognition of post-ischemic T wave abnormality in patient with ischemic heart disease is significant diagnostic application of electrocardiogram (ECG). However the cause of post-ischemic T wave changes, pointed coronary T wave, has been still obscure. The present study was designed to understand the relationships between the changes in the surface ECG and the shape of action potential during reoxygenation.
The transmembrane action potentials from canine endocardial muscle preparations were recorded by conventional microelectrode. The preparations were perfused with three kinds of ischemic-like solutions or ischemic solution containing lysophosphatidylcholine (LPC ; 0.2mM) for 20min, and then the persuate was switched to the normal Tyrode solution for 60min. After the duration of the action potential (APD) was shortened to 20-50% of the control value under the perfusion of ischemic-like solution, the reoxygenation was found to cause of the transient prolongation of APD than that of
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the control. The rebound phenomenon depended on the degree of metabolic inhibition. After the perfusion of ischemic-like solution containing LPC for 20min, APD was prolonged and persisted longer than the control during the reoxygenation for 120min.
On the basis of the experimental results, computer simulation was performed with a model developed by Aoki and Harumi (IEEE 34 : 454, 1978). The heart model was constructed in the cubic close-packed structure consisting of 50,000 discrete element (model cell) in three dimensions. Action potential of model cell can be appointed individually and the wave form of that changed by use of the parameters. Antero-septal and lateral myocardial infarction (MI), different shapes of the lesion, prolonged APDs and reduction of conduction velocity in the vicinities of MI were examined with model. The shapes of MI zone in the model are broader (type I) or narrower (type II) in endocardial area than epicardial area. On the assumption that APDs were 40% shoter than normal at the closed zone on MI and 25% longer in the middle of border zone, the T waves were inverted in correponding leads in both type I models. It was assumed that conduction speed in the border zone was reduced to 50% of the control value, the shape of T waves became more deeply and symmetrically.
The results indicated that the post-ischemic T wave was obtained if the APD is lengthened in peripheral zones around MI. The secondary T wave changes was another contributing factor to the post-ischemic T wave change. It is inferred from the result of LPC that the long lasting T wave inversion is resulted in the influence of membrane permeability induced by any structural change of the myocardial cell membrane. Less
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