1997 Fiscal Year Final Research Report Summary
MECHANISMS OF VENTRICULAR ARRHYTHMIAS IN HEART FAILURE
| Project/Area Number |
08670782
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | SHIGA UNIVERSITY OF MEDICAL SCIENCE |
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Principal Investigator |
ITO Makoto SHIGA UNIVERSITY OF MEDICAL SCIENCE,ASSOCIATE PROFESSOR, 医学部, 講師 (70159911)
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| Co-Investigator(Kenkyū-buntansha) |
WADA Atsuyuki SHIGA UNIVERSITY OF MEDICAL SCIENCE,ASSISTANT PROFESSOR, 医学部, 助手 (10273400)
SUGIMOTO Yoshihisa SHIGA UNIVERSITY OF MEDICAL SCIENCE,ASSISTANT PROFESSOR, 医学部, 助手 (30216337)
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| Project Period (FY) |
1996 – 1997
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| Keywords | RAPID VENTRICULAR PACING / HEART FAILURE / ACTION POTENTIAL / VENTRICULAR ARRHYTHMIA / CARDIAC SYMPATHETIC NERVOUS SYSTEM |
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| Research Abstract |
We have made a heart failure model with using rapid ventricular pacing in canine hearts. After ventricular pacing rate 270 bpm for 14 days, dogs showed congestive heart failure with enlarged heart, pleural effusion, and ascitis. Dogs exhibited abnormalities in neurohumoral factors such as increased ANP, BNP, enhanced renin-angiotensin-aldosterone system, and endotheline.
In dog hearts with heart failure, monophasic action potential duration recorded from ventricle was shorter compared with normal heart. This result was different from other chronic heart failure model with microsphare-induced ischemic dog hearts.
We have also made rapid pacing model in rabbit hearts. Ventricular pacing rate from 300 to 350 bpm shortened a duration of monophasic action potential in vivo. Shortening of action potential duration recovered by 4-aminopyridine which blocks the transient outward current (Ito). We concluded that short period of rapid ventricular pacing enhanced Ito. Such different results might b
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e affected by heart failure models and/or species.
Washout rate of 1-123 metaiodobenzylguanidine which reflects cardiac sympathetic neural function was greater in patients with ventricular tachycardia/fibrillation compared to the patients without ventricular tachycardia/fibrillation, although cardiac function was comparable between groups. with and without VT/VF.We concluded that cardiac sympathetic function was abnormal in the patients with malignant ventricular tachyarrhythmias compared to the patients without malignant ventricular tachyarrhythmias in chronic non-ischemic heart failure. Moreover, regional sympathetic imbalance reflected by heterogeneous washout of MIBG exists in symptomatic patients with long QT syndrome. Such abnormal sympathetic neural function can exacerbate malignant ventricular tachyarrhythmias in long QT syndrome. We also demonstrated that fatty acid metabolism was abnormal in coronary artery disease which is major cause of heart failure. Successful angioplasty restores fatty acid metabolism. Ischemia shortened ventricular action potential duration via activation of ATP-sensitive potassium channels. Opening of ATP-sensitive potassium channels preserves ischemic changes of epicardial ECG. Less
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