1993 Fiscal Year Final Research Report Summary
Experimental Research about Etiology of Long QT Syndrome and Torsades dePointes
| Project/Area Number |
04670552
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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 | Wakayama Medical College |
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Principal Investigator |
UENO Yuji Wakayama Medical College, Department of Cardiology, Associated Professor, 医学部・循環器内科, 助教授 (50151824)
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| Co-Investigator(Kenkyū-buntansha) |
HOSHIYA Hironobu Wakayama Medical College, Department of Cardiology, Assistant, 医学部・循環器内科, 助手 (00244723)
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| Project Period (FY) |
1992 – 1993
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| Keywords | Long QT Syndrome / Early After Depolarization / Monophasic Action Potential / Torsades de Pointes / Quinidine / Ansae-Subclaviae Stimulation |
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| Research Abstract |
The purpose of this study is to clarify the mechanisms responsible for QTU abnormality and Torsades de Pointes (Tdp) in patients with congenital and acquired long QT syndrome (LQTS). We recorded body surface electrocardiogram (ECG) and monophasic action potential (MAP) in vivo heart using the contact electrode technique, in patients with congenital LQTS and in dogs, and evaluated QT interval (QT), MAP duration at 90% repolarization (MAP90) and early after depolarization (EAD).
1. Clinical evaluation : ECGs and MAPs were obtained from the right and left ventricular endocardium (RV-and LV-MAP) in 4 patients with congenital LQTS (LQTS group : 12 recording sites) and in 3 patients with sick sinus syndrome (control group : 9 recording sites). EADs were recorded in all of the LQTS group at 4 recording sites, but not in the control group. After isoproterenol (Isp) infusion QT and MAP90 were significantly prolonged (p<0.02) associated with EAD enlargement in the LQTS group, whereas these change
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s were not found in the control group.
2. Effects of ansae subclaviae stimulation on ECG and MAP in dogs : We recorded ECGs, RV-MAPs and LV-MAPs in 9 adult mongrel dogs before and after left, right and bilateral ansae subclaviae stimulation (LAS,RAS and BAS). QT and MAP90 were significantly shortened after LAS and BAS, but not after RAS, EADs were not recorded before and after any types of ansae subclaviae stimulation (LAS,RAS and BAS).
3. Quinidine induced QTU abnormalities and EADs in dogs : ECGs, LV-MAPs and RV-MAPs were recorded before and after quinidine (Qi) infusion in 9 adult beagle dogs, and the effect of BAS and verapamil (Ver) infusion on EAD were evaluated EADs were not recorded during control state at any MAP recording sites. 60 minutes after Qi infusion, QT,LV-MAP90 and RV-MAP90 were significantly prolonged (p<0.01), and EADs were recorded 6 recording sites. EADs were depended upon bradycardia and enlarged after BAS but diminished after Ver infusion.
Conclusion : EADs play the important role in the etiologies of QTU abnormalities and Torsades de Pointes in patients with congenital and quinidine-induced LQTS. Less
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