PHYSIOLOGICAL AND PATHOLOGICAL RESPONSES OF TU WAVES TO CLASS IA ANTIARRHYTHMIC DRUGS

被引:8
作者
MARUYAMA, T [1 ]
OHE, T [1 ]
KURITA, T [1 ]
AIHARA, N [1 ]
SHIMIZU, W [1 ]
机构
[1] NATL CARDIOVASC CTR,DIV CARDIOL,SUITA,OSAKA 565,JAPAN
关键词
U WAVE; TORSADES DE POINTES; CLASS IA ANTIARRHYTHMIC DRUGS;
D O I
10.1093/oxfordjournals.eurheartj.a060971
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Abnormal repolarization associated with torsades de pointes is expressed as QT prolongation. The physiological response to class Ia antiarrhythmic drugs is also reflected in prolongation of the QT interval. However, the essential difference between pathological and physiological prolongation is not clear. The purpose of this investigation was to differentiate between pathological and physiological changes in the repolarization waves of surface electrocardiograms (ECG) induced by class Ia drugs. In 18 patients without a history of torsades de pointes or syncope (control group), TU waves were compared before and after the administration of class Ia drugs (physiological response). In eight patients with torsades de pointes induced by class Ia drugs (torsades de pointes group), the TU waves at torsades de pointes were compared with those before drug administration (pathological response). In the control group, although the QTc (measured in lead II and corrected for heart rate by Bazett's formula) was increased significantly (0.04 +/- 0.04 to 0.44 +/- 0.05 s, P < 0.001), the U-amp (amplitude of the U wave measured in a precordial lead where the T and U waves were clearly differentiated) remained unchanged. In the torsades de points group, however, the QTc was increased (0.42 +/- 0.04 to 0.54 +/- 0.07 s, P < 0.02); the U-amp was also increased, significantly (0.09 +/- 0.07 to 0.27 +/- 0.18 mV, P < 0.05). Thus, enlargement of the U wave may help to differentiate between the physiological and pathological responses to class Ia drugs.
引用
收藏
页码:667 / 673
页数:7
相关论文
共 22 条
[1]  
Bazett HC, 1920, HEART-J STUD CIRC, V7, P353
[2]   RECORDING OF MONOPHASIC ACTION-POTENTIALS OF THE RIGHT VENTRICLE IN LONG QT SYNDROMES COMPLICATED BY SEVERE VENTRICULAR ARRHYTHMIAS [J].
BONATTI, V ;
ROLLI, A ;
BOTTI, G .
EUROPEAN HEART JOURNAL, 1983, 4 (03) :168-179
[3]   BRADYCARDIA-DEPENDENT TRIGGERED ACTIVITY - RELEVANCE TO DRUG-INDUCED MULTIFORM VENTRICULAR-TACHYCARDIA [J].
BRACHMANN, J ;
SCHERLAG, BJ ;
ROSENSHTRAUKH, LV ;
LAZZARA, R .
CIRCULATION, 1983, 68 (04) :846-856
[4]  
CLELAND JGF, 1992, BRIT HEART J, V67, P1
[5]   QUINIDINE-INDUCED ACTION-POTENTIAL PROLONGATION, EARLY AFTERDEPOLARIZATIONS, AND TRIGGERED ACTIVITY IN CANINE PURKINJE-FIBERS - EFFECTS OF STIMULATION RATE, POTASSIUM, AND MAGNESIUM [J].
DAVIDENKO, JM ;
COHEN, L ;
GOODROW, R ;
ANTZELEVITCH, C .
CIRCULATION, 1989, 79 (03) :674-686
[6]   QUINIDINE-INDUCED LONG QTU INTERVAL AND TORSADE-DE-POINTES - ROLE OF BRADYCARDIA-DEPENDENT EARLY AFTERDEPOLARIZATIONS [J].
ELSHERIF, N ;
BEKHEIT, SS ;
HENKIN, R .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1989, 14 (01) :252-257
[7]   QTU PROLONGATION AND POLYMORPHIC VENTRICULAR TACHYARRHYTHMIAS DUE TO BRADYCARDIA-DEPENDENT EARLY AFTERDEPOLARIZATIONS - AFTERDEPOLARIZATIONS AND VENTRICULAR ARRHYTHMIAS [J].
ELSHERIF, N ;
ZEILER, RH ;
CRAELIUS, W ;
GOUGH, WB ;
HENKIN, R .
CIRCULATION RESEARCH, 1988, 63 (02) :286-305
[8]  
GAVRILESCU S, 1978, BRIT HEART J, V40, P1014
[9]   PARADOXICAL EFFECTS OF EXERCISE ON THE QT INTERVAL IN PATIENTS WITH POLYMORPHIC VENTRICULAR-TACHYCARDIA RECEIVING TYPE-IA ANTIARRHYTHMIC AGENTS [J].
KADISH, AH ;
WEISMAN, HF ;
VELTRI, EP ;
EPSTEIN, AE ;
SLEPIAN, MJ ;
LEVINE, JH .
CIRCULATION, 1990, 81 (01) :14-19
[10]   ETIOLOGY, WARNING SIGNS AND THERAPY OF TORSADE DE POINTES - A STUDY OF 10 PATIENTS [J].
KEREN, A ;
TZIVONI, D ;
GAVISH, D ;
LEVI, J ;
GOTTLIEB, S ;
BENHORIN, J ;
STERN, S .
CIRCULATION, 1981, 64 (06) :1167-1174