Conversion of atrial flutter by ibutilide is associated with increased atrial cycle length variability

被引:44
作者
Guo, GBF
Ellenbogen, KA
Wood, MA
Stambler, BS
机构
[1] HARVARD UNIV,SCH MED,W ROXBURY VET AFFAIRS MED CTR,DIV CARDIOL,BOSTON,MA 02132
[2] VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DIV CARDIOL,RICHMOND,VA 23298
[3] MCGUIRE DEPT VET AFFAIRS MED CTR,RICHMOND,VA
关键词
D O I
10.1016/0735-1097(95)00607-9
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objectives. This study was designed to test the hypothesis that conversion of atrial butter in humans by ibutilide, a new class III antiarrhythmic agent, is characterized by an increase in atrial cycle length variability. Background. Conversion of tachyarrhythmias has been associated with increased oscillations of cycle length. Methods. Electrograms and monophasic action potentials from the right atrium in 35 patients,vith spontaneous, sustained atrial butter were recorded before, during and after intravenous ibutilide (0.005 to 0.025 mg/kg body weight, n = 25) or placebo (n = 10). Atrial cycle length, cycle length variability (coefficient of variation), diastolic interval and diastolic interval variability were measured from 10 consecutive cycles at baseline and 3 min before, 1 min before, 30 s before and immediately before conversion. Similar measurements were made in patients who received ibutilide or placebo but did not convert. Results. Ibutilide converted atrial flutter in 14 of 25 patients 25 +/- 16 min (mean +/- SD) after initiation of the infusion, whereas placebo converted no patients. Atrial cycle length was prolonged to the same extent in ibutilide converters and nonconverters (36 +/- 19 vs. 38 +/- 21 ms, p = NS) and was not affected by placebo. Beat-to-beat variability in atrial cycle length (baseline 1.2 +/- 0.7 vs. preconversion 7.3 +/- 4.9, p < 0.01) and diastolic interval (baseline 11 +/- 8 vs. preconversion 33 +/- 23, p < 0.05) increased significantly just before atrial flutter conversion and remained unchanged in ibutilide nonconverters and placebo group patients. Conclusions. Ibutilide prolongs atrial butter cycle length, but conversion of atrial flutter by ibutilide is characterized by increased variability in atrial cycle length and diastolic interval.
引用
收藏
页码:1083 / 1089
页数:7
相关论文
共 26 条
[1]   ACTIVATION MAPPING OF REENTRY AROUND AN ANATOMICAL BARRIER IN THE CANINE ATRIUM - OBSERVATIONS DURING THE ACTION OF THE CLASS-III AGENT, D-SOTALOL [J].
BOYDEN, PA ;
GRAZIANO, JN .
JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, 1993, 4 (03) :266-279
[2]   EFFECTS OF IBUTILIDE ON SPONTANEOUS AND INDUCED VENTRICULAR ARRHYTHMIAS IN 24-HOUR CANINE MYOCARDIAL-INFARCTION - A COMPARATIVE-STUDY WITH SOTALOL AND ENCAINIDE [J].
BUCHANAN, LV ;
KABELL, G ;
TURCOTTE, UM ;
BRUNDEN, MN ;
GIBSON, JK .
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 1992, 19 (02) :256-263
[3]   CHARACTERIZATION OF SPONTANEOUS TERMINATION OF SUSTAINED VENTRICULAR-TACHYCARDIA ASSOCIATED WITH CORONARY-ARTERY DISEASE [J].
CALLANS, DJ ;
MARCHLINSKI, FE .
AMERICAN JOURNAL OF CARDIOLOGY, 1991, 67 (01) :50-54
[4]   ELECTROCARDIOGRAPHIC CORRELATES OF SPONTANEOUS TERMINATION OF VENTRICULAR-TACHYCARDIA IN PATIENTS WITH CORONARY-ARTERY DISEASE [J].
DUFF, HJ ;
MITCHELL, LB ;
GILLIS, AM ;
SHELDON, RS ;
CHUDLEIGH, L ;
CASSIDY, P ;
CHIAMVIMONVAT, N ;
WYSE, G .
CIRCULATION, 1993, 88 (03) :1054-1062
[5]  
ELLENBOGEN KA, 1994, J AM COLL CARDIOL, V23, pA227
[6]   OSCILLATIONS OF CONDUCTION, ACTION-POTENTIAL DURATION, AND REFRACTORINESS - A MECHANISM FOR SPONTANEOUS TERMINATION OF REENTRANT TACHYCARDIAS [J].
FRAME, LH ;
SIMSON, MB .
CIRCULATION, 1988, 78 (05) :1277-1287
[7]   SPONTANEOUS TERMINATION OF REENTRY AFTER ONE CYCLE OR SHORT NONSUSTAINED RUNS - ROLE OF OSCILLATIONS AND EXCESS DISPERSION OF REFRACTORINESS [J].
FRAME, LH ;
RHEE, EK .
CIRCULATION RESEARCH, 1991, 68 (02) :493-502
[8]   EFFECTS OF ANTIARRHYTHMIC DRUGS ON CANINE ATRIAL-FLUTTER DUE TO REENTRY - ROLE OF PROLONGATION OF REFRACTORY PERIOD AND DEPRESSION OF CONDUCTION TO EXCITABLE GAP [J].
INOUE, H ;
YAMASHITA, T ;
NOZAKI, A ;
SUGIMOTO, T .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1991, 18 (04) :1098-1104
[9]  
LAMMERS W J E P, 1991, Journal of Cardiovascular Electrophysiology, V2, P375, DOI 10.1111/j.1540-8167.1991.tb01337.x
[10]  
LEE KS, 1992, J PHARMACOL EXP THER, V262, P99