Abstract
This open-label, multicenter study was designed to assess the electrophysiological properties of intravenous recainam, an investigational Class I antiarrhythmic agent. In 25 patients undergoing electrophysiological studies for the evaluation of arrhythmias, recainam was administered intravenously in a loading infusion (0.1 mg/kg/min) for 40 minutes, followed by a maintenance infusion (0.02 mg/kg/min) until the completion of the study. Electrophysiological measurements were obtained at baseline, 30 minutes after initiation of the loading infusion, and 30 minutes after termination of the infusion during washout. Conduction intervals, refractory periods, and sinus node recovery times were measured during sinus rhythm and during atrial or ventricular pacing. Vital signs were obtained and recorded before, during, and after recainam infusion. The results showed no change in mean arterial pressure, but heart rate increased slightly by 4 beats/min following recainam infusion. Recainam produced a generalized slowing of intracardiac conduction. The mean intraatrial conduction time, measured at an atrial paced cycle length of 600 msec, increased during recainam loading infusion by 44%, from 38.8 ± 2.8 to 53.0 ± 5.4 msec; intranodal conduction time increased by 10%, from 102.0 ± 5.5 to 112.1 ± 5.2 msec; and infranodal conduction time increased by 31% from 53.1 ± 3.0 to 70.7 ± 3.8 msec. Slowed conduction persisted during washout. The mean right atrial effective refractory period was significantly prolonged (+7% at 600 msec cycle length and +8% at 450 msec cycle length, P < 0.05 and P < 0.01, respectively) during recainam loading and remained so during washout. However, the mean effective refractory period of the atrioventricular node was significantly prolonged only during the recainam loading infusion while pacing at 450-msec cycle length (+8%, P < 0.05). In contrast, the mean effective refractory period of the right ventricle was not changed during or immediately after the infusion, but was significantly shortened 30 minutes later (-4%, P < 0.05). Two of 25 patients (8%) developed adverse reactions requiring termination of the infusion. Five other patients (20%) developed less serious side effects during the recainam infusion, all of which resolved spontaneously and did not require termination of the infusion. The results demonstrate that recainam prolongs conduction in atrial, ventricular, and specialized cardiac conduction tissues. Recainam also prolongs atrial refractory periods, but has little or no effect on the sinus node or on AV nodal and right ventricular refractory periods. Thus, recainam is a Class I antiarrhythmic agent with a combination of electrophysiological properties suggesting its potential utility in the treatment of atrial and ventricular arrhythmias.
| Original language | English |
|---|---|
| Pages (from-to) | 1129-1137 |
| Number of pages | 9 |
| Journal | PACE - Pacing and Clinical Electrophysiology |
| Volume | 14 |
| Issue number | 7 |
| State | Published - Jan 1 1991 |
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ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Clinical electrophysiological effects of intravenous recainam : An antiarrhythmic drug under investigation for the treatment of ventricular and supraventricular arrhythmias. / Feld, G. K.; Luceri, R. M.; Greenspon, A. J.; Singh, B. N.; Horowitz, L. N.; Capuzzi, D. M.; Frame, V. B.; Myerburg, Robert J.
In: PACE - Pacing and Clinical Electrophysiology, Vol. 14, No. 7, 01.01.1991, p. 1129-1137.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Clinical electrophysiological effects of intravenous recainam
T2 - An antiarrhythmic drug under investigation for the treatment of ventricular and supraventricular arrhythmias
AU - Feld, G. K.
AU - Luceri, R. M.
AU - Greenspon, A. J.
AU - Singh, B. N.
AU - Horowitz, L. N.
AU - Capuzzi, D. M.
AU - Frame, V. B.
AU - Myerburg, Robert J
PY - 1991/1/1
Y1 - 1991/1/1
N2 - This open-label, multicenter study was designed to assess the electrophysiological properties of intravenous recainam, an investigational Class I antiarrhythmic agent. In 25 patients undergoing electrophysiological studies for the evaluation of arrhythmias, recainam was administered intravenously in a loading infusion (0.1 mg/kg/min) for 40 minutes, followed by a maintenance infusion (0.02 mg/kg/min) until the completion of the study. Electrophysiological measurements were obtained at baseline, 30 minutes after initiation of the loading infusion, and 30 minutes after termination of the infusion during washout. Conduction intervals, refractory periods, and sinus node recovery times were measured during sinus rhythm and during atrial or ventricular pacing. Vital signs were obtained and recorded before, during, and after recainam infusion. The results showed no change in mean arterial pressure, but heart rate increased slightly by 4 beats/min following recainam infusion. Recainam produced a generalized slowing of intracardiac conduction. The mean intraatrial conduction time, measured at an atrial paced cycle length of 600 msec, increased during recainam loading infusion by 44%, from 38.8 ± 2.8 to 53.0 ± 5.4 msec; intranodal conduction time increased by 10%, from 102.0 ± 5.5 to 112.1 ± 5.2 msec; and infranodal conduction time increased by 31% from 53.1 ± 3.0 to 70.7 ± 3.8 msec. Slowed conduction persisted during washout. The mean right atrial effective refractory period was significantly prolonged (+7% at 600 msec cycle length and +8% at 450 msec cycle length, P < 0.05 and P < 0.01, respectively) during recainam loading and remained so during washout. However, the mean effective refractory period of the atrioventricular node was significantly prolonged only during the recainam loading infusion while pacing at 450-msec cycle length (+8%, P < 0.05). In contrast, the mean effective refractory period of the right ventricle was not changed during or immediately after the infusion, but was significantly shortened 30 minutes later (-4%, P < 0.05). Two of 25 patients (8%) developed adverse reactions requiring termination of the infusion. Five other patients (20%) developed less serious side effects during the recainam infusion, all of which resolved spontaneously and did not require termination of the infusion. The results demonstrate that recainam prolongs conduction in atrial, ventricular, and specialized cardiac conduction tissues. Recainam also prolongs atrial refractory periods, but has little or no effect on the sinus node or on AV nodal and right ventricular refractory periods. Thus, recainam is a Class I antiarrhythmic agent with a combination of electrophysiological properties suggesting its potential utility in the treatment of atrial and ventricular arrhythmias.
AB - This open-label, multicenter study was designed to assess the electrophysiological properties of intravenous recainam, an investigational Class I antiarrhythmic agent. In 25 patients undergoing electrophysiological studies for the evaluation of arrhythmias, recainam was administered intravenously in a loading infusion (0.1 mg/kg/min) for 40 minutes, followed by a maintenance infusion (0.02 mg/kg/min) until the completion of the study. Electrophysiological measurements were obtained at baseline, 30 minutes after initiation of the loading infusion, and 30 minutes after termination of the infusion during washout. Conduction intervals, refractory periods, and sinus node recovery times were measured during sinus rhythm and during atrial or ventricular pacing. Vital signs were obtained and recorded before, during, and after recainam infusion. The results showed no change in mean arterial pressure, but heart rate increased slightly by 4 beats/min following recainam infusion. Recainam produced a generalized slowing of intracardiac conduction. The mean intraatrial conduction time, measured at an atrial paced cycle length of 600 msec, increased during recainam loading infusion by 44%, from 38.8 ± 2.8 to 53.0 ± 5.4 msec; intranodal conduction time increased by 10%, from 102.0 ± 5.5 to 112.1 ± 5.2 msec; and infranodal conduction time increased by 31% from 53.1 ± 3.0 to 70.7 ± 3.8 msec. Slowed conduction persisted during washout. The mean right atrial effective refractory period was significantly prolonged (+7% at 600 msec cycle length and +8% at 450 msec cycle length, P < 0.05 and P < 0.01, respectively) during recainam loading and remained so during washout. However, the mean effective refractory period of the atrioventricular node was significantly prolonged only during the recainam loading infusion while pacing at 450-msec cycle length (+8%, P < 0.05). In contrast, the mean effective refractory period of the right ventricle was not changed during or immediately after the infusion, but was significantly shortened 30 minutes later (-4%, P < 0.05). Two of 25 patients (8%) developed adverse reactions requiring termination of the infusion. Five other patients (20%) developed less serious side effects during the recainam infusion, all of which resolved spontaneously and did not require termination of the infusion. The results demonstrate that recainam prolongs conduction in atrial, ventricular, and specialized cardiac conduction tissues. Recainam also prolongs atrial refractory periods, but has little or no effect on the sinus node or on AV nodal and right ventricular refractory periods. Thus, recainam is a Class I antiarrhythmic agent with a combination of electrophysiological properties suggesting its potential utility in the treatment of atrial and ventricular arrhythmias.
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M3 - Article
VL - 14
SP - 1129
EP - 1137
JO - PACE - Pacing and Clinical Electrophysiology
JF - PACE - Pacing and Clinical Electrophysiology
SN - 0147-8389
IS - 7
ER -