TY - JOUR
T1 - Electrophysiologic evaluation of pirmenol for sustained ventricular tachycardia secondary to coronary artery disease
AU - Easley, Arthur R.
AU - Mann, David E.
AU - Reiter, Michael J.
AU - Sakun, Valerie
AU - Sullivan, Susan M.
AU - Magro, Sharon A.
AU - Luck, Jerry C.
AU - Wyndham, Christopher R.C.
N1 - Funding Information:
From the Cardiology Division, University of Colorado Health Sciences Center, Denver, Colorado, and the Cardiology Division, Baylor College of Medicine, Houston, Texas. This study was supported by a grant from Warner-Lambert/Parke-Davis Laboratories, Ann Arbor, Michigan. Manuscript received November 4,1985; revised manuscript received February l&1986, accepted February 19,1986.
PY - 1986/7/1
Y1 - 1986/7/1
N2 - The efficacy and electrophysiologic effects of pirmenol were evaluated in 21 patients with a history of sustained ventricular tachycardia (VT) and coronary artery disease. Intravenous pirmenol (0.7- to 1.1-mg/kg bolus, followed by a 35- to 40-μg/kg/min infusion) significantly prolonged the PR, QRS, QT and corrected QT intervals, HV interval and right ventricular effective refractory period, and shortened the sinus cycle length and atrioventricular nodal block cycle length. All 21 patients had inducible VT (20 sustained, 1 nonsustained) during programmed stimulation in the control state. After intravenous pirmenol, 5 patients (24%) no longer had inducible VT. In those in whom VT was still inducible, the VT cycle length was prolonged significantly. The 5 patients who responded to intravenous pirmenol were given oral pirmenol (200 to 250 mg every 8 hours) for 1 to 3 days and retested with programmed stimulation. In 4 of these 5, VT could not be induced with oral pirmenol administration; in 1 patient sustained VT was induced and pirmenol therapy was discontinued. Oral pirmenol suppressed recurrent VT during a follow-up of 315 ± 133 days in 4 patients. However, pirmenol therapy was discontinued in 2 patients because of possible deleterious effects (worsened heart failure in 1 patient and elevated liver function test results in 1). Thus, pirmenol, a type IA antiarrhythmic drug, had an overall efficacy of approximately 19% in patients with sustained VT secondary to coronary artery disease.
AB - The efficacy and electrophysiologic effects of pirmenol were evaluated in 21 patients with a history of sustained ventricular tachycardia (VT) and coronary artery disease. Intravenous pirmenol (0.7- to 1.1-mg/kg bolus, followed by a 35- to 40-μg/kg/min infusion) significantly prolonged the PR, QRS, QT and corrected QT intervals, HV interval and right ventricular effective refractory period, and shortened the sinus cycle length and atrioventricular nodal block cycle length. All 21 patients had inducible VT (20 sustained, 1 nonsustained) during programmed stimulation in the control state. After intravenous pirmenol, 5 patients (24%) no longer had inducible VT. In those in whom VT was still inducible, the VT cycle length was prolonged significantly. The 5 patients who responded to intravenous pirmenol were given oral pirmenol (200 to 250 mg every 8 hours) for 1 to 3 days and retested with programmed stimulation. In 4 of these 5, VT could not be induced with oral pirmenol administration; in 1 patient sustained VT was induced and pirmenol therapy was discontinued. Oral pirmenol suppressed recurrent VT during a follow-up of 315 ± 133 days in 4 patients. However, pirmenol therapy was discontinued in 2 patients because of possible deleterious effects (worsened heart failure in 1 patient and elevated liver function test results in 1). Thus, pirmenol, a type IA antiarrhythmic drug, had an overall efficacy of approximately 19% in patients with sustained VT secondary to coronary artery disease.
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U2 - 10.1016/0002-9149(86)90246-8
DO - 10.1016/0002-9149(86)90246-8
M3 - Article
C2 - 3728337
AN - SCOPUS:0022546745
SN - 0002-9149
VL - 58
SP - 86
EP - 89
JO - The American Journal of Cardiology
JF - The American Journal of Cardiology
IS - 1
ER -