TY - JOUR
T1 - Control of late postoperative ventricular arrhythmias with phenytoin in young patients
AU - Garson, Arthur
AU - Kugler, John D.
AU - Gillette, Paul C.
AU - Simonelli, Americo
AU - McNamara, Dan G.
N1 - Funding Information:
From The Lillie Frank Abercrombie Section of Cardiology, Department of Pediatrics, Baylor College of Medicine, Houston, Texas. This study was supported in parl by Grant HL-07 190 from the U.S. Public Health Service, and Grant RR-00188 from the General Clinical Research Branch, the National institutes of Health, Bethesda, Maryland; and by a grant from The J. S. Abercrombie Foundation, and The Danny Matthys Cardiac Research Fund, Houston, Texas. Manuscript received August 21, 1979; revised manuscript received December 28, 1979, accepted January 8, 1980. l Recipient of career development award HL00571 from the Rational Institutes of Health, Bethesda, Maryland.
PY - 1980
Y1 - 1980
N2 - Ventricular arrhythmias probably initiate the events leading to sudden death in patients who have recovered uneventfully from surgery for congenital heart disease. It is therefore recommended that antiarrhythmic therapy be given to all patients who have had surgery for congenital heart defects and who have ventricular arrhythmias found in a routine electrocardiogram taken after the immediate postoperative period. The response of ventricular arrhythmias to treatment was studied in six ambulatory patients aged 7 to 27 years (mean 16.5) who had had surgery a mean of 10.7 years before the arrhythmia was recognized. Four patients had unsatisfactory repair of the congenital defect; the two other patients had only a palliative operation. Each patient's electrocardiogram was monitored continually by tape recording. Each received phenytoin, 3.75 mg/kg body weight, every 6 hours for four doses, then 1.9 mg/kg every 6 hours until the serum concentration of phenytoin was 15 to 20 μg/ml. This serum concentration was maintained with the daily administration of 2.5 to 3 mg/kg every 12 hours. In the 24 hours before treatment, two patients had ventricular tachycardia, two had paired premature ventricular complexes and two had 10 or more single premature ventricular complexes/hour. After treatment, all patients had “effective control” (one or less premature ventricular complex/hour for 12 consecutive hours). This control was achieved with phenytoin in five patients, but one patient required the addition of disopyramide (2 mg/kg every 6 hours). All five patients undergoing a treadmill test before treatment had premature ventricular complexes during or after exercise; after treatment, only one had premature ventricular complexes after exercise. The patient who required two drugs was unable to perform a treadmill test. The mean effective serum phenytoin concentration, 15.7 μg/ml (range 8.5 to 20.0), was reached at a mean time of 61.2 hours (range 42 to 80) after the start of phenytoin therapy. Ataxia occurred in two patients with serum phenytoin concentrations of 16 and 20 μg, but not in the other four, three of whom had serum concentrations greater than 20 μg/ml. Echocardiographic, hematopoletic, hepatic and renal function indexes remained constant with treatment. It is concluded that (1) phenytoin suppressed ventricular arrhythmias in six children and young adults after surgery for congenital heart disease; (2) the effective serum concentration of phenytoin was approximately 15 μg/ml, but varied widely; and (3) this concentration was achieved within 48 to 72 hours when an oral loading dose was administered.
AB - Ventricular arrhythmias probably initiate the events leading to sudden death in patients who have recovered uneventfully from surgery for congenital heart disease. It is therefore recommended that antiarrhythmic therapy be given to all patients who have had surgery for congenital heart defects and who have ventricular arrhythmias found in a routine electrocardiogram taken after the immediate postoperative period. The response of ventricular arrhythmias to treatment was studied in six ambulatory patients aged 7 to 27 years (mean 16.5) who had had surgery a mean of 10.7 years before the arrhythmia was recognized. Four patients had unsatisfactory repair of the congenital defect; the two other patients had only a palliative operation. Each patient's electrocardiogram was monitored continually by tape recording. Each received phenytoin, 3.75 mg/kg body weight, every 6 hours for four doses, then 1.9 mg/kg every 6 hours until the serum concentration of phenytoin was 15 to 20 μg/ml. This serum concentration was maintained with the daily administration of 2.5 to 3 mg/kg every 12 hours. In the 24 hours before treatment, two patients had ventricular tachycardia, two had paired premature ventricular complexes and two had 10 or more single premature ventricular complexes/hour. After treatment, all patients had “effective control” (one or less premature ventricular complex/hour for 12 consecutive hours). This control was achieved with phenytoin in five patients, but one patient required the addition of disopyramide (2 mg/kg every 6 hours). All five patients undergoing a treadmill test before treatment had premature ventricular complexes during or after exercise; after treatment, only one had premature ventricular complexes after exercise. The patient who required two drugs was unable to perform a treadmill test. The mean effective serum phenytoin concentration, 15.7 μg/ml (range 8.5 to 20.0), was reached at a mean time of 61.2 hours (range 42 to 80) after the start of phenytoin therapy. Ataxia occurred in two patients with serum phenytoin concentrations of 16 and 20 μg, but not in the other four, three of whom had serum concentrations greater than 20 μg/ml. Echocardiographic, hematopoletic, hepatic and renal function indexes remained constant with treatment. It is concluded that (1) phenytoin suppressed ventricular arrhythmias in six children and young adults after surgery for congenital heart disease; (2) the effective serum concentration of phenytoin was approximately 15 μg/ml, but varied widely; and (3) this concentration was achieved within 48 to 72 hours when an oral loading dose was administered.
UR - http://www.scopus.com/inward/record.url?scp=0018967007&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0018967007&partnerID=8YFLogxK
U2 - 10.1016/0002-9149(80)90073-9
DO - 10.1016/0002-9149(80)90073-9
M3 - Article
C2 - 7405844
AN - SCOPUS:0018967007
SN - 0002-9149
VL - 46
SP - 290
EP - 294
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 2
ER -