Drug Safety Site.com Taking Amiodarone during pregnancy and breastfeeding

• Home
• Index
• Appendix
• Instructions

AMIODARONE

Fetal Risk Summary

Amiodarone is an antiarrhythmic agent used for difficult or resistant cases of arrhythmias. The drug contains about 75 mg of iodine per 200-mg dose (1,2 and 3).

Amiodarone was maternal and embryo toxic (increased fetal resorptions, decreased live litter size, growth retardation, and retarded sternum and metacarpal ossification) in rats administered an IV infusion of 100 mg/kg/day (approximately 1.4 times the maximum recommended human dose [MRHD] on a body surface area basis) (4). Dosages of 25 and 50 mg/kg/day (approximately 0.4 and 0.7 times the MRHD) produced no embryo toxicity (4). In pregnant rabbits administered 5, 10, or 25 mg/kg IV (about 0.1, 0.3, and 0.7 times the MRHD), embryo toxicity was observed at 10 mg/kg/day and above. At 75 mg/kg/day (about 2.7 times the MRHD), more than 90% of the animals aborted. No teratogenic effects were observed in any of the rabbit groups (4).

Amiodarone and its metabolite, desethylamiodarone, cross the placenta to the fetus (1,2 and 3,5,6,7,8 and 9). In the 10 infants described in these reports, cord blood concentrations of the parent compound were 0.05–0.35 µg/mL, representing cord:maternal ratios of 0.10–0.28 in nine cases (1,2 and 3, 5,6,7,8 and 9) and 0.6 in one case (9). Cord blood concentrations of the metabolite varied between 0.05 and 0.55 µg/mL, about one fourth of the maternal levels in 9 of the 10 cases. In one study, the amount of amiodarone crossing the placenta to the fetus was dependent on the degree of hydrops fetalis (10). The expected fetal concentrations of the drug were not achieved until substantial compensation of the fetus had occurred.

In 22 cases of amiodarone therapy during pregnancy, the antiarrhythmic was administered for maternal indications (1,2 and 3,5,7,8 and 9,11,12,13,14,15 and 16). One patient in the last 3 months of pregnancy was treated with 200 mg daily for resistant atrial tachycardia (1). She delivered a 2,780-g female infant at 40 weeks' gestation. Both the mother and the infant had a prolonged QT interval on electrocardiogram (ECG). A second woman was also treated by these investigators under similar conditions. Both infants were normal (infant sex, weight, and gestational age were not specified for the second case), including having normal thyroid function. In another report, a woman was treated at 34 weeks' gestation when quinidine failed to control her atrial fibrillation (2). After an initial dose of 800 mg/day for 1 week, the dose was decreased to 400 mg/day and continued at this level until delivery at 41 weeks' gestation. The healthy 3220-g infant experienced bradycardia during labor induction (104–120 beats/minute) and during the first 48 hours after birth. No other adverse effects were observed in the infant, who had normal thyroid and liver function tests. A woman was treated during the 37th–39th weeks of pregnancy with daily doses of 600 mg, 400 mg, and 200 mg, each for 1 week, for atrial tachycardia that was resistant to propranolol, digoxin, and verapamil (3). No bradycardia or other abnormalities were noted in the newborn. The infant's thyroid-stimulating hormone (TSH) level on the 4th day was 9 mU/L, a normal value. Goiter was not observed and the infant was clinically euthyroid.

A 1985 report described the treatment of two women with amiodarone for maternal heart conditions (5). One of these patients, a 31-year-old woman with atrial fibrillation, was treated with amiodarone, 200 mg/day, and diuretics throughout gestation. She delivered a healthy 3500-g girl without goiter or corneal changes at 37 weeks' gestation. A cord blood thyroxine (T4) level was elevated (209 nmol/L) and was still elevated 1 week later (207 nmol/L), but TSH concentrations at these times were 3.2 mU/L and <1 mU/L (both normal), respectively. The second woman, a 27-year-old primigravida, was treated with amiodarone, 400–800 mg/day, starting at 22 weeks' gestation. Fetal bradycardia, 100–120 beats/minute, was observed at approximately 33 weeks' gestation. Spontaneous labor ensued at 39 weeks with delivery of a healthy 2900-g boy. Thyroid function studies were not reported, but the neonatal examinations were normal (5).

A woman in her 16th week of pregnancy presented with severe atrial fibrillation and was treated with amiodarone, 800 mg/day for 1 week followed by 200 mg/day for the remainder of her pregnancy (7). She delivered a growth-retarded 2660-g male in the 39th week of gestation who had no goiter and whose free T4 index, serum free triiodothyronine (T3), and serum TSH concentrations were all within normal limits. An ECG at 1 day of age showed a prolonged QT interval. Follow-up of the infant at 6 months was normal.

A healthy 3650-g male infant was delivered at term from a mother who had taken 200-400 mg/day of amiodarone throughout gestation (8). The infant's thyroid function was normal at birth; no goiter or corneal deposits were noted; and subsequent growth and thyroid function remained within normal limits. In another case, a woman was treated with propranolol and amiodarone, 400 mg/day for 4 days each week, throughout gestation (11). A healthy 2670-g female infant was delivered, but the gestational age was not specified. No goiter or corneal microdeposits were present in the infant and clinically she was euthyroid. The T4 and TSH levels in cord blood were both normal although a total serum iodine level (290 µg/dL) was markedly elevated (normal 5.5-17.4 µg/dL).

A 1991 report described the use of amiodarone in one woman with a history of symptomatic ventricular arrhythmia, and mitral and tricuspid valve prolapse through two complete pregnancies (12). She also had a history of right upper lobectomy for drug-resistant pulmonary tuberculosis. She was treated with 400 mg/day of amiodarone during the first 12 weeks of gestation of one pregnancy before the dose was reduced to 200 mg/day. She continued this dose during the remainder of this pregnancy and through a successive pregnancy. One of the newborns was growth retarded, a 2500-g female delivered at 38 weeks' gestation. The second infant, a 2960-g male, was delivered prematurely at 35.5 weeks' gestation. Except for the growth retardation in the one infant, the newborns were physically normal and had no clinical or biochemical signs of hypothyroidism (12). The concentration of amiodarone and its metabolite, desethylamiodarone, were <0.3 µg/mL in the first-born infant (not determined in the second newborn).

In two other reports, treatment was begun at 25 and 32 weeks' gestation (13,14). Delivery occurred at 31 weeks in one case (sex and birth weight not given), and the infant died 2 days after delivery (13). In the second report, the infant (sex and birth weight not given) was born at 37 weeks' gestation (14). Amiodarone and desethylamiodarone concentrations in the cord blood were 0.1 and 0.2 µg/mL, respectively. The drug and its metabolite were not detected in the infant's serum at 3 and 6 days after birth. A prolonged QT interval was observed on the infant's ECG.

Five pregnancies in four women treated with amiodarone for various cardiac arrhythmias were described in a 1992 Reference (9). The drug was used throughout gestation in four pregnancies and during the last 6 weeks in a fifth. One infant delivered at 34 weeks' gestation was growth retarded (birth weight, length, and head circumference were all at the 10th percentile or less), but the other four newborns were of normal size. No adverse effects — such as goiter, corneal microdeposits, pulmonary fibrosis, or dermatologic or neurologic signs — were observed (9). The infants were clinically euthyroid, but one of the five newborns had transient biochemical signs of hypothyroidism (low T4 concentration) that responded to treatment. This latter infant, whose mother had taken the b-blocker, metoprolol, throughout gestation and amiodarone only during the last 6 weeks, had delayed motor development and impaired speech performance at 5 years of age. He had been delivered at 40 weeks' gestation with a birth weight of 2880 g (10th percentile) and a length of 50 cm (50th percentile). The other four infants had normal follow-up examinations at periods ranging from 8 months to 5 years.

Congenital hypothyroidism with goiter was described in a growth-retarded 2,450-g male newborn whose mother had taken 200 mg/day of amiodarone from the 13th week of gestation until delivery at 38 weeks for treatment of Wolff-Parkinson-White syndrome (15). The mother had no signs or symptoms of hypothyroidism. Thyroid tests of cord blood revealed a TSH level of >100 mU/L (normal 10–20 mU/L), a T4 of 35.9 µg/L (normal 60–170 µg/L), and no thyroid antibodies. In addition to a homogeneous goiter, the newborn had persistent hypotonia and bradycardia, large anterior and posterior fontanels, and macroglossia, but no corneal microdeposits. The bradycardia resolved after several days. Greater than normal amounts of urinary iodine were measured from birth (144 µg/dL; normal <15 µg/dL) until the 6th week of life. The infant's plasma concentrations of amiodarone and desethylamiodarone on day 5 were 140 ng/mL and 260 ng/mL, respectively, and were still detectable after 1 month. His bone age at birth and at 20 months of age was estimated to be 28 weeks and 12 months, respectively. Treatment with levothyroxine during the first 20 months resulted in the complete disappearance of the goiter at about 3 months of age, but his psychomotor development was retarded.

A 1994 report described three pregnancies in two women who were being treated with amiodarone (16). Recurrent ventricular fibrillation was treated in one woman with an implanted defibrillator and amiodarone, 400 mg/day. She became pregnant 4 years after beginning this therapy and eventually delivered a premature, 2540-g male infant at 35 weeks' gestation with a holosystolic murmur and an umbilical hernia. At 2 weeks of age, the infant experienced mild congestive heart failure with labored breathing. A large midmuscular ventricular septal defect, with marked left ventricular and left atrial dilatation and left ventricular hypertrophy, was observed by echocardiogram (16). The defect was still present at 21 months of age. A second pregnancy in this woman, at the same amiodarone dose, was electively terminated at approximately 11 weeks' gestation. The thorax and limbs of the fetus were normal and contained 1.55 and 5.8 µg/g of amiodarone and desethylamiodarone, respectively. The second woman had been treated with amiodarone, 600 mg/day, for 2 years for recurrent sustained ventricular tachycardia (Chagas' disease) before conception. She eventually delivered a term 3,300 g male infant with mild bradycardia (110 beats/minute) at birth. Both liveborn infants were clinically euthyroid without goiter or corneal changes.

Six cases of amiodarone therapy for refractory fetal tachycardia have been described in the literature (6,10,17,18,19 and 20). In the first of these, a fetus at 27 weeks' gestation experienced tachycardia, 260 beats/minute, that was unresponsive to digoxin and propranolol (17). Lidocaine and procainamide lowered the heart rate somewhat but were associated with unacceptable maternal toxicity. Amiodarone combined with verapamil was successful in halting the tachycardia and reversing the signs of congestive heart failure. An amiodarone maintenance dose of 400 mg/day was required for control. Spontaneous labor occurred after 39 days of therapy, with delivery of a 2700-g male infant at 33 weeks' gestation. Atrial flutter with a 2:1 block and a ventricular rate of 200 beats/minute were converted on the 3rd day by electrical cardioversion. No adverse effects from the drug therapy were mentioned.

A fetus with supraventricular tachycardia, 220 beats/minute, showed evidence of congestive heart failure at 32 weeks' gestation (6). Maternal therapy with digoxin alone or in combination with sotalol (a b-blocker) or verapamil failed to stop the abnormal rhythm. Digoxin was then combined with amiodarone, 1600 mg/day for 4 days, then 1200 mg/day for 3 days, then 800 mg/day for 6 weeks. The fetal heart rate fell to 140 beats/minute after 14 days of therapy, and the signs of congestive heart failure gradually resolved. Neonatal thyroid indices at birth (about 38 weeks' gestation) and at 1 month were as follows (normal values are shown in parentheses): free T3 index, 3.4 and 5.6 pmol/L (4.3-8.6 pmol/L); free T4 index, 5.4 and 25 pmol/L (9–26 pmol/L); T3, 1.7 and 2.7 nmol/L (1.2–3.1 nmol/L); T4, 196 and 300 nmol/L (70–175 nmol/L); and TSH, 30 and 4.12 mU/L (<5 mU/L). The elevated T4 level returned to normal at a later unspecified time. It was not mentioned whether a goiter was present at birth. At 10 months of age, all thyroid function tests were within normal limits.

A third case involved a fetus at 30 weeks' gestation with tachycardia, 220 beats/minute, with congestive heart failure that had not responded to digoxin and propranolol (18). At 32 weeks' gestation, digoxin and amiodarone lowered the rate to 110–180 beats/minute with improvement in the congestive failure. Amiodarone was given at 1200 mg/day for 3 days, then 600 mg/day until delivery 3 weeks later. The newborn had tachycardia of up to 200 beats/minute that was treated with digoxin, furosemide, and propranolol. Hypothyroidism was diagnosed based on the presence of a goiter and abnormal thyroid tests (normal values are in parentheses): T4, 48 µg/mL (70–180 µg/mL); free T4, 0.5 µg/mL (>1.5 µg/mL); and TSH, >240 mU/L (<30 mU/L). The infant was treated with 10 mg/day of T4 until age 3 months, at which time his cardiac and thyroid functions were normal. Follow-up at 15 months was normal.

A 27-week fetus with refractory supraventricular tachycardia and hydrops fetalis was treated with repeated injections of amiodarone into the umbilical vein after maternal therapy with amiodarone and multiple other antiarrhythmic drugs failed to resolve the fetal condition (10). Subtherapeutic transplacental passage of amiodarone and digoxin was documented that did not improve until substantial resolution of the hydrops had occurred with direct administration of amiodarone to the fetus. A male infant was delivered at 37 weeks' gestation because of growth retardation, but thyroid function and other tests were within normal limits, and no corneal deposits were observed.

In a similar case, a 27-week fetus with severe hydrops secondary to congenital sinoatrial disease-induced sinus bradycardia and atrial flutter was treated with amiodarone via the intravenous, intraperitoneal, and transplacental routes (19). Prior maternal therapy with oral sotalol and flecainide had failed to reverse the worsening right heart failure. A 15-mg IV dose was administered to the fetus concurrently with initiation to the mother of 200 mg orally every 8 hours. Approximately 24 hours later, an additional 15-mg dose of amiodarone was given intraperitoneally to the fetus. The fetal ascites resolved over the next 3 weeks. A 2686-g female infant in good condition was eventually delivered at 37 weeks' gestation. Cardiac function was normal in the neonatal period and at 3-month follow-up, as were thyroid tests at 6 days of age.

A 1994 report described the use of amiodarone, 1600 mg/day (25 mg/kg/day), for the treatment of fetal supraventricular tachycardia that had failed to respond to flecainide at 33 weeks' gestation (20). The tachycardia recurred 2 weeks later and a cesarean section was performed under epidural anesthesia with lidocaine to deliver a 3,380-g male infant (follow-up of the infant not specified).

A historic cohort study, first published as an abstract (21) and then as a full report (22), described the fetal effects of maternal treatment with amiodarone. Twelve women, with various heart conditions requiring amiodarone therapy, were treated with individualized therapeutic doses (mean dose 321 mg/day) during gestation. Seven patients were treated throughout their pregnancies with one suffering a spontaneous abortion at 10 weeks. b-blockers were used concurrently in the six pregnancies that delivered live newborns, but in one the b-blocker was stopped after 14 weeks. In the other five women, treatment with amiodarone was begun in the 2nd or 3rd trimesters, and concurrent b-blockers were used in three for various intervals. The 11 infants were delivered at term (>37 weeks' gestation). Amiodarone was detected in two of three cord blood samples. The level in one was 0.2 µg/mL (maternal serum not detectable), and the cord blood level in the other was 21.3% of the maternal concentration. One of the newborns was hyperthyroid (asymptomatic, transient) and one was hypothyroid. Fetal bradycardia occurred in three of the infants, two of whom had been exposed to b-blockers (acebutolol and propranolol). Four infants were small for gestational age (<3rd percentile corrected for gestational age) and three of these had been exposed to b-blockers throughout pregnancy (22). Two infants had birth defects, only one of whom had been exposed during the 1st trimester. This infant had congenital jerk nystagmus with synchronous head titubation (exposed to amiodarone and propranolol throughout, quinidine during the 1st 3 weeks). The other newborn had hypotonia, hypertelorism, and micrognathia (exposed to amiodarone from the 20th week, atenolol from 18 to 20 weeks, and phenoxybenzamine during week 39), and delayed motor development assessed at 18 months (normal speech but milestone delay of about 3 months as indicated by lifting head, sitting unaided, crawling, standing, and walking) (22). The child's birth weight and Apgar scores had been normal for gestational age and his neonatal course, other than a meconium plug, had been unremarkable. Other than this case, the other exposed infants had normal development (mean age at follow-up 30 months, range 0 months to 11.5 years).

In summary, serious fetal adverse effects directly attributable to amiodarone have been observed. Congenital goiter/hypothryoidism and hyperthyroidism may occur after in utero exposure. Congenital defects have been observed in two newborns, but any association between amiodarone and the defects may be fortuitous. Ventricular septal defects reportedly occur at an incidence of 1–3/1000 (16), and the cause of the neurotoxicity in the second case is unknown (22). The transient bradycardia and prolonged QT interval observed in some amiodarone-newborns are direct effects of the drug but apparently lack clinical significance. Intrauterine growth retardation occurs frequently in infants exposed in utero to amiodarone, but it is uncertain whether this is a consequence of amiodarone, the mother's disease, other drug therapy (such as b-blockers), or a combination of these and other factors. Growth retardation has also been observed in animal studies. Because of the above outcomes and the limited data available, the drug should be used cautiously during pregnancy. As a result of the potential for fetal and newborn toxicity, it is not recommended as a first-line drug in uncomplicated cases of fetal supraventricular tachycardia (23).

Following chronic administration, amiodarone has a very long elimination half-life of 14–58 days (24). Therefore, the drug must be stopped several months before conception to avoid exposure in early gestation. A 1987 review of the management of cardiac arrhythmias during pregnancy recommends that amiodarone be restricted to refractory cases (25). Similarly, a 1992 review of maternal drug therapy for fetal disorders suggests caution, if it is used at all, before amiodarone is prescribed during pregnancy (26). Newborns exposed to amiodarone in utero should have thyroid function studies performed because of the large proportion of iodine contained in each dose.

Breast Feeding Summary

The effects on suckling rats of amiodarone obtained from breast milk were investigated in a study published in 1992 (27). No effect on neonatal weight gain was observed, but treatment did result in a decrease in maternal weight gain compared to controls. Accumulations of both amiodarone and its metabolite, desethylamiodarone, were demonstrated in neonatal lung and liver.

Amiodarone is excreted into human breast milk (2,3,8,9). The drug contains about 75 mg of iodine/200-mg dose (2,3,5). One woman, consuming 400 mg/day, had milk levels of amiodarone and its metabolite, desethylamiodarone (activity unknown), determined at varying times between 9 and 63 days after delivery (2). Levels of the two substances in milk were highly variable during any 24-hour period. Peak levels of amiodarone and the metabolite ranged from 3.6–16.4 µg/mL and 1.3-6.5 µg/mL. The milk:plasma (M:P) ratio of the active drug at 9 weeks postpartum ranged from 2.3 to 9.1 and that of desethylamiodarone from 0.8 to 3.8. The authors calculated that the nursing infant received about 1.4–1.5 mg/kg/day of active drug. Plasma levels of amiodarone in the infant remained constant at 0.4 µg/mL (about 25% of maternal plasma) from birth to 63 days. In a second case, a mother taking 200 mg/day did not breast-feed, but milk levels of the drug and the metabolite on the 2nd and 3rd days after delivery were 0.5–1.8 µg/mL and 0.4–0.8 µg/mL, respectively (3). A mother taking 400 mg/day had milk concentrations of amiodarone and the metabolite during the first postpartum month ranging from 1.06–3.65 µg/mL and 0.50–1.24 µg/mL, respectively (8). No adverse effects were observed in her nursing infant.

Mothers of three breast-feeding infants had taken amiodarone, 200 mg/day, during pregnancy and continued the same dose in the postpartum period (9). Milk concentrations of the drug at various times after delivery in the three mothers were 1.70 µg/mL (2 days postpartum) and 3.04 µg/mL (3 weeks postpartum), 0.55 µg/mL (4 weeks postpartum) and 0.03 µg/mL (6 weeks postpartum), and 2.20 µg/mL (at birth), respectively. The milk:plasma ratios at these times varied widely from 0.4 to 13.0, as did the milk concentrations of the metabolite (0.002 to 1.81 µg/mL). Two of the infants had concentrations of amiodarone in their plasma of 0.01 to 0.03 µg/mL.

Although no adverse effects were observed in the one breast-fed infant, relatively large amounts of the drug and its metabolite are available through the milk. Amiodarone, after chronic administration, has a very long elimination half-life of 14–58 days in adults (24). Data in pediatric patients suggest a more rapid elimination, but the half-life in newborns has not been determined. The effects of chronic neonatal exposure to this drug are unknown. Because of this uncertainty, and also because of the high proportion of iodine contained in each dose (see also Potassium Iodide), breast feeding is not recommended if the mother is currently taking amiodarone or has taken it chronically within the past several months.

References

1. Candelpergher G, Buchberger R, Suzzi GL, Padrini R. Trans-placental passage of amiodarone: electrocardiographic and pharmacologic evidence in a newborn. G Ital Cardiol 1982;12:79–82.
2. McKenna WJ, Harris L, Rowland E, Whitelaw A, Storey G, Holt D. Amiodarone therapy during pregnancy. Am J Cardiol 1983;51:1231–3.
3. Pitcher D, Leather HM, Storey GAC, Holt DW. Amiodarone in pregnancy. Lancet 1983;1:597–8.
4. Product information. Cordarone. Wyeth-Ayerst Laboratories, 2000.
5. Robson DJ, Jeeva Raj MV, Storey GAC, Holt DW. Use of amiodarone during pregnancy. Postgrad Med J 1985;61:75–7.
6. Arnoux P, Seyral P, Llurens M, Djiane P, Potier A, Unal D, Cano JP, Serradimigni A, Rouault F. Amiodarone and digoxin for refractory fetal tachycardia. Am J Cardiol 1987;59:166–7.
7. Penn IM, Barrett PA, Pannikote V, Barnaby PF, Campbell JB, Lyons NR. Amiodarone in pregnancy. Am J Cardiol 1985;56:196–7.
8. Strunge P, Frandsen J, Andreasen F. Amiodarone during pregnancy. Eur Heart J 1988;9:106–9.
9. Plomp TA, Vulsma T, de Vijlder JJM. Use of amiodarone during pregnancy. Eur J Obstet Gynecol Reprod Biol 1992;43:201–7.
10. Gembruch U, Manz M, Bald R, Rúddel H, Redel DA, Schlebusch H, Nitsch J, Hansmann M. Repeated intravascular treatment with amiodarone in a fetus with refractory supraventricular tachycardia and hydrops fetalis. Am Heart J 1989;118:1335–8.
11. Rey E, Bachrach LK, Burrow GN. Effects of amiodarone during pregnancy. Can Med Assoc J 1987;136:959–60.
12. Widerhorn J, Bhandari AK, Bughi S, Rahimtoola SH, Elkayam U. Fetal and neonatal adverse effects profile of amiodarone treatment during pregnancy. Am Heart J 1991;122:1162–6.
13. Wladimiroff JW, Steward PA. Treatment of fetal cardiac arrhythmias. Br J Hosp Med 1985;34:134– 40. As cited by Widerhorn J, Bhandari AK, Bughi S, Rahimtoola SH, Elkayam U. Fetal and neonatal adverse effects profile of amiodarone treatment during pregnancy. Am Heart J 1991;122:1162– 6.
14. Foster CJ, Love HG. Amiodarone in pregnancy: case report and review of literature. Int J Cardiol 1988;20:307–6.
15. De Wolf D, De Schepper J, Verhaaren H, Deneyer M, Smitz J, Sacre-Smits L. Congenital hypothyroid goiter and amiodarone. Acta Paediatr Scand 1988;77:616–8.
16. Ovadia M, Brito M, Hoyer GL, Marcus FI. Human experience with amiodarone in the embryonic period. Am J Cardiol 1994;73:316–7.
17. Rey E, Duperron L, Gauthier R, Lemay M, Grignon A, LeLorier J. Transplacental treatment of tachycardia-induced fetal heart failure with verapamil and amiodarone: a case report. Am J Obstet Gynecol 1985;153:311–2.
18. Laurent M, Betremieux P, Biron Y, LeHelloco A. Neonatal hypothyroidism after treatment by amiodarone during pregnancy. Am J Cardiol 1987;60:942.
19. Flack NJ, Zosmer N, Bennett PR, Vaughan J, Fisk NM. Amiodarone given by three routes to terminate fetal atrial flutter associated with severe hydrops. Obstet Gynecol 1993;82:714–6.
20. Fulgencio JP, Hamza J. Anaesthesia for caesarean section in a patient receiving high dose amiodarone for fetal supraventricular tachycardia. Anaesthesia 1994;49:406–8.
21. Magee LA, Taddio A, Downar E, Sermer M, Boulton BC, Cameron D, Rosengarten M, Waxman M, Allen LC, Koren G. Pregnancy outcome following gestational exposure to amiodarone (abstract). Teratology 1994;49:398.
22. Magee LA, Downar E, Sermer M, Boulton BC, Allen LC, Koren G. Pregnancy outcome after gestational exposure to amiodarone in Canada. Am J Obstet Gynecol 1995;172:1307–11.
23. Ito S, Magee L, Smallhorn J. Drug therapy for fetal arrhythmias. Clin Perinatol 1994;21:543–72.
24. Sloskey GE. Amiodarone: a unique antiarrhythmic agent. Clin Pharm 1983;2:330–40.
25. Rotmensch HH, Rotmensch S, Elkayam U. Management of cardiac arrhythmias during pregnancy: current concepts. Drugs 1987;33:623–33.
26. Ward RM. Maternal drug therapy for fetal disorders. Semin Perinatol 1992;16:12–20.
27. Hill DA, Reasor MJ. Effects of amiodarone administration during lactation in Fischer-344 rats. Toxicol Lett 1992;62:119–25.
    
    

Q&A about Amiodarone

Pharmacy

• we make easy buying drugs online

Index

• A  B  C  D  E  F  G  H  I   K  L  M  N  O  P  Q  R  S  T  U  V  W  Z

Popular Meds

• Acyclovir
• Allopurinol
• Alprazolam
• Amiodarone
• Amitriptyline
• Amoxicillin
• Atenolol
• Atorvastatin
• Azithromycin
• Bupropion
• Buspirone
• Butalbital
• Carisoprodol
• Cefixime
• Celecoxib
• Cephalexin
• Cetirizine
• Ciprofloxacin
• Clomiphene
• Clonazepam
• Clonidine
• Codeine
• Cyclobenzaprine
• Diazepam
• Diethylpropion
• Diltiazem
• Doxycycline
• Enalapril
• Ephedrine
• Erythromycin
• Estradiol
• Fluconazole
• Fluoxetine
• Furosemide
• Gitalin
• Hydrocodone
• Lorazepam
• Losartan
• Metformin
• Metronidazole
• Minoxidil
• Naproxen
• Ondansetron
• Oxycodone
• Pantoprazole
• Passion Flower
• Phendimetrazine
• Phentermine
• Pioglitazone
• Pravastatin
• Propranolol
• Pseudoephedrine
• Quinine
• Ramipril
• Ranitidine
• Rosiglitazone
• Sertraline
• Simvastatin
• Sumatriptan
• Tamoxifen
• Terbinafine
• Tetracycline
• Thyroid
• Tramadol
• Trazodone
• Valerian
• Vitamin C
• Zolpidem

Copyright © 2003-2008 DRUGSAFETYSITE.COM All rights reserved.