Aust NZ J Obstet Gynaecol 1992; 32: 2: 169
Undiagnosed Maternal Fallot Tetralogy Presenting in Pregnancy P. Larsen-Disney: BSc(Hons), MBBS, D. Price: FRACOG and I. Meredith: BSc(Hons), PhD, FRACP Monash Medical Centre, Melbourne EDITORIAL COMMENT: We accepted this case reportfor publication not on& because we wish to help spread the authors’ message regarding team management during pregnancy of high risk patients with cardiac disease, but also to remind readers that significant cardiac anomalies may be recognized for thefirst time during routine antenatal examination.
Tetralogy of Fallot accounts for 75% of cyanotic congenital heart disease encountered in children, adults and pregnant mothers (1). Fifty percent of all children with surgically untreated Fallot tetralogy will not survive beyond 5 years of age (2), and 95% will die prior to age 25, their deaths being attributable to ventricular arrhythmias, cerebrovascular accident, bacterial endocarditis and rarely congestive cardiac failure or hypoxia (3). Classically, tetralogy of Fallot is characterized by the following structural cardiac abnormalities: 1. Pulmonary stenosis. 2. Ventricular septal defect. 3. Overriding or dextroposition of the aorta. 4. Right ventricular hypertrophy. The clinical presentation of the afflicted patient will be determined primarily by the size of the ventricular septal defect and the severity of the pulmonary valve stenosis. The physician may be alerted to the possibility of Fallot tetralogy by a history revealing dyspnoea on exertion, episodic cyanosis and squatting to relieve dyspnoea and faintness. Examination may reveal central cyanosis, physical underdevelopment and digital clubbing. Cardiovascular examination and investigation, including echocardiography, will confirm the diagnosis (4). This report describes the antenatal course and the subsequent delivery of a 28-year-old woman with previously undiagnosed Fallot tetralogy. Her pregnancy was further complicated by the development of preeclampsia requiring delivery at 33 weeks’ gestation.
Case report A 28-year-old primigravida initially presented to antenatal clinic at approximately 11 weeks’ gestation on uncertain menstrual dates. She was of Philippino extraction and had no relevant past medical history with the exception of a cardiac murmur, apparently detected 1. Registrar in Obstetrics and Gynaecology. 2. Consultant Obstetrician. 3. Senior Registrar in Cardiology. Address for correspondence: Dr. P. Larsen-Disney, 8/16 Cromwell Road, South Yarra, Victoria, 3141.
at birth. On specific questioning, the patient suggested that she may have had rheumatic fever as a child; however she received no treatment at that time and achieved normal developmental milestones. At no stage during her childhood or adolescence did she experience shortness-of-breath, cyanotic episodes or syncope. The patient had 7 siblings, each of whom was also well. Since her arrival in Australia in 1988, the patient had remained well and quite asymptomatic of cardiac disease, being able to perform her daily activities without hindrance. The patient’s antenatal course at the time of her first consultation had been unremarkable. General examination at that time revealed a 151 cm tall, well-looking woman with clubbing of the fingers and toes in the absence of obvious cyanosis. The patient weighed 36.4 kg, had a blood pressure of 95/70, pulse rate of 76 per minute with regular pulse volume and form. Her jugular venous pressure was + 2 cm. Precordial examination of the patient revealed a left parasternal heave and associated thrill. On auscultation, she had 2 heart sounds with a loud ejection systolic murmur at the upper left sternal edge with radiation over the entire precordium. Gynaecological examination of the patient demonstrated an ll-week gravid uterus and no specific abnormalities were detected. Urine analysis was normal and her haemoglobin value at presentation was 14.5 g/dl.
Investigations and clinical course The patient had an ECG performed which demonstrated sinus rhythm and right axis deviation in the presence of right ventricular hypertrophy and right heart strain. A chest X-ray showed clear lung fields and a normal sized cardiac shadow, and also revealed a rightsided aortic knuckle. The patient was referred to the Cardiology Unit for further assessment and an echocardiogram was performed which demonstrated the classical features of Fallot tetralogy with an overriding aorta and large outlet ventricular septal defect. Infundibular stenosis and possible pulmonary valve stenosis were also noted with a mean pulmonary valve gradient of 48 mmHg. The left ventricle was of normal size; however obvious enlargement of the right ventricle was reported.
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A routine pregnancy ultrasound was performed which confirmed an expected gestation of 17 weeks and fetal normality. An echocardiogram was also performed on the fetus and this revealed no evidence of cardiac anomaly. These findings were confirmed on a repeat echocardiogram 4 weeks later. The patient was regularly reviewed by the obstetric and cardiology units over subsequent months and remained well with the exception of slight tiredness and occasional shortness-of-breath. Arterial blood gases performed at 30 weeks’ gestation revealed an oxygen saturation of 91%. At 32 weeks’ gestation, the patient was found to have proteinuria in the absence of oedema and hypertension (blood pressure 110/70). She was subsequently hospitalized for observation and further assessment. Despite remaining asymptomatic, soon after admission, the patient’s blood pressure became elevated (diastolic pressure 90-95) and mild generalized oedema became apparent; neurological assessment revealed moderate hyperreflexia in the absence of papilloedema. Proteinuria remained constant at 1/8 to 1/10 solid on boiled midstream urine specimens. Laboratory tests performed on admission, showed normal urea and electrolytes, but elevated uric acid (457 mmol/l) and hypoalbuminaemia (29 mmol/l). Full blood examination was normal. A 24-hour urine collection demonstrated a reduced creatinine clearance of 54 ml/minute and a total protein excretion of 1.8 g/day. A full fetal assessment was also performed and ultrasound confirmed the clinical impression of a small baby with all criteria of measurement less than the tenth percentile. Liquor volume, however, was normal. Cardiotocography (CTG) recordings were also normal; however umbilical arterial blood flow resistance was marginally elevated wth A:B ratio = 4.0 (normal 5 mmHg. Urine output remained satisfactory at greater than 50 ml/hour. Labour progressed well and full cervical dilatation was achieved after 7 hours and 45 minutes. The liquor remained clear and despite no short-term variability, adequate long-term variability and reactivity were seen on the cardiotocograph. Second stage took 29 minutes and a normal vaginal delidery of a healthy male infant weighing 1,424 g resulted. The infant was transferred to the Special Care Nursery where thorough examination revealed no evidence of cardiac abnormality. The third stage of labour was completed with controlled cord traction and total blood loss was estimated to be 150 ml. Syntocinon 10 units I.V. was given after completion of the third stage and a Syntocinon infusion was commenced.
Postpartum management Postpartum, the patient remained well, with complete resolution of hypertension and proteinuria after 24 hours and she was transferred from CCU on Day 2. On return to the postnatal ward, ambulation was encouraged, and heparin and phenytoin were ceased. The patient was discharged home on Day 4. The patient was reviewed in the Cardiology outpatients 4 weeks postpartum and arrangements were made for cardiac catherization and angiography to be performed. The results of these studies were as follows: 1. Presence of tetralogy of Fallot with evidence of an abnormal doming of the pulmonary valve and significant infundibular stenosis. 2. A gradient of approximately 90 mmHg between a normal pulmonary circulation and the right ventricle. 3. A large malalignment ventricular septal defect. 4. Evidence of an atrial septal defect. 5. A normal-sized left ventricle and good left ventricular function. 6. Normal aortic root and aortic valve. 7. No evidence of anomalous coronary vasculature. After discussion at a cardiac unit conference, it was decided that in view of the patient’s lack of symptoms, total corrective surgery could be deferred until her infant was older and the patient had ceased breast-feeding. At review by the obstetric unit 6 weeks postpartum, the patient appeared well and was managing admirably with breast feeding and domestic duties.
P. LARSEN-DISNEY ET AL
DISCUSSION Pregnancy in the patient with Fallot tetralogy has received scant review in the literature. Some assessment of the clinical experience of such patients was made by Mendelson ( 5 ) who reviewed 33 cases reported prior to 1959. Since that time, further patients have been added to the literature (6,9). Review was previously hampered by the lack of complete obstetric information and unequivocal assessment of the precise cardiac malformation present. Today, the high incidence of shunt procedures and definitive surgical correction in the patient with Fallot tetralogy, has resulted in a paucity of clinical expertise in the management of the uncorrected condition during pregnancy. To obtain accurate information on the natural history of tetralogy of Fallot one must look to literature produced on the subject over 30 years ago; there is no recent series reported. It is usual for the patient with tetralogy of Fallot to suffer a gradual increase in the severity of pulmonary stenosis with exacerbation of symptoms and increasing cyanosis. The long-term prognosis is extremely poor in the absence of surgical correction, with a greatly reduced life-expectancy. The haemodynamic fluxes of pregnancy may severely compromise the patient with tetralogy of Fallot and may also result in fetal complications. The fall in peripheral vascular resistance which occurs in pregnancy can lead to the development of, or an increase in, shunting of blood from the right to the left side of the heart. The increased circulating blood volume of pregnancy and increased venous return, can in themselves lead to increased right-to-left shunting and heart failure may ensue. Careful management of the labour and delivery in these patients is critical. Hypotension resulting from intrapartum haemorrhage or fall in the peripheral resistance can further exacerbate the right-to-left shunt and result in cyanosis, hypoxia and circulatory collapse. A further risk which must not be overlooked is that of paradoxical embolism and cerebrovascular accident. Uncorrected tetralogy of Fallot carries a 4% risk of maternal death and a 30% fetal mortality related to hypoxia (5). The incidence of congenital heart disease in the neonate of the afflicted mother is variously quoted as 1.1% (7) to 14% (8). A recent article by Shime et a1 (7) describes 144 pregnancies in 74 women with congenital heart disease. Twenty-four of these women had cyanotic lesions and of these, 9 had proven Fallot tetralogy (2 of whom had not been treated by total corrective surgery). This study revealed a spontaneous abortion rate of 19.4% and a perinatal mortality of 13% in the cyanotic group of patients. In addition, it suggested that preterm births and small for gestational date infants were more common in the cyanotic group than in the acyanotic group and in the general population. Interestingly, pregnancy induced hypertension occurred in 14.9% of women with congenital heart disease and an on-going pregnancy (compared with 4.3% in the total obstetric population
171
during the same period); however, no case occurred in the group of women with treated or untreated tetralogy of Fallot. Patients who have had total correction of their Fallot tetralogy tolerate pregnancy well with only minimal increased risk to mother and infant (7,8,10,11). Patients who have had only palliative procedures including anastomoses between the pulmonary arterial system and the subclavian artery, descending or ascending aorta, still carry a significantly increased risk of cardiac deterioration during their pregnancies (8). The greatest risk however, is carried by the untreated patient. Some assessment of this risk may be established by seeking poor prognostic signs which include: a maternal haematocrit > 60%; peripheral arterial oxygen saturation < 80%; right ventricular hypertension and a clinical history of syncopal attacks (3). The case described reaffirms our belief that patients with significant cardiac anomalies, such as Fallot tetralogy, must be jointly managed throughout their pregnancy by an experienced team of cardiologists and obstetricians. Staff and facilities must be available to regularly review these patients and manage any deterioration in their condition. To provide optimal care for the pregnant cardiac patient, prompt access to a coronary care unit is mandatory and the delivery should occur in this unit, to ensure adequate monitoring of the patient’s cardiac status.
Acknowledgements The authors wish to express their thanks to Associate Professor Geoffrey Bishop for his suggestions during the preparation of this paper. We also wish to thank Eileen Taylor and Maureen Langdon, Secretaries in Suite G at the Monash Medical Centre for their assistance.
References 1. Campbell M. Natural history of cyanotic malformations and
2. 3. 4. 5.
6. 7.
8. 9. 10. 11.
comparison of all common cardiac malformations. Br Heart J 1972; 34: 3-8. Ikeda M, Hirosawa K. Tetralogy of Fallot. Circulation 1968; 38: (suppl. V): 21. Elkayam U. Congenital Heart Disease and Pregnancy. In Cardiac Problems in Pregnancy. 2nd Edition. New York. Alan R. Liss Inc. 1988. Braunwald E. Congenital Heart Disease in Infancy and Childhood. In Heart Disease 3rd Edition. Phila WB Saunders Company. 1988. Medelson C.L. Cardiac Disease in Pregnancy. Phila F.A. Davis Co. 1960. Jacoby WJ. Pregnancy with Tetralogy and Pentalogy of Fallot. Am J Cardiol 1964; 14: 866-871. Shime J, Mocarski EJ, Hastings D, Webb GD, McLaughlin PR. Congenital heart disease in pregnancy: short- and long-term implications: published erratum appears in Am J Obstet Gynecol 1987; 156: 1361. Am J Obstet Gynecol 1987; 156: 313-322. Whittemore R, Hobbins JC, Engle MA. Pregnancy and its outcome in the woman with and without surgical treatment of congenital disease. Am J Cardiol 1982; 50: 641-651. Meyer EC, Tulsky AS, Sigmann P, Silber EN. Pregnancy in the presence of tetralogy of fallot: observations on two patients. Am J Cardiol 1964; 14: 874-879. Neilson G, Calea EG, Blunt A. Congenital heart disease and pregnancy. Med J Aust 1970; 1: 1086-1088. Loh TF, Tan NC. Fallot’s Tetralogy in pregnancy: A report of a successful pregnancy after complete correction. Med J Aust 1971; 2: 141-145.
Undiagnosed Maternal Fallot Tetralogy Presenting in Pregnancy P. Larsen-Disney: BSc(Hons), MBBS, D. Price: FRACOG and I. Meredith: BSc(Hons), PhD, FRACP Monash Medical Centre, Melbourne EDITORIAL COMMENT: We accepted this case reportfor publication not on& because we wish to help spread the authors’ message regarding team management during pregnancy of high risk patients with cardiac disease, but also to remind readers that significant cardiac anomalies may be recognized for thefirst time during routine antenatal examination.
Tetralogy of Fallot accounts for 75% of cyanotic congenital heart disease encountered in children, adults and pregnant mothers (1). Fifty percent of all children with surgically untreated Fallot tetralogy will not survive beyond 5 years of age (2), and 95% will die prior to age 25, their deaths being attributable to ventricular arrhythmias, cerebrovascular accident, bacterial endocarditis and rarely congestive cardiac failure or hypoxia (3). Classically, tetralogy of Fallot is characterized by the following structural cardiac abnormalities: 1. Pulmonary stenosis. 2. Ventricular septal defect. 3. Overriding or dextroposition of the aorta. 4. Right ventricular hypertrophy. The clinical presentation of the afflicted patient will be determined primarily by the size of the ventricular septal defect and the severity of the pulmonary valve stenosis. The physician may be alerted to the possibility of Fallot tetralogy by a history revealing dyspnoea on exertion, episodic cyanosis and squatting to relieve dyspnoea and faintness. Examination may reveal central cyanosis, physical underdevelopment and digital clubbing. Cardiovascular examination and investigation, including echocardiography, will confirm the diagnosis (4). This report describes the antenatal course and the subsequent delivery of a 28-year-old woman with previously undiagnosed Fallot tetralogy. Her pregnancy was further complicated by the development of preeclampsia requiring delivery at 33 weeks’ gestation.
Case report A 28-year-old primigravida initially presented to antenatal clinic at approximately 11 weeks’ gestation on uncertain menstrual dates. She was of Philippino extraction and had no relevant past medical history with the exception of a cardiac murmur, apparently detected 1. Registrar in Obstetrics and Gynaecology. 2. Consultant Obstetrician. 3. Senior Registrar in Cardiology. Address for correspondence: Dr. P. Larsen-Disney, 8/16 Cromwell Road, South Yarra, Victoria, 3141.
at birth. On specific questioning, the patient suggested that she may have had rheumatic fever as a child; however she received no treatment at that time and achieved normal developmental milestones. At no stage during her childhood or adolescence did she experience shortness-of-breath, cyanotic episodes or syncope. The patient had 7 siblings, each of whom was also well. Since her arrival in Australia in 1988, the patient had remained well and quite asymptomatic of cardiac disease, being able to perform her daily activities without hindrance. The patient’s antenatal course at the time of her first consultation had been unremarkable. General examination at that time revealed a 151 cm tall, well-looking woman with clubbing of the fingers and toes in the absence of obvious cyanosis. The patient weighed 36.4 kg, had a blood pressure of 95/70, pulse rate of 76 per minute with regular pulse volume and form. Her jugular venous pressure was + 2 cm. Precordial examination of the patient revealed a left parasternal heave and associated thrill. On auscultation, she had 2 heart sounds with a loud ejection systolic murmur at the upper left sternal edge with radiation over the entire precordium. Gynaecological examination of the patient demonstrated an ll-week gravid uterus and no specific abnormalities were detected. Urine analysis was normal and her haemoglobin value at presentation was 14.5 g/dl.
Investigations and clinical course The patient had an ECG performed which demonstrated sinus rhythm and right axis deviation in the presence of right ventricular hypertrophy and right heart strain. A chest X-ray showed clear lung fields and a normal sized cardiac shadow, and also revealed a rightsided aortic knuckle. The patient was referred to the Cardiology Unit for further assessment and an echocardiogram was performed which demonstrated the classical features of Fallot tetralogy with an overriding aorta and large outlet ventricular septal defect. Infundibular stenosis and possible pulmonary valve stenosis were also noted with a mean pulmonary valve gradient of 48 mmHg. The left ventricle was of normal size; however obvious enlargement of the right ventricle was reported.
170
AUST.AND N . Z . JOURNAL OF OBSTETRlCS AND GYNAECOLOGY
A routine pregnancy ultrasound was performed which confirmed an expected gestation of 17 weeks and fetal normality. An echocardiogram was also performed on the fetus and this revealed no evidence of cardiac anomaly. These findings were confirmed on a repeat echocardiogram 4 weeks later. The patient was regularly reviewed by the obstetric and cardiology units over subsequent months and remained well with the exception of slight tiredness and occasional shortness-of-breath. Arterial blood gases performed at 30 weeks’ gestation revealed an oxygen saturation of 91%. At 32 weeks’ gestation, the patient was found to have proteinuria in the absence of oedema and hypertension (blood pressure 110/70). She was subsequently hospitalized for observation and further assessment. Despite remaining asymptomatic, soon after admission, the patient’s blood pressure became elevated (diastolic pressure 90-95) and mild generalized oedema became apparent; neurological assessment revealed moderate hyperreflexia in the absence of papilloedema. Proteinuria remained constant at 1/8 to 1/10 solid on boiled midstream urine specimens. Laboratory tests performed on admission, showed normal urea and electrolytes, but elevated uric acid (457 mmol/l) and hypoalbuminaemia (29 mmol/l). Full blood examination was normal. A 24-hour urine collection demonstrated a reduced creatinine clearance of 54 ml/minute and a total protein excretion of 1.8 g/day. A full fetal assessment was also performed and ultrasound confirmed the clinical impression of a small baby with all criteria of measurement less than the tenth percentile. Liquor volume, however, was normal. Cardiotocography (CTG) recordings were also normal; however umbilical arterial blood flow resistance was marginally elevated wth A:B ratio = 4.0 (normal 5 mmHg. Urine output remained satisfactory at greater than 50 ml/hour. Labour progressed well and full cervical dilatation was achieved after 7 hours and 45 minutes. The liquor remained clear and despite no short-term variability, adequate long-term variability and reactivity were seen on the cardiotocograph. Second stage took 29 minutes and a normal vaginal delidery of a healthy male infant weighing 1,424 g resulted. The infant was transferred to the Special Care Nursery where thorough examination revealed no evidence of cardiac abnormality. The third stage of labour was completed with controlled cord traction and total blood loss was estimated to be 150 ml. Syntocinon 10 units I.V. was given after completion of the third stage and a Syntocinon infusion was commenced.
Postpartum management Postpartum, the patient remained well, with complete resolution of hypertension and proteinuria after 24 hours and she was transferred from CCU on Day 2. On return to the postnatal ward, ambulation was encouraged, and heparin and phenytoin were ceased. The patient was discharged home on Day 4. The patient was reviewed in the Cardiology outpatients 4 weeks postpartum and arrangements were made for cardiac catherization and angiography to be performed. The results of these studies were as follows: 1. Presence of tetralogy of Fallot with evidence of an abnormal doming of the pulmonary valve and significant infundibular stenosis. 2. A gradient of approximately 90 mmHg between a normal pulmonary circulation and the right ventricle. 3. A large malalignment ventricular septal defect. 4. Evidence of an atrial septal defect. 5. A normal-sized left ventricle and good left ventricular function. 6. Normal aortic root and aortic valve. 7. No evidence of anomalous coronary vasculature. After discussion at a cardiac unit conference, it was decided that in view of the patient’s lack of symptoms, total corrective surgery could be deferred until her infant was older and the patient had ceased breast-feeding. At review by the obstetric unit 6 weeks postpartum, the patient appeared well and was managing admirably with breast feeding and domestic duties.
P. LARSEN-DISNEY ET AL
DISCUSSION Pregnancy in the patient with Fallot tetralogy has received scant review in the literature. Some assessment of the clinical experience of such patients was made by Mendelson ( 5 ) who reviewed 33 cases reported prior to 1959. Since that time, further patients have been added to the literature (6,9). Review was previously hampered by the lack of complete obstetric information and unequivocal assessment of the precise cardiac malformation present. Today, the high incidence of shunt procedures and definitive surgical correction in the patient with Fallot tetralogy, has resulted in a paucity of clinical expertise in the management of the uncorrected condition during pregnancy. To obtain accurate information on the natural history of tetralogy of Fallot one must look to literature produced on the subject over 30 years ago; there is no recent series reported. It is usual for the patient with tetralogy of Fallot to suffer a gradual increase in the severity of pulmonary stenosis with exacerbation of symptoms and increasing cyanosis. The long-term prognosis is extremely poor in the absence of surgical correction, with a greatly reduced life-expectancy. The haemodynamic fluxes of pregnancy may severely compromise the patient with tetralogy of Fallot and may also result in fetal complications. The fall in peripheral vascular resistance which occurs in pregnancy can lead to the development of, or an increase in, shunting of blood from the right to the left side of the heart. The increased circulating blood volume of pregnancy and increased venous return, can in themselves lead to increased right-to-left shunting and heart failure may ensue. Careful management of the labour and delivery in these patients is critical. Hypotension resulting from intrapartum haemorrhage or fall in the peripheral resistance can further exacerbate the right-to-left shunt and result in cyanosis, hypoxia and circulatory collapse. A further risk which must not be overlooked is that of paradoxical embolism and cerebrovascular accident. Uncorrected tetralogy of Fallot carries a 4% risk of maternal death and a 30% fetal mortality related to hypoxia (5). The incidence of congenital heart disease in the neonate of the afflicted mother is variously quoted as 1.1% (7) to 14% (8). A recent article by Shime et a1 (7) describes 144 pregnancies in 74 women with congenital heart disease. Twenty-four of these women had cyanotic lesions and of these, 9 had proven Fallot tetralogy (2 of whom had not been treated by total corrective surgery). This study revealed a spontaneous abortion rate of 19.4% and a perinatal mortality of 13% in the cyanotic group of patients. In addition, it suggested that preterm births and small for gestational date infants were more common in the cyanotic group than in the acyanotic group and in the general population. Interestingly, pregnancy induced hypertension occurred in 14.9% of women with congenital heart disease and an on-going pregnancy (compared with 4.3% in the total obstetric population
171
during the same period); however, no case occurred in the group of women with treated or untreated tetralogy of Fallot. Patients who have had total correction of their Fallot tetralogy tolerate pregnancy well with only minimal increased risk to mother and infant (7,8,10,11). Patients who have had only palliative procedures including anastomoses between the pulmonary arterial system and the subclavian artery, descending or ascending aorta, still carry a significantly increased risk of cardiac deterioration during their pregnancies (8). The greatest risk however, is carried by the untreated patient. Some assessment of this risk may be established by seeking poor prognostic signs which include: a maternal haematocrit > 60%; peripheral arterial oxygen saturation < 80%; right ventricular hypertension and a clinical history of syncopal attacks (3). The case described reaffirms our belief that patients with significant cardiac anomalies, such as Fallot tetralogy, must be jointly managed throughout their pregnancy by an experienced team of cardiologists and obstetricians. Staff and facilities must be available to regularly review these patients and manage any deterioration in their condition. To provide optimal care for the pregnant cardiac patient, prompt access to a coronary care unit is mandatory and the delivery should occur in this unit, to ensure adequate monitoring of the patient’s cardiac status.
Acknowledgements The authors wish to express their thanks to Associate Professor Geoffrey Bishop for his suggestions during the preparation of this paper. We also wish to thank Eileen Taylor and Maureen Langdon, Secretaries in Suite G at the Monash Medical Centre for their assistance.
References 1. Campbell M. Natural history of cyanotic malformations and
2. 3. 4. 5.
6. 7.
8. 9. 10. 11.
comparison of all common cardiac malformations. Br Heart J 1972; 34: 3-8. Ikeda M, Hirosawa K. Tetralogy of Fallot. Circulation 1968; 38: (suppl. V): 21. Elkayam U. Congenital Heart Disease and Pregnancy. In Cardiac Problems in Pregnancy. 2nd Edition. New York. Alan R. Liss Inc. 1988. Braunwald E. Congenital Heart Disease in Infancy and Childhood. In Heart Disease 3rd Edition. Phila WB Saunders Company. 1988. Medelson C.L. Cardiac Disease in Pregnancy. Phila F.A. Davis Co. 1960. Jacoby WJ. Pregnancy with Tetralogy and Pentalogy of Fallot. Am J Cardiol 1964; 14: 866-871. Shime J, Mocarski EJ, Hastings D, Webb GD, McLaughlin PR. Congenital heart disease in pregnancy: short- and long-term implications: published erratum appears in Am J Obstet Gynecol 1987; 156: 1361. Am J Obstet Gynecol 1987; 156: 313-322. Whittemore R, Hobbins JC, Engle MA. Pregnancy and its outcome in the woman with and without surgical treatment of congenital disease. Am J Cardiol 1982; 50: 641-651. Meyer EC, Tulsky AS, Sigmann P, Silber EN. Pregnancy in the presence of tetralogy of fallot: observations on two patients. Am J Cardiol 1964; 14: 874-879. Neilson G, Calea EG, Blunt A. Congenital heart disease and pregnancy. Med J Aust 1970; 1: 1086-1088. Loh TF, Tan NC. Fallot’s Tetralogy in pregnancy: A report of a successful pregnancy after complete correction. Med J Aust 1971; 2: 141-145.
