Briiish Journal of Obstetrics and Gynaecology June 1975. Vol. 82. pp. 505-507

MYOCARDIAL INFARCTION AND RHEUMATIC HEART DISEASE IN PREGNANCY CASE REPORT BY

T. B. J. HUGHES Lecturer Department of Obstetrics and GynaecoIogy University of Liverpool Summary Myocardial infarction is a rare complication of pregnancy, only 45 proven cases having been reported. In only one patient was rheumatic heart disease an associated factor (Goldberger and Pokress, 1950).

cardiomegally and engorgement of the pulmonary vessels consistent with advanced rheumatic heart disease. The serum asparate aminotransferase (SGOT) was elevated to 108 lU/l; serum lactic dehydrogenase (LDH) was elevated to 680 units/ml and the serum alanine aminotransferase was 8 IU/l which was within the normal range. Initially, she was treated with 10 mg. of diamorphine intramuscularly and with 4-hourly intravenous injections of 5000 1U of heparin for 12 days after which time anticoagulant therapy was reduced gradually over a 48-hour period, stopped and the patient then mobilized. She was discharged from hospital at 30 weeks gestation after a total of one month in-patient care. Thereafter she attended the antenatal clinic at weekly intervals. She remained normotensive; her haemoglobin was in excess of 1 I .O g/100 ml. and there was no evidence of cardiac decompensation. At 266 days gestation she was readmitted into hospital for rest and went into spontaneous labour at 279 days gestation. Intramuscular ampicillin, 500 mgs. 6 hourly, was commenced. The first stage of labour lasted 2 hours 25 minutes during which time she received a single intramuscular injection of 15 mg. of morphine intramuscularly for analgesia. A prophylactic

CASEREPORT A WOMAN, aged 43 years, gravida 4, para 3, was admitted to hospital as an emergency at 26 weeks gestation in her fourth pregnancy with severe retrosternal chest pain of sudden onset accompanied by breathlessness and sweating. She had had rheumatic fever at the age of 13 years and was known to have rheumatic heart disease. During the antenatal period prior to her admission she had been examined at fortnightly intervals by a physician who had detected no evidence of cardiac decompensation. Apart from pre-eclampsia during her first pregnancy at the age of 25 years, she had remained well throughout her previous confinements with no episodes of cardiac failure. On examination, she had “mitral facies” and was slightly dyspnoeic at rest. Her blood pressure was 130/80 mm. Hg. and her pulse 80 beats per minute in sinus rhythm. Crepitations were present at both lung bases. Examination of her heart revealed cardiac enlargement, the apex beat being displaced laterally to the anterior axillary line, and murmurs commensurate with a diagnosis of mitral stenosis, mitral incompetence and aortic stenosis. An electrocardiogram showed ST depression in chest leads Vs-VB indicating an inferior myocardial infarction. Her chest X-ray confirmed 505

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forceps delivery was performed and a healthy female infant with an Apgar scorz of 10 at one minute was delivered. The baby weighed 3.095 kg. Immediately after delivery, the patient became dyspnoeic and cyanosed and crepitations were audible at both lung bases. She experienced no chest pain. Oxygen was given via a face mask and 40 mg. of frusemide was administered intravenously. Oxytocics were initially withheld but a sudden postpartum haemorrhage of 1000 ml. from a uterus which remained atonic despite bimanual massage, necessitated the intravenous administration of 0.25 mg. of ergometrine. The vaginal haemorrhage ceased and her cardiovascular status rapidly improved. An electrocardiograph at this time revealed no evidence of fresh infarction. On the first day after delivery she was mobilized and treatment with 40 mg. of oral frusemide daily and potassium supplements commenced. Oral ampicillin, 500 mg., was given six-hourly for the first five postpartum days. Anticoagulant therapy was considered unnecessary and oestrogens were withheld for suppressing lactation, mild analgesics and firm breast binding being used to overcome mild engorgement. The haemoglobin concentration 72 hours following delivery was 10.8 gjl00 ml. The patient remained well throughout the puerperium and was discharged on the fourteenth day postpartum on potassium supplements, diuretic and haematinic therapy. Postnatal examination at 6 weeks showed no evidence of cardiorespiratory embarrassment and the diuretic and potassium supplements were discontinued. Because of the risk of a similar thrombotic episode in a future pregnancy, sterilization was advised. However her husband had elected to have a vasectomy operation performed in the near future.

DISCUSSION Reviewing myocardial infarction during pregnancy, Husaini (1971) shows that in only one previous case was rheumatic heart disease a complicating factor (Goldberger and Pokress, 1950). In this particular case, the patient, aged 37 was also known to have tertiary syphilis. Diagnosis of myocardial infarction in the

pregnant patient presents clinical difficulties. Fletcher et al. (1967) and Ginz (1970) state that the most reliable evidence of obstructive coronary disease depends on electrocardiographic analysis after allowing for normal pregnancy changes. Management of myocardial infarction in pregnancy involves treatment of the acute episode and attention to the safest method of management for the remainder of the pregnancy. Initial therapy does not differ from that used in non-pregnant patients with the exception that anticoagulants are used more liberally. Thirteen of the 45 previously described patients with myocardial infarction in pregnancy received anticoagulants. Hirsh et al. (1970) state that choice of anticoagulant and careful control are important and its maintenance after mobilization of the patient of questionable value, a policy which was adopted in this patient. Should angina persist following treatment, termination of the pregnancy would appear to be of therapeutis value (Pfaffenschlager, 1964; Listo and Bjorkenheim, 1966; Husaini, 1971). The management of labour poses certain difficulties. Spontaneous onset of labour should be anticipated, but if for other reasons induction of labour is indicated it is suggested that a technique of low amniotomy with simultaneous intravenous infusion of prostaglandin be adopted under antibiotic cover. The antidiuretic effect of oxytocin at term (Abdul-Karim and Assali, 1961; Assali et al., 1960; Douglas, 1965) and intrinsic ability of oxytocin to affect myocardial function and coronary flow (Pauerstein, 1973) contraindicate its use for the induction of labour. Prostaglandins have no antidiuretic properties or detrimental effects upon the cardiovascular system of pregnant women (Karim et al., 1971). Indeed, animal experiments have shown that prostaglandins, particularly the E series have pronounced coronary vasodilator action (Mantegazza, 1965; Vergraesen et al., 1967 and Willebrands and Tasseron, 1968). Theoretically, therefore, prostaglandin E2 would appear to be the drug of choice for induction of labour. Analgesia in labour may conveniently be obtained by the epidural route. Prophylactic shortening of the second stage of labour, as for any patient with heart disease, is advised.

MYOCARDIAL INFARCTION IN PREGNANCY

It is generally recommended that oxytocics be withheld during the third stage of labour due to their potential vasoconstrictive activity, and used only in emergency. Caesarean section is not indicated unless obstetric indications supervene. Only 12 of the previously reported patients were delivered by this means. REFERENCES Abdul-Karim, R., and Assali, N. S. (1961): Journal of Laboratory Clinical Medicine, 51, 522. Assali, N. S., Digram, W. J., and Longo, L. (1960): Journal of Clinical Endocrinology, 20, 58. Douglas, C. P. (1965): Clinical Science, 28, 39. Fletcher, E., Knox, E. W. and Morton, P. (1967): British Medical Journal, 3, 586. Ginz, B. (1970): Journal of Obstetrics and Gynaecology of the British Commonwealth, 11,610.

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Goldberger, E. and Pokress, M. J. (1950): New York State Journal of Medicine, 50, 95. Hirsch, J., Cade, J. F., and Sullivan, E. F. (1970): British Medical Journal, 1, 270. Husaini, M. H . (1971): Postgraduate Medical Journal, 47, 660. Karim, S. M. M., Hillier, K., Somers, K. and Trussell, R. R. (1971): Journal of Obstetrics and Gynaecology of the British Commonwealth, 78, 172. Listo, M., and Bjorkenheim, G. (1966): Acta obstetricia et gynecologica Scandinavica, 45, 268. Mmtegazza, P. (1965): Atti della Accademia rnedica lombarda, 20. 66. Pauerstein, C. J. (1973): Clinical Obstetrics and Cynecology, Vol. 16, No. 4, 279. Pfaffenschlager, F. (1964): Wiener Klinische Wochenschrifr, 16, 297. Vergraesen, A. J., De Boer, J., and Gottenbos, J. J. (1967): Prostaglandins. Edited by S. Bergstrom and B. Sammuelsson. Almqvist and Wiksell, p. 21 1. Willebrands, A. F., and Tasseron, S. J. A. (1968): American Journal of Physiology, 215, 1089.

Myocardial infarction and rheumatic heart disease in pregnancy. Case report.

Myocardial infarction is a rare complication of pregnancy, only 45 proven cases having been reported. In only one patient was rheumatic heart disease ...
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