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A 28 year old white woman had an unplanned home birth due to a short second stage of labour. A healthy boy was delivered vaginally with a midwife in attendance. Before delivering the placenta the patient was given 1 ml of intramuscular Syntometrine (ergometrine maleate 500 μg, oxytocin 5 units; Novartis, Surrey, UK). The placenta and membranes were delivered completely with minimal blood loss. Fifteen minutes later the patient complained of severe central chest tightness radiating to both arms and associated with profuse sweating, nausea, and breathlessness. She was transferred to a local maternity hospital for further assessment.
On admission her ECG showed ST segment elevation across the chest leads with 6 mm of ST elevation in leads V4 and V5 confirming an acute anterior myocardial infarction (MI). She was transferred to the coronary care unit at a nearby district general hospital. Thrombolysis was withheld due to the risk of postpartum haemorrhagic complications and she was immediately transferred to a tertiary referral centre 25 miles away where she underwent emergency cardiac catheterisation.
The patient had been well previously with no cardiac symptoms and two entirely uncomplicated pregnancies. However, she was a heavy smoker and hypercholesterolaemia was diagnosed after both parents died from coronary artery disease in their early 40s.
Coronary angiography revealed diffuse three vessel coronary artery disease with an acute occlusion in the proximal left anterior descending coronary artery (TIMI grade 0 flow) (fig 1A). The occlusion was dilated with a 3 mm balloon followed by insertion of a 9 mm NIR stent with a good angiographic result (fig 1B). TIMI grade 3 flow was restored to the infarct related artery within half an hour of arrival at the tertiary centre (5.5 hours after the onset of chest pain). A subsequent ECG showed resolution of ST elevation and Q waves in leads V1–4. Creatinine kinase (CK) peaked at 9858 U/l (8% CK-MB isoenzyme). Echocardiography showed anteroseptal hypokinesis but other segments of the left ventricle contracted well. Her recovery was uncomplicated.
Acute MI occurs rarely in women of childbearing age and has a reported incidence in pregnancy of 1 in 10 000.1 MI is more frequent during the third trimester and puerperium of the first and second pregnancies and most commonly involves the left anterior descending artery territory. In the immediate postpartum period spontaneous coronary artery dissection is the most common cause of MI.2 In 20% of cases of MI in pregnancy, thrombus is identified without angiographically visible atherosclerotic disease. A combination of transient coronary artery spasm and the hypercoagulable state of pregnancy may lead to coronary thrombosis.
In most maternity units Syntometrine is given routinely at the time of delivery of the placenta and membranes to reduce postpartum haemorrhage. Ergometrine is a potent vasoconstrictor, which is also used in provocation testing for coronary vasospasm. Refractory vasospasm culminating in MI is a recognised complication in this setting, and occlusive coronary artery spasm leading to in situ thrombosis has been shown angiographically.3 However, there have been only two previous reports of MI resulting from postpartum use of ergometrine.4 ,5 In both reports the patients had angiographically normal coronary arteries. In our report the patient had extensive coronary atherosclerosis, which may have enhanced the vasoconstrictor response to ergometrine.
Treatment of MI in pregnancy and the puerperium is complicated as thrombolytics are contraindicated. PTCA is a viable alternative, although there are only eight reported cases of PTCA in pregnancy and the puerperium. To our knowledge this is the first reported case of primary PTCA carried out immediately after delivery and only the second report of intracoronary stenting for acute MI in pregnancy.
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