Dr Nayomi Perera1,2,3, Dr Freya Berenyi3, Dr Jessica V Yao3,4, Dr Sarah Price1,2
1Department of Obstetric Medicine, Royal Women's Hospital, Parkville, Australia, 2Department of Endocrinology, Royal Melbourne Hospital, Parkville, Australia, 3Department of General Medicine, Royal Melbourne Hospital, Parkville, Australia , 4Department of Cardiology, Royal Melbourne Hospital, Parkville, Australia
Biography:
Nayomi is currently the obstetric medicine fellow at the Royal Women's hospital. She has completed her training in Endocrinology and General medicine.
Abstract:
Introduction: Coronary events during pregnancy are uncommon, but represent a significant cause of morbidity and mortality in young females. The majority of these events occur in non-atherosclerotic coronary arteries, such as spontaneous coronary artery dissection, coronary spasms, thrombosis, and embolism. Physiological changes in pregnancy can increase the risk of cardiovascular events; however, a portion of individuals may also have underlying pathology.
Case: AJ 33F G2P1 34 /40 presents with chest pain, troponin 2384ng/L and an electrocardiogram with ST depression inferolateral leads. Antenatal care prior had been routine. Medical history included high risk diffuse sclerosing papillary thyroid cancer, managed with thyroidectomy, radioactive iodine and ongoing TSH suppression of <0.01ug/L. She had left sided atypical cystic kidney disease with normal renal function.
Coronary angiogram and echocardiogram were unremarkable. She was diagnosed with myocardial infarction non-occlusive coronary artery, likely triggered by TSH suppression. Thyroxine dose was reduced in consultation with Endocrinology. She was discharged with metoprolol, aspirin and multidisciplinary plan for induction of labour at 37 weeks, shortened second stage with post-partum cardiac monitoring. AJ delivered after 20 minutes of pushing, day two post-partum was complicated by chest pain and troponin 62ng/L. Cardiac MR identified a localized mid inferolateral wall lesion with late gadolinium enhancement consistent with an embolic phenomenon. Additionally, a large 12cm left sided lesion was noted thought to be consistent with known cystic disease. Bubble study was negative.
Outpatient investigation revealed grossly elevated metanephrins and normetanephrins. Dedicated adrenal imaging confirmed pheochromocytoma. Despite unopposed beta blockade and stress of normal vaginal delivery, the patient remained normotensive and asymptomatic for a pheochromocytoma crisis. Prazosin was commenced, and the patient underwent an urgent open adrenalectomy.
Conclusion: This case highlights the necessity to search for underlying causes that may be precipitating coronary events, even when other plausible explanations, such as thyroid suppression, are present.