Broad complex tachycardia caused by adrenal tumour and atrial septal defect

P Velavan¹, JL Morris²,  
¹ Academic Cardiology Unit (University of Hull), Castle Hill Hospital, Kingston upon Hull. HU16 5JQ, United Kingdom
² Cardiothoracic Centre, Thomas Drive, Liverpool. L14 3PE, United Kingdom

Correspondence Address:
P Velavan
Academic Cardiology Unit (University of Hull), Castle Hill Hospital, Kingston upon Hull. HU16 5JQ
United Kingdom

Full Text

Sir,

Catecholamine secreting tumors are under-diagnosed due to a marked variation in and intermittent nature of the presenting symptoms. We describe a patient with atrial septal defect (ASD) and adrenal tumor presenting with intermittent broad complex tachycardia.

A 49 year old man was admitted with recurrent pre-syncopal episodes associated with palpitations over 2 months. He had been started on propranolol recently, but these episodes continued. On admission, he was cold, clammy, sweating and tachycardic, but the blood pressure was normal. Examination of the chest revealed basal crackles. Electrocardiogram (ECG) showed broad complex tachycardia (atrial flutter with 1:1 conduction) with a rate of 210/m. He was cardioverted to sinus rhythm with intravenous amiodarone. Serum amylase was normal but troponin T was elevated at 0.43mg/l. He was treated as myocardial infarction and echocardiography showed an isolated ostium primum ASD with mild mitral regurgitation and good left ventricular function. A 24 hour urinary catecholamine measurement showed an elevated norepinephrine level (1644 nmol/24hrs). He continued to have further episodes of broad complex tachycardia associated with presyncope. He was then started on warfarin and amiodarone was continued orally.

A CT scan of his abdomen showed a left adrenal mass measuring 26 x 27 mm. MRI scan suggested a pheochromocytoma but MIBG scan was negative. Cardiac catheterisation demonstrated normal coronary arteries and left to right shunt through the ASD (flow ratio of 2.7:1). Elevated catecholamine levels in the left adrenal venous blood [Table 1], but further 24 hour urinary catecholamine levels were normal.

He continued to have episodes of broad complex tachycardia [Figure 1] associated with sweating, dizziness, hypertension (170/110 mmHg) and pre-syncope, despite treatment with metoprolol (200 mg bd) and phenoxybenzamine (110 mg bd). Left adrenalectomy was performed and a nodular left adrenal mass measuring 32×24×20 mm (weight 10.5 g) was found. Histology revealed a well circumscribed encapsulated cortical adenoma with no evidence of malignancy and adrenal medulla appeared normal. Immuno-histochemical evaluation was not done.

His alpha and beta blockade were discontinued following adrenalectomy and he had remained well and asymptomatic with normal subsequent 24 hour urinary catecholamine measurements. He later underwent surgical repair of ASD.

This case illustrates that catecholamine secreting tumours can present in a very atypical manner, as it was associated with an ASD and caused paroxysmal atrial flutter and troponin rise due to catecholamine release.

Adrenal cortical adenomas causing clinical features of phaeochromocytoma and elevated 24 hour urinary catecholamines have been reported rarely,[1] although many cortical adenomas are usually detected incidentally (incidentalomas).[2] Neuroendocrine differentiation, supported by immunohistochemical studies has been proposed as the mechanism of catecholamine release.[1],[3] Patients with hypertension and those on long-term beta-blocker treatment may have an increased urinary norepinephrine excretion.[4] Hence multiple 24 hour urine collections are recommended. MIBG scanning may be useful when an extra-medullary tumor is suspected, but false negative results are common. Supra-ventricular tachycardia, atrial fibrillation and ventricular tachycardia can rarely be associated with rise in troponin levels in patients with normal coronary arteries.[5]

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