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Avi Shimony, Sergiy Bereza, Aryeh Shalev, Harel Gilutz, Reuben Ilia and Doron Zahger
American Heart Hospital Journal Volume 7 No.1

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We describe a case of a young adult in whom sudden cardiac death due to ventricular fibrillation was the presenting manifestation of an adrenocortical carcinoma. The arrhythmia was precipitated by severe hypokalemia induced by the aldosterone-secreting tumor. Sudden death has not been previously described as a manifestation of this adrenal neoplasm. Unexplained persistent hypokalemia after resuscitated sudden death (especially when combined with hypertension) should prompt investigation for an underlying secondary hypertension, particularly adrenal pathology. Adrenocortical carcinoma should be considered in the differential diagnosis of unexplained sudden death associated with unexplained hypokalemia.

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Various endocrine disorders, mainly those affecting the thyroid or adrenal glands, can lead to lethal cardiac arrhythmias including torsade de pointes and ventricular fibrillation (VF) through excess or insufficient hormone activity and electrolyte imbalance.^1-3Severe hypokalemia is frequent in most forms of adrenal tumor, but sudden death is a most unusual presentation of an adrenal tumor. We describe for the first time a case of an aldosterone-producing adrenocortical carcinoma presenting as VF due to severe hypokalemia.

Case Description
A 31-year-old male patient was admitted to our intensive cardiac care unit (ICCU) after out-of-hospital cardiac arrest. The patient was married with no children and was taking no medications. Apart from smoking, there were no known coronary risk factors. There was no personal history of substance abuse and no family history of sudden death. A week prior to admission, the patient complained of new-onset 'heartburn,' which was treated by an antacid.

On the day of admission the patient collapsed without preceding signs during his morning prayers. Basic life support was not provided. Paramedics found him 15 minutes later in VF and administered defibrillation and advanced cardiac life support. Upon admission to the ICCU the patient experienced two more episodes of VF, which were successfully terminated by defibrillation. Physical examination upon admission was normal except for a blood pressure of 200/130mmHg. The admission electrocardiogram (ECG) was normal. Induced hypothermia was initiated using external cooling for 24 hours. Laboratory tests were unremarkable except for a potassium level of 2.3mmol/l. Echocardiography revealed preserved biventricular function, no left ventricular hypertrophy, and normal valvular function. The patient was extubated 48 hours after admission and was quickly ambulated. He remained neurologically intact except for mild amnesia. Coronary angiography revealed normal coronary arteries. The patient continued to demonstrate persistent hypokalemia and high blood pressure for a few days, both of which responded to treatment with an angiotensin-converting enzyme inhibitor and spironolactone.

Further history obtained from family members shortly after admission indicated that the patient had been admitted to another hospital one month earlier due to right flank pain, which was demonstrated to be the result of a retroperitoneal hematoma surrounding and obscuring the right kidney. The patient was discharged and ambulatory magnetic resonance imaging (MRI) was scheduled one month later to allow for resolution of the hematoma. The patient sustained his episode of sudden death before the MRI could be performed.

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