SAT-595 Ventricular Fibrillation as a Manifestation of Hyperthyroidism

Background: Thyrotoxicosis is a known cause of atrial arrhythmias however, ventricular arrhythmias in this setting are rare. We report a case of ventricular fibrillation (VF) in a patient with Graves hyperthyroidism in the absence of coronary disease. Clinical Case: A 55-year old woman with hypertension and a self-reported thyroid nodule presented with a two week history of general malaise, palpations, diarrhea and muscle aches. Her mother had a goiter and paternal aunt required a thyroidectomy. Both her father and paternal uncle died at age 58 and 60 respectively of myocardial infarction. She was tachycardic to 125 beats per minute (bpm) and had a firm goiter with no bruit and normal reflexes. TSH was <0.01, free T4 > 6.99 ng/dL (n= 0.7-2.19 ng/dL), total T3 > 7.81 ng/mL (n=0.97 -1.7 ng/mL), thyroid stimulating immunoglobulin 516 % (n= <140%), and thyroid binding inhibitory immunoglobulin was 82.5% (n=<16%). Treatment with dexamethasone, methimazole, and propranolol was initiated. Homogenous increased uptake was seen in the thyroid gland on nuclear medicine scan. On day two of admission, her total T3 remained > 7.81 ng/mL despite therapy but her heart rate was better controlled at 100 bpm. However, that night she suffered a 40- minute cardiac arrest from VF. Spontaneous circulation was restored after multiple shocks, amiodarone and lidocaine, and then temporary pacing for bradycardia. She received a total of 440mg of propranolol and 40mg of methimazole prior to cardiac arrest. Serum potassium was normal pre arrest but rose to 6.9 mmol/L (n=3.5-5.1 mmol/L) after. Given the bradycardia, glucagon was given for possible beta blocker toxicity although this was thought to be unlikely as telemetry did not reveal pre-arrest bradycardia. There was no evidence of a coronary event since admission troponin was negative and post arrest troponin was only mild elevated with a flat trend. No wall motion abnormality was see on echocardiogram and ventricular function was preserved. Cardiac catheterization was deferred due to declining renal function. Subsequent myocardial perfusion imaging displayed only an apical cap artifact and coronary CT angiogram was free from atherosclerosis. She had no further arrhythmias. An implantable cardioverter defibrillator was placed prior to discharge for secondary prevention of ventricular arrhythmias. Conclusion: VF in the absence of underlying coronary disease or heart failure is rare in thyrotoxicosis. Thyroid hormone induced coronary vasospasm and activation of regionally varied beta-adrenergic receptors are proposed mechanisms for VF. Further, some individuals may have genetic predisposition to this in the setting of hyperthyroidism. This case highlights the urgency of achieving a euthyroid state and closely monitoring individuals with a family or personal history of ventricular arrhythmias or sudden cardiac death.