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SUN-248 A Case of Ventricular Fibrillation Triggered by Thyroid Storm

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Abstract Disclosure: A. Deswal: None. A. Marrium: None. A. Kumar: None. Introduction: Hyperthyroidism is known to induce supraventricular arrhythmias, including atrial fibrillation and atrial flutter, with atrial fibrillation occurring in approximately 20% of affected patients. Ventricular arrhythmias are uncommon in hyperthyroidism. The majority of reported cases of ventricular fibrillation are associated with hypokalemia in the context of thyroid periodic paralysis. This case report highlights an unusual manifestation of thyroid storm leading to ventricular fibrillation (VF) in the absence of hypokalemia. Case presentation: A 41-year-old male with a medical history significant for hyperthyroidism, paroxysmal atrial fibrillation, and hypertension, who was non-compliant with his methimazole and metoprolol, presented to our facility after experiencing a ventricular fibrillation cardiac arrest at home. Upon arrival, he was in normal sinus rhythm with a heart rate of 128 and a BP of 100/72 mm Hg. Initial laboratory workup showed TSH < 0.010 uIU/mL ( 0.270-4.200 uIU/mL), T4 5.15 ng/dL (0.5-1.6 ng/dL), T3 266 ng/dL (80-187 ng/dL), high-sensitivity troponin of 3,886, potassium 4.1 mEq/L, and magnesium 2.6 mEq/L. Post-arrest EKG showed normal sinus rhythm. An echocardiogram revealed global hypokinesis with an ejection fraction (EF) of 10-15%. The patient was started on methimazole and hydrocortisone to manage his thyroid storm. Amiodarone was briefly used to stabilize his cardiac rhythm. He underwent cardiac catheterization, which showed no obstructive coronary arteries, and his EF improved to 45% within a week. He also developed atrial fibrillation with rapid ventricular response, which was treated with propranolol. Eventually, the patient underwent tracheostomy, PEG tube placement, and thyroidectomy. He was discharged home. Discussion: One of the mechanisms by which thyroid hormones may contribute to the onset of VF is by enhancing adrenergic receptor activity, which can trigger coronary artery spasm and silent myocardial ischemia, thereby precipitating ventricular arrhythmias.In this case, various potential etiologies for VF were considered, including ischemic heart disease, structural heart disease, and electrolyte imbalances such as hypo- or hyperkalemia. The initial echocardiogram revealed a low EF. This could either reflect pre-existing tachycardia-induced cardiomyopathy or an acute result of stunned myocardium following cardiac arrest. A coronary angiogram revealed clean coronary arteries, making ischemic heart disease an unlikely cause of the VF. Additionally, since the patient's potassium levels were normal, thyroid periodic paralysis was ruled out. Taking all these factors into account, ventricular fibrillation due to thyroid storm in conjunction with low EF of heart appears to be the most probable cause of this out-of-hospital cardiac arrest. Presentation: Sunday, July 13, 2025
Title: SUN-248 A Case of Ventricular Fibrillation Triggered by Thyroid Storm
Description:
Abstract Disclosure: A.
Deswal: None.
A.
Marrium: None.
A.
Kumar: None.
Introduction: Hyperthyroidism is known to induce supraventricular arrhythmias, including atrial fibrillation and atrial flutter, with atrial fibrillation occurring in approximately 20% of affected patients.
Ventricular arrhythmias are uncommon in hyperthyroidism.
The majority of reported cases of ventricular fibrillation are associated with hypokalemia in the context of thyroid periodic paralysis.
This case report highlights an unusual manifestation of thyroid storm leading to ventricular fibrillation (VF) in the absence of hypokalemia.
Case presentation: A 41-year-old male with a medical history significant for hyperthyroidism, paroxysmal atrial fibrillation, and hypertension, who was non-compliant with his methimazole and metoprolol, presented to our facility after experiencing a ventricular fibrillation cardiac arrest at home.
Upon arrival, he was in normal sinus rhythm with a heart rate of 128 and a BP of 100/72 mm Hg.
Initial laboratory workup showed TSH < 0.
010 uIU/mL ( 0.
270-4.
200 uIU/mL), T4 5.
15 ng/dL (0.
5-1.
6 ng/dL), T3 266 ng/dL (80-187 ng/dL), high-sensitivity troponin of 3,886, potassium 4.
1 mEq/L, and magnesium 2.
6 mEq/L.
Post-arrest EKG showed normal sinus rhythm.
An echocardiogram revealed global hypokinesis with an ejection fraction (EF) of 10-15%.
The patient was started on methimazole and hydrocortisone to manage his thyroid storm.
Amiodarone was briefly used to stabilize his cardiac rhythm.
He underwent cardiac catheterization, which showed no obstructive coronary arteries, and his EF improved to 45% within a week.
He also developed atrial fibrillation with rapid ventricular response, which was treated with propranolol.
Eventually, the patient underwent tracheostomy, PEG tube placement, and thyroidectomy.
He was discharged home.
Discussion: One of the mechanisms by which thyroid hormones may contribute to the onset of VF is by enhancing adrenergic receptor activity, which can trigger coronary artery spasm and silent myocardial ischemia, thereby precipitating ventricular arrhythmias.
In this case, various potential etiologies for VF were considered, including ischemic heart disease, structural heart disease, and electrolyte imbalances such as hypo- or hyperkalemia.
The initial echocardiogram revealed a low EF.
This could either reflect pre-existing tachycardia-induced cardiomyopathy or an acute result of stunned myocardium following cardiac arrest.
A coronary angiogram revealed clean coronary arteries, making ischemic heart disease an unlikely cause of the VF.
Additionally, since the patient's potassium levels were normal, thyroid periodic paralysis was ruled out.
Taking all these factors into account, ventricular fibrillation due to thyroid storm in conjunction with low EF of heart appears to be the most probable cause of this out-of-hospital cardiac arrest.
Presentation: Sunday, July 13, 2025.

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