SAT-468 Anticoagulation Conundrum: A Case Of Embolic Stroke Due To Thyrotoxic Atrial Fibrillation

Abstract

Background: Thyrotoxicosis is not incorporated into any of the atrial fibrillation (AF) CVA risk stratification methods, including CHADS2VASc, as neither the American College of Cardiology/American Heart Association nor the American College of Chest Physicians view it as an independent risk factor of CVA. However, the literature has reported numerous cases of patients with thyrotoxic AF and low CHADS2VASc scores who developed CVA. It is unclear which patients with thyrotoxic AF would benefit from prophylactic anticoagulation (AC). Clinical Case: A 50-year-old male without past medical history presented for palpitations. He was found to be in AF with rapid ventricular rate. Labs revealed thyrotoxicosis (TSH <0.010 [RR 0.34-5.6 μIU/mL], FT4 3.57 [RR 0.61-1.64 ng/dL], FT3 5.26 [RR 2.5-4.5 pg/mL], and TSI negative). He was started on methimazole but no AC, as his CHADS2VASc score was 0. A few hours after admission, he developed a right-sided facial droop and weakness & aphasia. CT head showed acute left MCA infarct. CTA head/neck revealed occlusive embolus in the distal left M1 segment. He underwent IR-guided embolectomy and received intra-arterial tPA. Echocardiogram did not show thrombi or atrial level shunt but showed right atrial dilation. After extensive work-up, etiology of CVA was determined most likely a cardioembolic source due to thyrotoxic AF. Patient was treated with PTU and steroids initially for two days due to recent contrast exposure (CTA and embolectomy) and poor neurologic status, in order to obtain the added benefit of decreased T4 to T3 peripheral conversion. Patient was started on AC two weeks after his CVA (given initial risk of hemorrhagic conversion due to large CVA burden), at which time his weakness and aphasia were slowly improving, but he remained with significant neurologic deficits. Discussion: The current thought that thyrotoxicosis is not an independent risk factor of CVA in patients with AF has led to recommendations against prophylactic AC for this specific group. Although recent research has suggested that patients with thyrotoxic AF are at a lower risk of CVA than patients with non-thyrotoxic AF, there have still been many reported cases of CVA in patients who have thyrotoxic AF but no other risk factors for CVA. This discrepancy in association between thyrotoxic AF and CVA needs to be clarified. Conclusion: This case of a middle-aged man with thyrotoxic AF who developed a debilitating CVA after being treated according to his CHADS2VASC score of 0 (he was not given prophylactic AC) mirrors multiple cases in the literature. It highlights the potential benefit of examining thyrotoxic patients with AF more closely in order to more effectively risk stratify them for CVA or further exploring the relationship between thyrotoxicosis and CVA. This may help to identify more patients who could benefit from AC and thus prevent devastating consequences of CVA.