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Thyroid storm: A rare and life-threatening cause of acute neurological manifestations during urgent percutaneous coronary intervention for acute coronary syndrome.

Acute neurological complications during coronary angiography (CAG) are extremely uncommon with an incidence of < 0.1% [1] but they remain a challenging clinical problem, particularly in patients with acute coronary syndrome. Periprocedural ischemic or hemorrhagic stroke remains the most common cause with an incidence of 0.07–0.38% and is associated with high rates of morbidity and mortality [2]. However, sudden-onset neurological symptoms during diagnostic CAG or percutaneous coronary intervention (PCI) may result from rarer albeit fatal neurological or endocrine conditions, such as seizure, encephalopathy, contrast media-induced neurotoxicity or acute thyrotoxicosis [3]. Thyroid storm (TS) is a life-threatening endocrine emergency that represents the extreme manifestation of acute thyrotoxicosis and is associated with high morbidity and mortality (10%) rates if left untreated [3, 4]. Herein is reported a 70-year-old woman with arterial hypertension, pacemaker implantation for sick sinus syndrome and paroxysmal atrial fibrillation on long-term amiodarone therapy, who was admitted to the emergency department with acute typical chest pain. The patient underwent previous coronary artery bypass grafting with left internal mammary artery (LIMA) to the left anterior descending artery (LAD) and saphenous vein graft to the right coronary artery (RCA) 16 years earlier, followed by PCI to the distal RCA with a drugeluting stent 9 years later. Three weeks prior to admission, the patient presented with weight loss, tremor and palpitations suggestive of thyrotoxicosis, with decreased levels of thyroid stimulating hormone (< 0.005 mIU/L, normal range 0.4– –4.0 mIU/L), and elevated levels of free thyroxine (T4) (93 pmol/L, normal range 11–27 pmol/L) and free tri-iodothyronine (T3) (16.5 pmol/L, normal range 0.8–2.7 pmol/L), suggestive of amiodarone-induced thyrotoxicosis (anti-TSH receptor antibody: < 3 U/L). Amiodarone therapy was discontinued and an antithyroid drug (carbimazole 20 mg/day) was initiated with reduction of free T4 (70 pmol/L) and T3 (15 pmol/L) levels at 3-week follow-up. The thyroid ultrasound showed a slightly enlarged and heterogeneous thyroid gland, but excluded a nodular formation as well as hypervascularisation. Upon present admission, electrocardiogram demonstrated ST-segment depression from V3 to V6 leads and cardiac biomarkers were elevated. The CAG demonstrated a 3-vessel coronary artery disease with occlusion of the saphenous vein graft to RCA, involution of the LIMA graft to LAD, 50% distal left main coronary artery stenosis, obtuse marginal branches and intermediate artery stenoses, 50% distal RCA in-stent restenosis, and hemodynamically significant proximal LAD stenosis. The patient underwent PCI to the proximal LAD with a drug-eluting stent. During the procedure, the patient developed acute neurological symptoms including headache, agitation, delirium, confusion, nausea and vomiting, that required CLINICAL CARDIOLOGY