Thyroid hormones, mainly triiodothyronine, have genomic and non-genomic effects on cardiomyocytes related to the contractile function of the heart. Thyrotoxicosis, which is the set of signs and symptoms derived from the excess of circulating thyroid hormones, leads to increased cardiac output and decreased systemic vascular resistance, increasing the volume of circulating blood and causing systolic hypertension. In addition, the shortening of the refractory period of cardiomyocytes produces sinus tachycardia and atrial fibrillation. This leads to heart failure. Approximately 1% of patients with thyrotoxicosis develop thyrotoxic cardiomyopathy, a rare but potentially fatal form of dilated cardiomyopathy. Thyrotoxic cardiomyopathy represents a diagnosis of exclusion, and prompt identification is crucial as it is a reversible cause of heart failure, and heart function can be recovered after achieving a euthyroid state using antithyroid drugs. Radioactive iodine therapy and surgery are not the best initial therapeutic approach. Moreover, it is important to manage cardiovascular symptoms, for which beta blockers are the first-line therapeutic option.

Challenging differential diagnosis Background:High-risk pulmonary embolism (PE) occurs when the pulmonary circulation is suddenly occluded by a thrombus and is a life-threatening medical emergency. In young and otherwise healthy individuals, there may be undiagnosed underlying risk factors for PE that require investigation. This report presents the case of a 25-yearold woman admitted as an emergency with a high-risk large and occlusive PE, later diagnosed with primary antiphospholipid syndrome (APS) and hyperhomocysteinemia. Case Report:A 25-year-old woman presented with sudden-onset dyspnea after elective cholecystectomy. One year earlier, the patient had lower limb deep vein thrombosis without an identified predisposing cause, and she received anticoagulation for 6 months. On physical examination, she had right leg edema. Laboratory tests revealed elevated levels of troponin, pro-B-type natriuretic peptide, and D-dimer. Computed tomography pulmonary angiography (CTPA) demonstrated a large and occlusive PE, and an echocardiogram showed right ventricular dysfunction. Successful thrombolysis was performed with alteplase. On repeat CTPA, a significant reduction in filling defects in the pulmonary vasculature was observed. The patient evolved uneventfully and was discharged home on a vitamin K antagonist. Due to unprovoked recurrent thrombotic events, suspicion of underlying thrombophilia was raised, and hypercoagulability studies confirmed primary APS and hyperhomocysteinemia. Conclusions:This report presents the case of a life-threatening high-risk PE in a previously healthy young woman and highlights the importance of emergency management followed by investigation and treatment of underlying risk factors for venous thromboembolism, including APS and hyperhomocysteinemia.