Storm and STEMI: a case report of unexpected cardiac complications of thyrotoxicosis

Abstract

Background: Thyroid storm is a rare condition with well-known cardiovascular manifestations including tachycardia, atrial fibrillation, heart failure, and myocardial infarction (MI). Several uncommon conditions that can mimic MI are associated with thyrotoxicosis and discussed in this case.

Case summary: A 23-year-old previously healthy male presented after the onset of generalized weakness and inability to rise from bed in the setting of 35 kg of unintentional weight loss, and was found to have profound hypokalaemia, elevated thyroid hormone, and suppressed thyroid-stimulating hormone consistent with thyrotoxicosis secondary to Grave's disease. Following hospital admission, he developed worsening tachycardia with dynamic anteroseptal ST-segment elevations and elevated cardiac biomarkers concerning for MI. He was treated with aspirin, ticagrelor, and a heparin infusion, but was unable to tolerate beta-blockade acutely due to hypotension. Echocardiography demonstrated a severely dilated left ventricle (left ventricular end-diastolic volume index 114 mL/m²) and severely reduced systolic function (ejection fraction 23%) with global hypokinesis. Following initiation of propylthiouracil, iodine solution, and stress-dosed steroids his tachycardia and ST-elevations resolved. Computed tomography (CT) coronary angiography demonstrated no evidence of coronary stenosis. He was discharged on methimazole, metoprolol, and lisinopril and found to have recovered left ventricular systolic function at 2-month follow-up.

Discussion: Thyrotoxicosis can rarely cause coronary vasospasm, stress cardiomyopathy, and autoimmune myocarditis. These conditions should be suspected in hyperthyroid patients with features of MI and normal coronary arteries. Workup should include laboratory evaluation, electrocardiography (ECG), echocardiography, and non-invasive or invasive ischaemic evaluation.

Keywords: Cardiomyopathy; Case report; Myocardial infarction; Myocarditis; Thyrotoxicosis; Vasospasm.

Figure 1

12-lead ECG upon transfer to our hospital (top panel) demonstrating sinus tachycardia with minimal ST-elevations in V1–V3. Second ECG following admission to the medical intensive care unit (bottom panel) demonstrating worsening sinus tachycardia with increasing ST-elevations in leads V1–V4 (arrows). Note the lack of reciprocal ST-depressions.

Figure 2

3D-reconstructed image from CT coronary angiography showing the left main, proximal left anterior descending, and proximal left circumflex coronary arteries. Full linear reconstructions of the right and left coronary arteries were unable to be obtained due to significant artefact. Following radiologist review of several cardiac phases, there was no evidence of atherosclerosis, stenosis, or thrombosis.