A 49-year-old man was brought to the Emergency Department in a comatose mental state. He had experienced nocturnal chest pain lasting a few minutes over the previous week. On the morning of presentation, he woke up with severe chest pain and collapsed. Cardiopulmonary resuscitation was initiated and continued en route to the hospital by emergency medical services personnel. Shortly after arrival, spontaneous circulation returned. He had no previous history of diabetes, hypertension, hepatitis, and pulmonary tuberculosis. He was a 30-pack-year current smoker. His family history was non-specific. His blood pressure was 127/83 mmHg and his pulse rate was 146 beats per minute. On auscultation of the chest, inspiratory crackles were heard in both lungs. His initial electrocardiogram (ECG) showed sinus tachycardia with marked ST-segment elevation in the precordial leads (Fig. 1A). A repeat ECG after successful resuscitation revealed resolution of ST-segment elevation (Fig. 1B). The levels of cardiac biomarkers were elevated: creatine kinase 2,854 U/L (35-172), CK-MB 186 U/L (2.3-9.5), and troponin I 56.49 ng/ml (0-0.05). The chest X-ray demonstrated bilateral pulmonary congestion.
Two-dimensional echocardiography showed, however, normal left ventricular systolic function (ejection fraction = 65%) without regional wall motion abnormality. After therapeutic hypothermia for 2 days, his mental state recovered and he was extubated on the 4th hospital day. A closer physical examination disclosed proptosis and anterior neck swelling, and the results of thyroid function testing were compatible with Graves’ disease: TSH <0.01 uIU/ml (0.35-5.5), free T4 3.97 ng/dl (0.89-1.76), and thyroid-binding inhibitory immunoglobulin 61% (0-15). Thyroid ultrasonography showed diffuse thyroid enlargement with hypervascularity (Fig. 2). Diagnostic coronary angiography was performed on hospital day 9, which revealed no significant fixed stenosis in either coronary artery (Fig. 3). Two days later, ergonovine provocation testing was performed to exclude coronary artery spasm. After the second bolus injection of ergonovine (10 ug), severe multiple spasms occurred in the left anterior descending artery (LAD) and left circumflex artery (LCx) (Fig. 4). The patient complained of chest pain, and his ECG showed ST depression in the anterior wall. Intracoronary injection of nitroglycerin promptly relieved the symptoms and the spasms. Intravenous ultrasound revealed mild soft plaque in the LAD and LCx (Fig. 5). He was discharged home on day 28, after an uneventful recovery, with a regimen of aspirin 100 mg, valsartan 160 mg, diltiazem hydrochloride 180 mg, isosorbide dinitrate 40 mg, nicorandil 10 mg, and propylthiouracil 300mg daily. At six-month follow-up, he remained symptom-free and his thyroid function returned to normal.
The cardiovascular effects of hyperthyroidism are well established and are related to a hyperadrenergic state and an agonist effect of calcium in the myocardium. Hyperthyroidism as a cofactor for coronary vasospasm has also been described, but the exact underlying mechanisms are not fully explained. Our case suggests causality in the association between hyperthyroidism and coronary vasospasm, which, if sufficiently prolonged, may provoke myocardial infarction and fatal arrhythmia, leading to sudden cardiac death. It also highlights the significance of searching for the signs of thyrotoxicosis and determining thyroid function in patients with sudden cardiac death secondary to coronary artery spasm. Treatment should include calcium channel blockers or nitrates in addition to anti-thyroid drugs. Once the diagnosis of hyperthyroidism is established, medical therapy usually suffices, although, in refractory cases, radioactive iodine ablation or surgery may be necessary.