Case Report

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American Journal of Emergency Medicine

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American Journal of Emergency Medicine 33 (2015) 983.e5-983.e10

Painless thyroiditis-induced acute myocardial infarction with Normal coronary arteries?,??

Acute myocardial infarction (AMI) is a common life-threatening dis- ease in the emergency department. However, it is rare that AMI is induced by painless thyroiditis in an individual with normal coronary arteries. Here, we describe a very rare case of thyroiditis-induced AMI and review the literature concerning patients with thyrotoxicosis-related AMI.

A 21-year-old man, without a history of Tobacco use, recreational drug abuse, or inherited Cardiovascular risk factors, presented with a sudden onset of chest pain when he slept. Three days prior, he had experienced a similar chest pain after drinking alcohol, which spontane- ously relieved after a few minutes. On presentation, his heart rate was 95 beats per minute, and blood pressure was 168/82 mm Hg. Marked ST-segment elevation in II, III, aVF, and V7 to V9 was found on electro- cardiogram (ECG) (Fig. 1). Levels of troponin I rose to 11.1 ng/mL and Creatine phosphokinase (CK)-MB to 27.70 ng/mL (Fig. 2). However, echocardiography showed no wall-motion abnormalities or ventricle dysfunction (ejection fraction, 54%). emergency coronary angiography revealed normal coronary arteries with no sign of coronary dissection or atherosclerosis (Fig. 3; Videos 1 and 2). No further procedures were implemented, and medical treatment was chosen.

The patient had no clinical or biological signs suggestive of myocar- ditis, myocardial bridging, early repolarization syndrome, Behcet disease, lupus erythematosus, Antiphospholipid syndrome, or Takayasu disease. Upon 2 days’ complaining of persistent palpitation (~ 95-110 beats per minute) and tremor, the patient was subjected to thyroid function testing. The test revealed thyrotoxicosis, but the titers for antithyrotropin receptor and thyroid-stimulating antibody were negative (Table). Thyroid ultrasound showed a smooth thyroid without focal lesions. A technetium Tc 99m pertechnetate scan indicated markedly low thyroid uptake, compatible with thyroiditis. We diag- nosed the patient with painless thyroiditis (thyrotoxic phase) and con- cluded that thyrotoxicosis had induced Coronary vasospasm, resulting in AMI. The patient was treated with diltiazem and propranolol. He did not report any chest pain during the 24-month follow-up period.

Thyrotoxicosis alters the cardiovascular hemodynamics by increasing the heart rate, cardiac contractility, and cardiac output and by decreasing systemic vascular resistance [4,5]. In this way, thyrotoxicosis increases the risk of angina pectoris and AMI by coronary vasospasm. Angina is a com- mon symptom in patients with hyperthyroidism; however, AMI, as oc- curred in our patient, is infrequently observed [1,3]. Our patient was first diagnosed with AMI, but the coronary angiographic results showed no signs of stenosis, occlusion, or atherosclerotic changes. Thus, we ex- cluded the possibility of thrombolytic myocardial infarction and assumed

? Conflict of interest: No conflict of interest.

?? Patient consent: Obtained.

that the symptoms were caused by a temporary coronary vasospasm. Subsequent tests suggested that the spasm could be induced by thyro- toxicosis associated with painless thyroiditis (thyrotoxic stage).

Painless thyroiditis, accounting for approximately 0.5% to 5% of all thy- rotoxicosis cases, is diagnosed by increased free T4 and free T3 levels for less than 3 months and/or later development of transient hypothyroidism without neck pain or tenderness [6,7]. This condition is caused by the destruction of thyroid follicles and the release of excess thyroid hormones into the circulation. Painless thyroiditis often manifests as transient thyro- toxicosis and displays symptoms similar to those of Graves disease. The combined application of thyroid function test, thyroid antibodies test, and scintigraphy is helpful in the differential diagnosis [2,8,9].

We reviewed all 21 AMI patients (including our patient) with thyro- toxicosis/thyroiditis who have been reported in the English literature since 2000 (Table). Most cases (15/21) presented between the ages of 20 and 60 years (mean age, 47 years), with a female predominance (female: male, 14:7). Patients usually had severe, persistent chest pain with onset at rest. Associated symptoms included arrhythmias (sinus tachycardia and atrial fibrillation), dyspnea, and sudden cardiac death. Approximately 25% of patients exhibited palpitation, tremor, or other hyperthyroid-state symptoms. A thyroid medical history or recent weight loss was valuable diagnostic clues in 6 of 21 patients. The physical examination was similar to that of other patients with AMI. A goiter or thyroid eye signs were sometimes found. Initial ECG manifested as typical AMI changes, but initial angiography often revealed normal coronary arteries (13/21) or coronary vasospasm (3/21) without thrombolytic occlusion. Patients were diagnosed with Graves disease (8/21), subclinical hyperthyroidism (6/21), painless thyroiditis (3/21), iatrogenic thyrotoxicosis (2/21), and postoperational thyrotoxicosis (1/21). Thyroid function and thyroid uptake of technetium Tc 99m provide evidence for diagnosis. ?-Blocker was the first choice of therapy in most patients, given the combination of AMI with thyrotoxicosis; however, nitrates and calcium antagonists should be considered because coronary vasospasm is also present. Symptoms were often self-limiting with excellent prognosis (18/21). Recurrent angina (1/21) or death (2/21) occasionally occurred.

In conclusion, thyrotoxicosis, especially induced by painless thyroid- itis, should be considered when patients manifest with typical AMI but with normal angiographic results and no cardiovascular disease risk factors. Age; sex; medical history; state of onset; characteristic symp- toms and signs; and unexplainable arrhythmia, such as sinus tachycar- dia or atrial fibrillation, could provide valuable diagnostic clues. We suggest that routine thyroid function tests should be performed for AMI patients with normal angiogram.

Supplementary data to this article can be found online at http://dx. doi.org/10.1016/j.ajem.2014.12.071.

0735-6757/(C) 2015

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Fig. 1. Evolution of ECG. A, The ECG on admission showed ST-segment elevation of lead II, III, aVF, and V7 to V9, diagnosed as an acute inferior and posterior myocardial infarction. B and C, A typical evolution of acute myocardial infarction including ST-segment resolution and Q-wave formation.

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Fig. 2. Changes in cardiac troponin I and CK-MB after admission. The evolution of cardiac enzymes was generally in accordance with changes typical of AMI. Earlier peak and quicker res- toration to normal level were observed because of less myocardial injury caused by spasm. Reference ranges of cardiac enzymes are as follows: cardiac troponin I, less than 0.034 ng/mL; CK-MB, less than 3.38 ng/mL.

Fig. 3. coronary angiogram. A and B, Normal coronary arteries were observed on angiogram.

Acknowledgment

The authors thank Medjaden Bioscience Limited for assisting in the preparation of this manuscript.

Wen Zheng, MD, PhD Yu-Jiao Zhang, MD, PhD Shu-Yan Li, MD, PhD

Department of Cardiology, the First Hospital of Jilin University, Changchun, China

E-mail addresses: [email protected] [email protected], [email protected]

Lu-Lun Liu, MD

Thyroid Surgery Department, the First Hospital of

Jilin University, Changchun, China E-mail address: [email protected]

Jian Sun, MD, PhD Department of Cardiology, the First Hospital of Jilin University, Changchun, China

Corresponding author. Department of Cardiology the First Hospital of Jilin University, Changchun, China, 130021. Tel.: +86-13943085420

E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2014.12.071

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Table

Summary of reported patients with thyrotoxicosis-induced AMI since 2000

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Abbreviations: TSH, thyroid-stimulating hormone; Free T3, free triiodothyronine; Free T4, free thyroxine; M, male; LAD, left anterior descending coronary artery; NA, not available or not mentioned; F, female; AF, atrial fibrillation; PST, Paroxysmal supraventricular tachycardia; LM, left main coronary artery; LCX, left circumflex coronary artery; RCA, right coronary artery.

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