American Journal of Emergency Medicine xxx (2015) xxx–xxx
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Painless thyroiditis-induced acute myocardial infarction with normal coronary arteries☆,☆☆ Acute myocardial infarction (AMI) is a common life-threatening disease 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 spontaneously 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 electrocardiogram (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 myocarditis, 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 diagnosed the patient with painless thyroiditis (thyrotoxic phase) and concluded 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 common symptom in patients with hyperthyroidism; however, AMI, as occurred 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 excluded 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 thyrotoxicosis associated with painless thyroiditis (thyrotoxic stage). Painless thyroiditis, accounting for approximately 0.5% to 5% of all thyrotoxicosis 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 thyrotoxicosis 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 thyrotoxicosis/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. β-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 thyroiditis, 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 symptoms and signs; and unexplainable arrhythmia, such as sinus tachycardia 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/© 2015 Elsevier Inc. All rights reserved.
Please cite this article as: Zheng W, et al, Painless thyroiditis-induced acute myocardial infarction with normal coronary arteries, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2014.12.071
2
W. Zheng et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
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.
Please cite this article as: Zheng W, et al, Painless thyroiditis-induced acute myocardial infarction with normal coronary arteries, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2014.12.071
W. Zheng et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
3
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 restoration 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
Please cite this article as: Zheng W, et al, Painless thyroiditis-induced acute myocardial infarction with normal coronary arteries, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2014.12.071
4
Author
Current study
Year
Age Sex Angiograpic findings
Arrhythmia
Characteristic symptoms and signs/thyroid medical history
Diagnosis
TSH level
Free T3 Free T4 (pg/mL) (ng/dL)
Treatment
Follow-up Outcomes
Aspirin, clopidogrel, isosorbide dinitrate, diltiazem, and propranolol Aspirin, clopidogrel, and isosorbide dinitrate
24 mo
Normal thyroid function & well
1 mo
Asymptomatic
(μUI/mL)
2014
21
M
Normal coronary arteries
Sinus tachycardia
Palpitation and tremor
Painless thyroiditis
0.034
7.21
33.76
Zheng et al [1] 2014
26
M
Sinus tachycardia
NA/medical history
Painless thyroiditis
NA
NA
NA
Bouabdallaoui 2013 et al [2]
23
F
NA
NA
Graves disease
b0.005
NA
NA
NA
3 mo/3 y
Patane et al [10] 2012
75
F
AF
NA/medical history
0.003
2.77
1.53
NA
NA
2012
48
F
NA
NA
Subclinical hyperthyroidism Graves disease
Thrombus disappearance/ well NA
Lee et al [11]
0.031
26
NA
Kauffels et al 2012 [12] Hama et al [13] 2012
55
F
0.04
11.4
5.15
Normal thyroid function/ well NA
F
b0.03
10.5
1.89
Carbimazole, isosorbide dinitrate, nifedipine Ivabradine, parathyroidectomy NA
2 mo/1.5 y NA
25
NA
Died
Kim et al [3]
2011
35
M
12 mo
Patane et al [14] 2010
78
M
Normal thyroid function NA
2010
31
F
Patane et al [16] 2010
90
M
Normal coronary arteries and myocardial bridging over LAD Normal coronary arteries and distal LAD thrombosis Normal coronary arteries Normal coronary arteries Normal coronary arteries Left coronary artery thrombosis (autopsy) Normal coronary arteries Severe 3 vessels diseases Spasm of LAD and narrowing of LAD apical segment NA
Lewandowski et al [15]
Sinus NA/medical history tachycardia Tachycardia Cardiopulmonary arrest/medical history
Thyrotoxicosis after parathyroidectomy Subclinical hyperthyroidism
NA
NA
Painless thyroiditis
0.04
NA
4.51
AF
NA
Subclinical hyperthyroidism Graves disease
0.068
2.07
0.02
Subclinical hyperthyroidism
0.071
Tachycardia Palpitation and tremor AF
NA
1.06
Diltiazem, isosorbide dinitrate NA
NA
3.24
12.78
Thiamazole
18 mo
Normal thyroid function
1.66
NA
NA
NA
NA
W. Zheng et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
Please cite this article as: Zheng W, et al, Painless thyroiditis-induced acute myocardial infarction with normal coronary arteries, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2014.12.071
Table Summary of reported patients with thyrotoxicosis-induced AMI since 2000
63
M
Iwanczuk [18]
2010
51
F
Patane et al [19] 2009
28
M
Patane et al [20] 2009
67
F
Patel et al [21] 2008
40
F
Ostial spasm of LM and RCA
Chudleigh et al 2007 [22]
36
F
Left main stem stenosis
Chudleigh et al 2007 [22] Gowda et al [23] 2003
59
F
51
F
Normal coronary arteries Normal coronary arteries Total occlusion of LAD and LCX due to vasospasm Normal coronary arteries
Lassnig et al [24]
2003
66
F
Timurkaynak et al [25]
2002
28
F
Normal coronary arteries NA
AF
Palpitation
Subclinical hyperthyroidism Thyroid storm
0.082
3.14
1.20
NA
NA
NA
NA
Cardiogenic shock
0.009
4.71
13.73
NA
NA
NA/ medical history
Iatrogenic hyperthyroidism
0.008
8.17
NA
Inotropic support, thiamazole, β-blockers, iodine solution, glucocorticoids, and diuretics Aspirin, intravenous heparin, nitroglycerin, tirofiban
Normal coronary arteries and myocardial bridging over the LAD Normal coronary arteries
NA
NA
NA
PST/AF
NA
Subclinical hyperthyroidism
0.009
3.04
1.4
NA
NA
Tachycardia Weight loss
Graves disease
b0.1
NA
3.7
Aspirin, intravenous heparin, nitroglycerin, tirofiban, clopidogrel, bisoprolol Isosorbide dinitrate, metoprolol, and methimazole
4 mo/1 y
Tachycardia Goiter with bruit, tremor and ophthalmopathy/ medical history NA Goiter
Graves disease
b0.02
NA
32.7
Propylthiouracil, propranolol, warfarin, and radioactive iodine
6 wk
Normal thyroid function/ recurrent angina with elevated fT4 Normal thyroid function
Graves disease
b0.02
NA
12.59
NA
NA
Iatrogenic hyperthyroidism Graves disease
b0.01
2.43
2.3
4 mo
Asymptomatic
0.01
6.48
43.6
Carbimazole, diltiazem, and conventional cardiac treatment Standard anti-ischemic therapy and levothyroxine Thiamazol, nitrates, anesthetized and mechanically ventilated
Graves disease
0.01
14.83
5.1
NA
NA/medical history
NA
Hyperthyroid state
Tachycardia NA
Propylthiouracil, β-blocker, and angiotensin receptor blocker
At Died discharge 6 mo
Normal thyroid function
W. Zheng et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
Please cite this article as: Zheng W, et al, Painless thyroiditis-induced acute myocardial infarction with normal coronary arteries, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2014.12.071
Patane et al [17] 2010
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.
5
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W. Zheng et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
References [1] Zheng Y, Shen BT, Dai YM, Zhao XZ, Zheng Y, Zhao W. Acute myocardial infarction associated with painless thyroiditis. Am J Med Sci 2014;348(3):266–7. http://dx.doi.org/10.1097/maj.0000000000000309 [published Online First: Epub Date]. [2] Bouabdallaoui N, Mouquet F, Ennezat PV. Acute myocardial infarction with normal coronary arteries associated with subclinical Graves disease. Am J Emerg Med 2013;31(12):1721.e1–2. http://dx.doi.org/10.1016/j.ajem.2013.07.023 [published Online First: Epub Date]. [3] Kim HJ, Jung TS, Hahm JR, Hwang SJ, Lee SM, Jung JH, et al. Thyrotoxicosisinduced acute myocardial infarction due to painless thyroiditis. Thyroid 2011; 21(10):1149–51. http://dx.doi.org/10.1089/thy.2010.0428 [published Online First: Epub Date]. [4] Klein I, Ojamaa K. Thyroid hormone and the cardiovascular system. N Engl J Med 2001;344(7):501–9. http://dx.doi.org/10.1056/NEJM200102153440707 [published Online First: Epub Date]. [5] Grais IM, Sowers JR. Thyroid and the heart. Am J Med 2014;127(8):691–8. http://dx. doi.org/10.1016/j.amjmed.2014.03.009 [published Online First: Epub Date]. [6] Schwartz F, Bergmann N, Zerahn B, Faber J. Incidence rate of symptomatic painless thyroiditis presenting with thyrotoxicosis in Denmark as evaluated by consecutive thyroid scintigraphies. Scand J Clin Lab Invest 2013;73(3):240–4. http://dx.doi.org/ 10.3109/00365513.2013.769623 [published Online First: Epub Date]. [7] Vitug AC, Goldman JM. Silent (painless) thyroiditis. Evidence of a geographic variation in frequency. Arch Intern Med 1985;145(3):473–5. [8] Hiraiwa T, Tsujimoto N, Tanimoto K, Terasaki J, Amino N, Hanafusa T. Use of color Doppler ultrasonography to measure thyroid blood flow and differentiate Graves' disease from painless thyroiditis. Eur Thyroid J 2013;2(2):120–6. http://dx.doi.org/ 10.1159/000350560 [published Online First: Epub Date]. [9] Intenzo CM, Capuzzi DM, Jabbour S, Kim SM, dePapp AE. Scintigraphic features of autoimmune thyroiditis. Radiographics 2001;21(4):957–64. http:// dx.doi.org/10.1148/radiographics.21.4.g01jl17957 [published Online First: Epub Date]. [10] Patane S, Marte F, Sturiale M. Acute myocardial infarction without significant coronary stenoses associated with endogenous subclinical hyperthyroidism. Int J Cardiol 2012;156(1):e1–3. http://dx.doi.org/10.1016/j.ijcard.2009.12.014 [published Online First: Epub Date]. [11] Lee CP, Lee WL, Lai HC, Ting CT, Wang KY, Liu TJ. Recurrent vasodilator-refractory acute coronary syndrome as the exclusive manifestation of Graves disease. Am J Emerg Med 2012;30(8):1656 e5–9. http://dx.doi.org/10.1016/j.ajem.2011.07.026 [published Online First: Epub Date]. [12] Kauffels A, Lee IO, Schilling MK, Slotta JE. Thyrotoxicosis after parathyroidectomy mimicking myocardial infarction: a case report and review of the literature. Clin Res Cardiol 2012;101(8):687–90. http://dx.doi.org/10.1007/s00392-012-0446-0 [published Online First: Epub Date].
[13] Hama M, Abe M, Kawaguchi T, et al. A case of myocardial infarction in a young female with subclinical hyperthyroidism. Int J Cardiol 2012;158(2):e23–5. http:// dx.doi.org/10.1016/j.ijcard.2011.10.038 [published Online First: Epub Date]. [14] Patane S, Marte F. Paroxysmal atrial fibrillation during acute myocardial infarction associated with subclinical hyperthyroidism, severe three vessels coronary artery disease and elevation of prostate-specific antigen after TURP. Int J Cardiol 2010; 138(2):e28–30. http://dx.doi.org/10.1016/j.ijcard.2008.06.040 [published Online First: Epub Date]. [15] Lewandowski KC, Rechcinski T, Krzeminska-Pakula M, Lewinski A. Acute myocardial infarction as the first presentation of thyrotoxicosis in a 31-year old woman - case report. Thy Res 2010;3(1). http://dx.doi.org/10.1186/1756-6614-3-1 [published Online First: Epub Date]. [16] Patane S, Marte F. Paroxysmal ventricular tachycardia and paroxysmal atrial fibrillation associated with subclinical hyperthyroidism, chronic renal failure and elevation of prostate-specific antigen during acute myocardial infarction. Int J Cardiol 2010; 138(3):e44–6. http://dx.doi.org/10.1016/j.ijcard.2008.06.062 [published Online First: Epub Date]. [17] Patane S, Marte F. Atrial fibrillation and acute myocardial infarction without significant coronary stenoses associated with subclinical hyperthyroidism and erythrocytosis. Int J Cardiol 2010;145(1):e36–9. http://dx.doi.org/10.1016/j.ijcard.2008.12.135 [published Online First: Epub Date]. [18] Iwanczuk W. Myocardial infarction and shock associated with thyrotoxicosis. Anestezjol Intens Ter 2010;42(3):142–6. [19] Patane S, Marte F, Patane F, Di Bella G, Chiofalo S, Cinnirella G, et al. Acute myocardial infarction in a young patient with myocardial bridge and elevated levels of free triiodothyronine. Int J Cardiol 2009;132(1):140–2. http://dx.doi.org/10.1016/j. ijcard.2007.07.153 [published Online First: Epub Date]. [20] Patane S, Marte F, Di Bella G, Turiano G. Acute myocardial infarction and subclinical hyperthyroidism without significant coronary stenoses. Int J Cardiol 2009;134(3):e135–7. http://dx.doi.org/10.1016/j.ijcard.2008.03.011 [published Online First: Epub Date]. [21] Patel R, Peterson G, Rohatgi A, Ghayee HK, Keeley EC, Auchus RJ, et al. Hyperthyroidismassociated coronary vasospasm with myocardial infarction and subsequent euthyroid angina. Thyroid 2008;18(2):273–6. http://dx.doi.org/10.1089/thy.2007.0131 [published Online First: Epub Date]. [22] Chudleigh RA, Davies JS. Graves' thyrotoxicosis and coronary artery spasm. Postgrad Med J 2007;83(985):e1–2. http://dx.doi.org/10.1136/pgmj.2007.062299 [published Online First: Epub Date]. [23] Gowda RM, Khan IA, Soodini G, Vasavada BC, Sacchi TJ. Acute myocardial infarction with normal coronary arteries associated with iatrogenic hyperthyroidism. Int J Cardiol 2003;90(2–3):327–9. [24] Lassnig E, Berent R, Auer J, Eber B. Cardiogenic shock due to myocardial infarction caused by coronary vasospasm associated with hyperthyroidism. Int J Cardiol 2003;90(2–3):333–5. [25] Timurkaynak T, Aydogdu G, Cengel A. Acute myocardial infarction secondary to thyrotoxicosis. Acta Cardiol 2002;57(6):439–42.
Please cite this article as: Zheng W, et al, Painless thyroiditis-induced acute myocardial infarction with normal coronary arteries, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2014.12.071
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Painless thyroiditis-induced acute myocardial infarction with normal coronary arteries☆,☆☆ Acute myocardial infarction (AMI) is a common life-threatening disease 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 spontaneously 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 electrocardiogram (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 myocarditis, 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 diagnosed the patient with painless thyroiditis (thyrotoxic phase) and concluded 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 common symptom in patients with hyperthyroidism; however, AMI, as occurred 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 excluded 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 thyrotoxicosis associated with painless thyroiditis (thyrotoxic stage). Painless thyroiditis, accounting for approximately 0.5% to 5% of all thyrotoxicosis 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 thyrotoxicosis 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 thyrotoxicosis/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. β-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 thyroiditis, 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 symptoms and signs; and unexplainable arrhythmia, such as sinus tachycardia 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/© 2015 Elsevier Inc. All rights reserved.
Please cite this article as: Zheng W, et al, Painless thyroiditis-induced acute myocardial infarction with normal coronary arteries, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2014.12.071
2
W. Zheng et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
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.
Please cite this article as: Zheng W, et al, Painless thyroiditis-induced acute myocardial infarction with normal coronary arteries, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2014.12.071
W. Zheng et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
3
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 restoration 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
Please cite this article as: Zheng W, et al, Painless thyroiditis-induced acute myocardial infarction with normal coronary arteries, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2014.12.071
4
Author
Current study
Year
Age Sex Angiograpic findings
Arrhythmia
Characteristic symptoms and signs/thyroid medical history
Diagnosis
TSH level
Free T3 Free T4 (pg/mL) (ng/dL)
Treatment
Follow-up Outcomes
Aspirin, clopidogrel, isosorbide dinitrate, diltiazem, and propranolol Aspirin, clopidogrel, and isosorbide dinitrate
24 mo
Normal thyroid function & well
1 mo
Asymptomatic
(μUI/mL)
2014
21
M
Normal coronary arteries
Sinus tachycardia
Palpitation and tremor
Painless thyroiditis
0.034
7.21
33.76
Zheng et al [1] 2014
26
M
Sinus tachycardia
NA/medical history
Painless thyroiditis
NA
NA
NA
Bouabdallaoui 2013 et al [2]
23
F
NA
NA
Graves disease
b0.005
NA
NA
NA
3 mo/3 y
Patane et al [10] 2012
75
F
AF
NA/medical history
0.003
2.77
1.53
NA
NA
2012
48
F
NA
NA
Subclinical hyperthyroidism Graves disease
Thrombus disappearance/ well NA
Lee et al [11]
0.031
26
NA
Kauffels et al 2012 [12] Hama et al [13] 2012
55
F
0.04
11.4
5.15
Normal thyroid function/ well NA
F
b0.03
10.5
1.89
Carbimazole, isosorbide dinitrate, nifedipine Ivabradine, parathyroidectomy NA
2 mo/1.5 y NA
25
NA
Died
Kim et al [3]
2011
35
M
12 mo
Patane et al [14] 2010
78
M
Normal thyroid function NA
2010
31
F
Patane et al [16] 2010
90
M
Normal coronary arteries and myocardial bridging over LAD Normal coronary arteries and distal LAD thrombosis Normal coronary arteries Normal coronary arteries Normal coronary arteries Left coronary artery thrombosis (autopsy) Normal coronary arteries Severe 3 vessels diseases Spasm of LAD and narrowing of LAD apical segment NA
Lewandowski et al [15]
Sinus NA/medical history tachycardia Tachycardia Cardiopulmonary arrest/medical history
Thyrotoxicosis after parathyroidectomy Subclinical hyperthyroidism
NA
NA
Painless thyroiditis
0.04
NA
4.51
AF
NA
Subclinical hyperthyroidism Graves disease
0.068
2.07
0.02
Subclinical hyperthyroidism
0.071
Tachycardia Palpitation and tremor AF
NA
1.06
Diltiazem, isosorbide dinitrate NA
NA
3.24
12.78
Thiamazole
18 mo
Normal thyroid function
1.66
NA
NA
NA
NA
W. Zheng et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
Please cite this article as: Zheng W, et al, Painless thyroiditis-induced acute myocardial infarction with normal coronary arteries, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2014.12.071
Table Summary of reported patients with thyrotoxicosis-induced AMI since 2000
63
M
Iwanczuk [18]
2010
51
F
Patane et al [19] 2009
28
M
Patane et al [20] 2009
67
F
Patel et al [21] 2008
40
F
Ostial spasm of LM and RCA
Chudleigh et al 2007 [22]
36
F
Left main stem stenosis
Chudleigh et al 2007 [22] Gowda et al [23] 2003
59
F
51
F
Normal coronary arteries Normal coronary arteries Total occlusion of LAD and LCX due to vasospasm Normal coronary arteries
Lassnig et al [24]
2003
66
F
Timurkaynak et al [25]
2002
28
F
Normal coronary arteries NA
AF
Palpitation
Subclinical hyperthyroidism Thyroid storm
0.082
3.14
1.20
NA
NA
NA
NA
Cardiogenic shock
0.009
4.71
13.73
NA
NA
NA/ medical history
Iatrogenic hyperthyroidism
0.008
8.17
NA
Inotropic support, thiamazole, β-blockers, iodine solution, glucocorticoids, and diuretics Aspirin, intravenous heparin, nitroglycerin, tirofiban
Normal coronary arteries and myocardial bridging over the LAD Normal coronary arteries
NA
NA
NA
PST/AF
NA
Subclinical hyperthyroidism
0.009
3.04
1.4
NA
NA
Tachycardia Weight loss
Graves disease
b0.1
NA
3.7
Aspirin, intravenous heparin, nitroglycerin, tirofiban, clopidogrel, bisoprolol Isosorbide dinitrate, metoprolol, and methimazole
4 mo/1 y
Tachycardia Goiter with bruit, tremor and ophthalmopathy/ medical history NA Goiter
Graves disease
b0.02
NA
32.7
Propylthiouracil, propranolol, warfarin, and radioactive iodine
6 wk
Normal thyroid function/ recurrent angina with elevated fT4 Normal thyroid function
Graves disease
b0.02
NA
12.59
NA
NA
Iatrogenic hyperthyroidism Graves disease
b0.01
2.43
2.3
4 mo
Asymptomatic
0.01
6.48
43.6
Carbimazole, diltiazem, and conventional cardiac treatment Standard anti-ischemic therapy and levothyroxine Thiamazol, nitrates, anesthetized and mechanically ventilated
Graves disease
0.01
14.83
5.1
NA
NA/medical history
NA
Hyperthyroid state
Tachycardia NA
Propylthiouracil, β-blocker, and angiotensin receptor blocker
At Died discharge 6 mo
Normal thyroid function
W. Zheng et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
Please cite this article as: Zheng W, et al, Painless thyroiditis-induced acute myocardial infarction with normal coronary arteries, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2014.12.071
Patane et al [17] 2010
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.
5
6
W. Zheng et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
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Please cite this article as: Zheng W, et al, Painless thyroiditis-induced acute myocardial infarction with normal coronary arteries, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2014.12.071
