International Journal of Cardiology 171 (2014) e129–e130
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Acute pericarditis: Unique comorbidity of thyrotoxic crisis with Graves' disease Toru Inami a,⁎, Yoshihiko Seino a, Hiroki Goda b, Hirotake Okazaki b, Akihiro Shirakabe b, Masanori Yamamoto b, Fumitaka Okajima c, Naoya Emoto c, Noritake Hata b, Wataru Shimizu d a
Department of Cardiology, Nippon Medical School Chiba Hokusoh Hospital, Chiba, Japan Department of Intensive Care Unit, Nippon Medical School Chiba Hokusoh Hospital, Chiba, Japan Department of Endocrinolgy, Nippon Medical School Chiba Hokusoh Hospital, Chiba, Japan d Department of Cardiovascular Medicine, Nippon Medical School, Tokyo, Japan b c
a r t i c l e
i n f o
Article history: Received 22 September 2013 Accepted 20 December 2013 Available online 28 December 2013 Keywords: Acute pericarditis Graves' disease Thyroid crisis
Acute pericarditis is a common disorder caused by inflammation of the pericardium and relatively common in clinical practice. Pericarditis accounts for 0.1% of hospitalized patients and 5% of emergency department visits for chest pain without myocardial infarction [1]. The common etiologies of acute pericarditis were viral, bacterial, myocardial infarction, and autoimmune diseases [2], however the relationship between acute pericarditis and thyrotoxic crisis associated Graves' disease is very rare. A 69-year-old female was transported to the emergency department with retrosternal chest pain and fever. In the emergency room, she had disturbance of consciousness. The results of her examination were a body temperature of 38.0 °C, blood pressure of 184/70 mm Hg and heart rate of 150 beats per minute. Her medical history revealed rheumatoid arthritis which was well controlled and we could not find any exacerbating signs of rheumatoid arthritis. The chest pain increased with deep breathing and position change. Electrocardiogram showed diffuse ST-segment elevation in all leads except aVR and V1. Diffuse PR-segment depression was present except in lead aVR which showed ST elevation (Fig. 1A), though the elevation of troponin T was not documented. Transthoracic echocardiography showed normal left ventricular contraction and the absence of pericardial effusion. Chest computed tomography revealed thickening pericardium without pericardial effusion
⁎ Corresponding author at: Department of Cardiology, Nippon Medical School Chiba Hokusoh Hospital, 1715 Kamagari, Inzai, Chiba 270-1694, Japan. Tel.: +81 476 99 1111; fax: +81 476 99 1908. E-mail address: [email protected] (T. Inami).
0167-5273/$ – see front matter © 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.12.042
(Fig. 2A). Laboratory analysis revealed an elevation in the white-cell count, C-reactive protein, free T3 of more than 30.0 pg/mL, and free T4 of 5.47 ng/dL. Thyroid-stimulating hormone (TSH) was below 0.10 μIU/mL. TSH receptor antibody was 17.7 IU/L. Thyroid scan showed 23%uptake (Fig. 2B). The patient was diagnosed with acute pericarditis and thyrotoxic crisis associated with Graves' disease. There were no signs of increases of immunoglobulin M antibodies suggesting acute viral disease, such as coxsackie virus, adenovirus and echo virus. The patient was given ibuprofen and colchicine for pericarditis [3]. We also admitted beta adrenergic receptor blockade for tachycardia and methimazole for Graves' disease. The symptoms respond promptly and improved. ST elevation disappeared in one week (Fig. 1B). Four weeks after the administration, the patient showed a biochemically euthyroid state. Graves' disease is the disorder of the thyroid gland resulting primarily from autoimmune processes, which stimulate the overproduction of thyroid hormones. The typical Graves' cardiac complications are atrial fibrillation, tachycardia induced cardiomyopathy, and heart failure. Pericardial effusion is a well-known complication of hypothyroidism, however thyrotoxicosis has been identified as a rare complication of acute pericarditis. A few reports noted the coexistence of Graves' thyrotoxicosis and acute pericarditis [4,5]. They did not describe the clear mechanism or etiological association between two diseases. It is very difficult to identify whether these two diseases represented coincident existence or underlying etiologic association between acute pericarditis and Graves' disease. There might be a possibility that the autoantibody or viral infection in Graves' disease contributes to the direct or indirect interaction with the some receptors on the pericardium, because the causes of acute pericarditis included systemic autoimmune diseases and viral infection. The most common types of pericardial involvement with autoimmune diseases are acute pericarditis. Data from several studies on acute pericarditis revealed that a systemic autoimmune disease was responsible for acute pericarditis in 2–7% of cases [6,7]. Autoimmunity and autoinflammation play an important role in the pathogenesis of idiopathic recurrent pericarditis [8]. As of viral infection, some noted that Epstein Barr virus (EBV) can be the cause of Graves' disease [9] and pericarditis [10]. There might be a possibility that the immune reaction plays an etiologic and mechanistic role in the development of acute pericarditis in the patient with Graves' disease.
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T. Inami et al. / International Journal of Cardiology 171 (2014) e129–e130
Fig. 1. Panel A showed that electrocardiogram revealed diffuse ST-segment elevation in all leads except aVR and V1. Panel B showed the time course of changes in the electrocardiogram.
Fig. 2. Panel A showed that chest computed tomography revealed thickening pericardium and bilateral pleural effusion. Thyroid scan showed 23%uptake in panel B.
The etiology of acute pericarditis is not clear in many of the cases, with about 20% of patients designated a specific etiological diagnosis [2]. Practical physicians should consider the possible existence of Graves' thyrotoxicosis as an underlying etiology in differential diagnosis of acute pericarditis. References [1] Spodick DH. Acute cardiac tamponade. N Engl J Med 2003;349:684–90. [2] Zayas R, Anguita M, Torres F, et al. Incidence of specific etiology and role of methods for specific etiologic diagnosis of primary acute pericarditis. Am J Cardiol 1995;75:378–82. [3] Lilly LS. Treatment of acute and recurrent idiopathic pericarditis. Circulation 2013;127:1723–6.
[4] Sugar SJ. Pericarditis as a complication of thyrotoxicosis. Arch Intern Med 1981;141:1242. [5] Tsai MS, Yang CW, Chi CL, Hsieh CC, Chen WJ, Huang CH. Acute pericarditis: a rare complication of Graves' thyrotoxicosis? Am J Emerg Med 2006;24:374–5. [6] Permanyer-Miralda G, Sagrista-Sauleda J, Soler-Soler J. Primary acute pericardial disease: a prospective series of 231 consecutive patients. Am J Cardiol 1985;56:623–30. [7] Imazio M, Cecchi E, Demichelis B, et al. Indicators of poor prognosis of acute pericarditis. Circulation 2007;115:2739–44. [8] Cantarini L, Imazio M, Brizi MG, et al. Role of autoimmunity and autoinflammation in the pathogenesis of idiopathic recurrent pericarditis. Clin Rev Allergy Immunol 2013;44:6–13. [9] Nagata K, Fukata S, Kanai K, et al. The influence of Epstein–Barr virus reactivation in patients with Graves' disease. Viral Immunol 2011;24:143–9. [10] Zafrir B, Aviv A, Reichman N, Flatau E. Epstein–Barr virus-associated pericarditis and pericardial effusion: case report and diagnostic aspects. Eur J Intern Med 2005;16:528–30.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Acute pericarditis: Unique comorbidity of thyrotoxic crisis with Graves' disease Toru Inami a,⁎, Yoshihiko Seino a, Hiroki Goda b, Hirotake Okazaki b, Akihiro Shirakabe b, Masanori Yamamoto b, Fumitaka Okajima c, Naoya Emoto c, Noritake Hata b, Wataru Shimizu d a
Department of Cardiology, Nippon Medical School Chiba Hokusoh Hospital, Chiba, Japan Department of Intensive Care Unit, Nippon Medical School Chiba Hokusoh Hospital, Chiba, Japan Department of Endocrinolgy, Nippon Medical School Chiba Hokusoh Hospital, Chiba, Japan d Department of Cardiovascular Medicine, Nippon Medical School, Tokyo, Japan b c
a r t i c l e
i n f o
Article history: Received 22 September 2013 Accepted 20 December 2013 Available online 28 December 2013 Keywords: Acute pericarditis Graves' disease Thyroid crisis
Acute pericarditis is a common disorder caused by inflammation of the pericardium and relatively common in clinical practice. Pericarditis accounts for 0.1% of hospitalized patients and 5% of emergency department visits for chest pain without myocardial infarction [1]. The common etiologies of acute pericarditis were viral, bacterial, myocardial infarction, and autoimmune diseases [2], however the relationship between acute pericarditis and thyrotoxic crisis associated Graves' disease is very rare. A 69-year-old female was transported to the emergency department with retrosternal chest pain and fever. In the emergency room, she had disturbance of consciousness. The results of her examination were a body temperature of 38.0 °C, blood pressure of 184/70 mm Hg and heart rate of 150 beats per minute. Her medical history revealed rheumatoid arthritis which was well controlled and we could not find any exacerbating signs of rheumatoid arthritis. The chest pain increased with deep breathing and position change. Electrocardiogram showed diffuse ST-segment elevation in all leads except aVR and V1. Diffuse PR-segment depression was present except in lead aVR which showed ST elevation (Fig. 1A), though the elevation of troponin T was not documented. Transthoracic echocardiography showed normal left ventricular contraction and the absence of pericardial effusion. Chest computed tomography revealed thickening pericardium without pericardial effusion
⁎ Corresponding author at: Department of Cardiology, Nippon Medical School Chiba Hokusoh Hospital, 1715 Kamagari, Inzai, Chiba 270-1694, Japan. Tel.: +81 476 99 1111; fax: +81 476 99 1908. E-mail address: [email protected] (T. Inami).
0167-5273/$ – see front matter © 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.12.042
(Fig. 2A). Laboratory analysis revealed an elevation in the white-cell count, C-reactive protein, free T3 of more than 30.0 pg/mL, and free T4 of 5.47 ng/dL. Thyroid-stimulating hormone (TSH) was below 0.10 μIU/mL. TSH receptor antibody was 17.7 IU/L. Thyroid scan showed 23%uptake (Fig. 2B). The patient was diagnosed with acute pericarditis and thyrotoxic crisis associated with Graves' disease. There were no signs of increases of immunoglobulin M antibodies suggesting acute viral disease, such as coxsackie virus, adenovirus and echo virus. The patient was given ibuprofen and colchicine for pericarditis [3]. We also admitted beta adrenergic receptor blockade for tachycardia and methimazole for Graves' disease. The symptoms respond promptly and improved. ST elevation disappeared in one week (Fig. 1B). Four weeks after the administration, the patient showed a biochemically euthyroid state. Graves' disease is the disorder of the thyroid gland resulting primarily from autoimmune processes, which stimulate the overproduction of thyroid hormones. The typical Graves' cardiac complications are atrial fibrillation, tachycardia induced cardiomyopathy, and heart failure. Pericardial effusion is a well-known complication of hypothyroidism, however thyrotoxicosis has been identified as a rare complication of acute pericarditis. A few reports noted the coexistence of Graves' thyrotoxicosis and acute pericarditis [4,5]. They did not describe the clear mechanism or etiological association between two diseases. It is very difficult to identify whether these two diseases represented coincident existence or underlying etiologic association between acute pericarditis and Graves' disease. There might be a possibility that the autoantibody or viral infection in Graves' disease contributes to the direct or indirect interaction with the some receptors on the pericardium, because the causes of acute pericarditis included systemic autoimmune diseases and viral infection. The most common types of pericardial involvement with autoimmune diseases are acute pericarditis. Data from several studies on acute pericarditis revealed that a systemic autoimmune disease was responsible for acute pericarditis in 2–7% of cases [6,7]. Autoimmunity and autoinflammation play an important role in the pathogenesis of idiopathic recurrent pericarditis [8]. As of viral infection, some noted that Epstein Barr virus (EBV) can be the cause of Graves' disease [9] and pericarditis [10]. There might be a possibility that the immune reaction plays an etiologic and mechanistic role in the development of acute pericarditis in the patient with Graves' disease.
e130
T. Inami et al. / International Journal of Cardiology 171 (2014) e129–e130
Fig. 1. Panel A showed that electrocardiogram revealed diffuse ST-segment elevation in all leads except aVR and V1. Panel B showed the time course of changes in the electrocardiogram.
Fig. 2. Panel A showed that chest computed tomography revealed thickening pericardium and bilateral pleural effusion. Thyroid scan showed 23%uptake in panel B.
The etiology of acute pericarditis is not clear in many of the cases, with about 20% of patients designated a specific etiological diagnosis [2]. Practical physicians should consider the possible existence of Graves' thyrotoxicosis as an underlying etiology in differential diagnosis of acute pericarditis. References [1] Spodick DH. Acute cardiac tamponade. N Engl J Med 2003;349:684–90. [2] Zayas R, Anguita M, Torres F, et al. Incidence of specific etiology and role of methods for specific etiologic diagnosis of primary acute pericarditis. Am J Cardiol 1995;75:378–82. [3] Lilly LS. Treatment of acute and recurrent idiopathic pericarditis. Circulation 2013;127:1723–6.
[4] Sugar SJ. Pericarditis as a complication of thyrotoxicosis. Arch Intern Med 1981;141:1242. [5] Tsai MS, Yang CW, Chi CL, Hsieh CC, Chen WJ, Huang CH. Acute pericarditis: a rare complication of Graves' thyrotoxicosis? Am J Emerg Med 2006;24:374–5. [6] Permanyer-Miralda G, Sagrista-Sauleda J, Soler-Soler J. Primary acute pericardial disease: a prospective series of 231 consecutive patients. Am J Cardiol 1985;56:623–30. [7] Imazio M, Cecchi E, Demichelis B, et al. Indicators of poor prognosis of acute pericarditis. Circulation 2007;115:2739–44. [8] Cantarini L, Imazio M, Brizi MG, et al. Role of autoimmunity and autoinflammation in the pathogenesis of idiopathic recurrent pericarditis. Clin Rev Allergy Immunol 2013;44:6–13. [9] Nagata K, Fukata S, Kanai K, et al. The influence of Epstein–Barr virus reactivation in patients with Graves' disease. Viral Immunol 2011;24:143–9. [10] Zafrir B, Aviv A, Reichman N, Flatau E. Epstein–Barr virus-associated pericarditis and pericardial effusion: case report and diagnostic aspects. Eur J Intern Med 2005;16:528–30.
