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Ventricular Fibrillation Associated With Dynamic Changes in J-Point Elevation in a Patient With Silent Thyroiditis

Ventricular Fibrillation Associated With Dynamic Changes in J-Point Elevation in a Patient With... ISSN 2472-1972 Ventricular Fibrillation Associated With Dynamic Changes in J-Point Elevation in a Patient With Silent Thyroiditis 1 2 1 Shigehiro Karashima, *ToyonobuTsuda, * Yusuke Wakabayashi, 1 1,3 2 2 Mitsuhiro Kometani, Masashi Demura, Taro Ichise, Masa-aki Kawashiri, 1 2 1,4 Yoshiyu Takeda, Kenshi Hayashi, and Takashi Yoneda Division of Endocrinology and Metabolism, Graduate School of Medical Science, Kanazawa University, Kanazawa 920-8691, Japan; Division of Cardiovascular Medicine, Graduate School of Medicine, Kanazawa University, Kanazawa 920-8691, Japan; Departments of Hygiene, Graduate School of Medical Science, Kanazawa University, Kanazawa 920-8691, Japan; and Program Management Office for Paradigms Establishing Center for Fostering Medical Researchers of the Future, Kanazawa University, Kanazawa 920-8691, Japan *These authors contributed equally to this study. A J wave is a common electrocardiographic finding in the general population. Individuals with prominent J waves in multiple electrocardiogram (ECG) leads have a higher risk of lethal arrhythmias than those with low-amplitude J waves. There are few reports about the relationship between thyroid function and J-wave amplitude. We report the case of a 45-year-old man who had unexpected ventricular fibrillation (VF). He had dynamic J-point elevation in multiple ECG leads. Possible early repolarization syndrome was diagnosed. He also had thyrotoxicosis caused by silent thyroiditis, and his J-wave amplitude decreased according to changes in thyroid function because of spontaneous remission of silent thyroiditis. There was a positive correlation between serum triiodothyronine levels and J-wave am- plitudes. The findings in case suggested silent thyroiditis may contribute to the occurrence of VF in a patient with dynamic changes in J-point elevation in multiple ECG leads. Thyrotoxicosis is a relatively common endocrine disease; therefore, clinicians should pay attention to J-wave amplitude in the ECG of patients with thyrotoxicosis. Copyright © 2018 Endocrine Society This article has been published under the terms of the Creative Commons Attribution Non- Commercial, No-Derivatives License (CC BY-NC-ND; https://creativecommons.org/licenses/by-nc- nd/4.0/). Freeform/Key Words: J-wave, silent thyroiditis, thyrotoxicosis, ventricular fibrillation 1. Case Report A 45-year-old man had visited his local hospital because of paroxysmal atrial fibrillation that had started 9 years earlier. He had been taking 80 mg of verapamil and 100 mg of pilsicainide each day. His electrocardiogram (ECG) showed J-point elevation in multiple leads (II, aVF, I, aVL, V3-V6) during outpatient visits [Fig. 1(A)]. His thyroid function had been within the normal range. His mother and his brother also had J-point elevation in multiple ECG leads. The patient was found in cardiopulmonary arrest by his wife in the early morning. Basic life support was performed immediately. An automated external defibrillator detected ventric- ular fibrillation (VF), and a defibrillation shock was delivered by ambulance attendants. He was transported to Kanazawa University Hospital. On arrival, his Glasgow Coma Scale score was 6 (E1V1M4); physical examination revealed a blood pressure of 125/68 mm Hg, heart rate Abbreviations: BS, Brugada syndrome; ECG, electrocardiogram; ERS, early repolarization syndrome; FT3, free triiodothyronine; FT4, free thyroxine; JWS, J-wave syndromes; TSH, thyroid-stimulating hormone VF, ventricular fibrillation. Received 8 June 2017 Accepted 1 December 2017 February 2018 | Vol. 2, Iss. 2 First Published Online 6 December 2017 doi: 10.1210/js.2017-00276 | Journal of the Endocrine Society | 135–139 Downloaded from https://academic.oup.com/jes/article-abstract/2/2/135/4693882 by Ed 'DeepDyve' Gillespie user on 22 March 2018 136 | Journal of the Endocrine Society | doi: 10.1210/js.2017-00276 Figure 1. Electrocardiography. (A) Twelve-lead electrocardiogram recorded in the local hospital. (B) Dynamic J-wave changes associated with thyroid function. Arrow points to J wave. of 108 beats/minute, and body temperature of 36.3°C. He had no obvious thyroid swelling or exophthalmos. Laboratory data, including complete blood cell counts, and cardiac enzyme, renal function, and electrolyte levels were also within normal limits. The patient’s C-reactive protein level was 0.6 mg/dL. A thyroid function test showed the following levels: free tri- iodothyronine (FT3), 8.6 (range, 2.3 to 4.0) pg/mL; free thyroxine (FT4), 3.7 (1.0 to 1.8) ng/dL; thyroid-stimulating hormone (TSH), ,0.01 (0.27 to 4.20) mIU/L; TSH receptor antibody, 0.6 (,2) IU/L); thyroglobulin, 2.0 (3.5 to 77) ng/mL; TSH-stimulating receptor antibody, 105% (,120%); thyroperoxidase antibody, 354 (,16.0) IU/mL; and thyroglobulin antibody, 575 (,28.0) IU/mL. His serum thyroid hormone levels indicated thyrotoxicosis. Thyroid ultra- sonography and Tc-99m scintigraphy were performed and showed results compatible with silent thyroiditis. The clinical course of his thyroid function and ECG are shown in [Fig. 1(B)]. Compared with the 12-lead ECG recorded in the outpatient clinic, his ECG on day 11 after admission showed increased J-point elevation (.0.1 mV) in multiple leads (II, aVF, I, aVL, V2-V6). According to the Proposed Shanghai Score System for diagnosis of early repolarization syndrome (ERS), he had 4.5 points in total and was possible ERS was diagnosed [1]. Echocardiography and coronary angiography showed no unusual findings. A sodium-channel blocker infusion test did not result in the typical ECG pattern of Brugada syndrome (BS), and the test attenuated J-point elevation in the inferolateral leads. The patient was not treated with any antithyroid agents, thyroid hormone replacement, or b-blockers. He underwent cardioverter defibrillator implantation on day 11 and was Downloaded from https://academic.oup.com/jes/article-abstract/2/2/135/4693882 by Ed 'DeepDyve' Gillespie user on 22 March 2018 doi: 10.1210/js.2017-00276 | Journal of the Endocrine Society | 137 discharged on day 33. On day 54, FT3 and FT4 levels had changed to hypothyroid status (FT3, 2.69 pg/mL; FT4, 0.66 ng/dL; TSH, 9.73 mIU/L). J-point elevation in the ECG was decreased compared with his ECG after admission. On day 131, his serum thyroid hormone levels had returned to almost normal (FT3, 3.25 pg/mL; FT4, 1.08 ng/dL; TSH, 4.29 mIU/L), and there was no change in J-point elevation in the ECG between day 54 and day 131. There were also correlations between FT3 levels and the J-wave amplitudes in the lateral leads [Fig. 2(A)], but there were not important correlations in the inferior leads [Fig. 2(B)]. The J-wave amplitudes were measured by a previously reported method [2]. In the outpatient clinic, interrogation of the implanted cardioverter defibrillator showed no lethal arrhythmic events. 2. Discussion We report the case of a 45-year-old man with possible ERS who had an episode of unexplained VF and dynamic changes in J-point elevation in multiple ECG leads. Silent thyroiditis also was diagnosed, and there was a correlation between thyroid hormone levels and J-wave amplitudes. A J-wave, which is a positive deflection immediately following the QRS complex of the surface ECG or is, in part, buried inside the QRS as notching or slurring, is often found in the general population [1]. J waves are associated with the occurrence of lethal arrhythmic events in patients with BS, ischemic heart disease, hypertrophic cardiomyopathy, and long-QT syndrome [1, 3]. J-wave syndromes (JWS) are a spectrum of ECG manifestations of prominent J waves with a risk of VF. JWS consist of ERS and BS. This patient’s condition could be diagnosed as possible ERS by the Proposed Shanghai Score System and was classified as type 3 ERS based on the early repolarization (ER) in multiple ECG leads. Nam et al. [4] em- phasized there is high risk of sudden death in type 3 ERS compared with BS. Figure 2. Correlation between free triiodothyronine levels and the amplitudes of J waves in the (A) lateral leads and (B) inferior leads. Downloaded from https://academic.oup.com/jes/article-abstract/2/2/135/4693882 by Ed 'DeepDyve' Gillespie user on 22 March 2018 138 | Journal of the Endocrine Society | doi: 10.1210/js.2017-00276 Individuals with prominent J waves in multiple leads have a higher risk of lethal ar- rhythmias than those with low-amplitude J waves [1]. In this patient, thyrotoxicosis was thought to cause the increased J-wave amplitude and the occurrence of VF. Thyroid hormone has an important effect on cardiac muscle, particularly via the sympa- thetic nervous system [5]. Cardiac tissue contains b1- and b2-adrenergic receptor subtypes. b-blockers and parasympathetic stimulation augment the elevation of J-point and ST segment; b-stimulators and sympathetic stimulation cause them to decline [6]. Hyperthyroid status leads to an increased sensitivity of the sympathoadrenal system with more b-adrenergic re- ceptors, stimulatory guanine nucleotide-regulatory protein, and Gs proteins, so hyperthyroid status is considered to cause the decline of the J point. However, in the patient reported here, J-wave amplitudes were enhanced when the high thyroid hormone levels were increased. There are two mechanisms thought to enhance J-wave amplitudes in this patient. First, the transient outward current is influenced by triiodothyronine. Thyrotoxicosis increases the expression of KCND3, the gene that encodes the a subunit (K 4.3) of the transient outward current (I ) channel. Accentuation of I may cause an ER pattern in the ECG characterized to to by J-point elevation [7]. Second, the J wave was observed in circadian variations [8]. The J-wave amplitude increased at night and early morning and decreased during the day in patients with JWS by changing vagal activity. VF occurred at early morning; para- sympathetic stimulation might trigger enhanced J-wave amplitude. The change of J-wave amplitude is regulated by sympathetic and parasympathetic stimulation; therefore, the factors causing elevated J wave might have been dominant, as a result, in this patient. Furthermore, Vestergaard et al. [9] investigated thyroid histological images in 25 cases with an unknown cause of death and diagnosed silent thyroiditis in three cases. They might suggest silent thyroiditis is considered as a differential diagnosis of cardiac arrhythmias. Although the relationship between thyroid function abnormalities and J-point elevation was closely related, we have to consider other possibilities. The patient had been receiving verapamil before the event and the drug was stopped after the event. ER pattern was induced by adding the I agonist and the calcium channel blocker [10]. Thus, verapamil may play a to role in the development of augmented J-point elevation in the thyrotoxic phase. Alternatively, the elevation of the J point after the event may have been due to the event itself and not the hyperthyroidism, and the decrease in the J-point elevation over time may be a resolution of the acute ischemia caused by the VF as well as the discontinuation of the verapamil. The other known triggers might have influenced the elevation of J-wave amplitudes; additional in- vestigation is needed. In summary, the present case suggested that silent thyroiditis may contribute to the occurrence of VF in a patient with dynamic J-point elevation in multiple ECG leads. His clinical course showed that there was a close relationship between thyroid function and J-wave amplitude. A J wave is a common electrocardiographic finding. Physicians should pay attention to J-wave amplitude of the ECG in patients with thyrotoxicosis, which is clinically important because of the risk of life-threatening arrhythmias. Acknowledgments Correspondence: Takashi Yoneda, MD, PhD, Program Management Office for Paradigms Estab- lishing Center for Fostering Medical Researchers of the Future, Kanazawa University, Kanazawa 920-8691, Japan. E-mail: endocrin@med.kanazawa-u.ac.jp; or Kenshi Hayashi, MD, PhD, Division of Cardiovascular Medicine, Graduate School of Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa, Ishikawa 920-8691, Japan. E-mail address: kenshi@med.kanazawa-u.ac.jp. Disclosure Summary: The authors have nothing to disclose. References and Notes 1. Antzelevitch C, Yan GX, Ackerman MJ, Borggrefe M, Corrado D, Guo J, Gussak I, Hasdemir C, Horie M, Huikuri H, Ma C, Morita H, Nam GB, Sacher F, Shimizu W, Viskin S, Wilde AA. J-wave syndromes Downloaded from https://academic.oup.com/jes/article-abstract/2/2/135/4693882 by Ed 'DeepDyve' Gillespie user on 22 March 2018 doi: 10.1210/js.2017-00276 | Journal of the Endocrine Society | 139 expert consensus conference report: emerging concepts and gaps in knowledge. J Arrhythm. 2016;32(5): 315–339. 2. Brosnan MJ, Kumar S, LaGerche A, Brown A, Stewart S, Kalman JM, Prior DL. Early repolarization patterns associated with increased arrhythmic risk are common in young non-Caucasian Australian males and not influenced by athletic status. Heart Rhythm. 2015;12(7):1576–1583. 3. Tsuda T, Hayashi K, Konno T, Sakata K, Fujita T, Hodatsu A, Nagata Y, Teramoto R, Nomura A, Tanaka Y, Furusho H, Takamura M, Kawashiri MA, Fujino N, Yamagishi M. J waves for predicting cardiac events in hypertrophic cardiomyopathy [published online ahead of print June 2017]. JACC Clin Electrophysiol. DOI:10.1016/j.jacep.2017.03.010. 4. Nam GB, Ko KH, Kim J, Park KM, Rhee KS, Choi KJ, Kim YH, Antzelevitch C. Mode of onset of ventricular fibrillation in patients with early repolarization pattern vs. Brugada syndrome. Eur Heart J. 2010;31(3):330–339. 5. Kahaly GJ, Dillmann WH. Thyroid hormone action in the heart. Endocr Rev. 2005;26(5):704–728. 6. Ueno A, Yamamoto T, Sato N, Tanaka K. Ventricular fibrillation associated with early repolarization in a patient with thyroid storm. J Interv Card Electrophysiol. 2010;29(2):93–96. 7. Shimoni Y, Fiset C, Clark RB, Dixon JE, McKinnon D, Giles WR. Thyroid hormone regulates postnatal expression of transient K+ channel isoforms in rat ventricle. J Physiol. 1997;500(Pt 1):65–73. 8. Miyazaki H, Nakagawa M, Shin Y, Wakisaka O, Shinohara T, Ezaki K, Teshima Y, Yufu K, Takahashi N, Hara M, Saikawa T. Comparison of autonomic J-wave modulation in patients with idiopathic ventricular fibrillation and control subjects. Circ J. 2013;77(2):330–337. 9. Vestergaard V, Drostrup DH, Thomsen JL. Sudden unexpected death associated with lymphocytic thyroiditis. Med Sci Law. 2007;47(2):125–133. 10. Patocskai B, Barajas-Martinez H, Hu D, Gurabi Z, Koncz I, Antzelevitch C. Cellular and ionic mechanisms underlying the effects of cilostazol, milrinone, and isoproterenol to suppress arrhyth- mogenesis in an experimental model of early repolarization syndrome. Heart Rhythm. 2016;13(6): 1326–1334. Downloaded from https://academic.oup.com/jes/article-abstract/2/2/135/4693882 by Ed 'DeepDyve' Gillespie user on 22 March 2018 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of the Endocrine Society Oxford University Press

Ventricular Fibrillation Associated With Dynamic Changes in J-Point Elevation in a Patient With Silent Thyroiditis

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Abstract

ISSN 2472-1972 Ventricular Fibrillation Associated With Dynamic Changes in J-Point Elevation in a Patient With Silent Thyroiditis 1 2 1 Shigehiro Karashima, *ToyonobuTsuda, * Yusuke Wakabayashi, 1 1,3 2 2 Mitsuhiro Kometani, Masashi Demura, Taro Ichise, Masa-aki Kawashiri, 1 2 1,4 Yoshiyu Takeda, Kenshi Hayashi, and Takashi Yoneda Division of Endocrinology and Metabolism, Graduate School of Medical Science, Kanazawa University, Kanazawa 920-8691, Japan; Division of Cardiovascular Medicine, Graduate School of Medicine, Kanazawa University, Kanazawa 920-8691, Japan; Departments of Hygiene, Graduate School of Medical Science, Kanazawa University, Kanazawa 920-8691, Japan; and Program Management Office for Paradigms Establishing Center for Fostering Medical Researchers of the Future, Kanazawa University, Kanazawa 920-8691, Japan *These authors contributed equally to this study. A J wave is a common electrocardiographic finding in the general population. Individuals with prominent J waves in multiple electrocardiogram (ECG) leads have a higher risk of lethal arrhythmias than those with low-amplitude J waves. There are few reports about the relationship between thyroid function and J-wave amplitude. We report the case of a 45-year-old man who had unexpected ventricular fibrillation (VF). He had dynamic J-point elevation in multiple ECG leads. Possible early repolarization syndrome was diagnosed. He also had thyrotoxicosis caused by silent thyroiditis, and his J-wave amplitude decreased according to changes in thyroid function because of spontaneous remission of silent thyroiditis. There was a positive correlation between serum triiodothyronine levels and J-wave am- plitudes. The findings in case suggested silent thyroiditis may contribute to the occurrence of VF in a patient with dynamic changes in J-point elevation in multiple ECG leads. Thyrotoxicosis is a relatively common endocrine disease; therefore, clinicians should pay attention to J-wave amplitude in the ECG of patients with thyrotoxicosis. Copyright © 2018 Endocrine Society This article has been published under the terms of the Creative Commons Attribution Non- Commercial, No-Derivatives License (CC BY-NC-ND; https://creativecommons.org/licenses/by-nc- nd/4.0/). Freeform/Key Words: J-wave, silent thyroiditis, thyrotoxicosis, ventricular fibrillation 1. Case Report A 45-year-old man had visited his local hospital because of paroxysmal atrial fibrillation that had started 9 years earlier. He had been taking 80 mg of verapamil and 100 mg of pilsicainide each day. His electrocardiogram (ECG) showed J-point elevation in multiple leads (II, aVF, I, aVL, V3-V6) during outpatient visits [Fig. 1(A)]. His thyroid function had been within the normal range. His mother and his brother also had J-point elevation in multiple ECG leads. The patient was found in cardiopulmonary arrest by his wife in the early morning. Basic life support was performed immediately. An automated external defibrillator detected ventric- ular fibrillation (VF), and a defibrillation shock was delivered by ambulance attendants. He was transported to Kanazawa University Hospital. On arrival, his Glasgow Coma Scale score was 6 (E1V1M4); physical examination revealed a blood pressure of 125/68 mm Hg, heart rate Abbreviations: BS, Brugada syndrome; ECG, electrocardiogram; ERS, early repolarization syndrome; FT3, free triiodothyronine; FT4, free thyroxine; JWS, J-wave syndromes; TSH, thyroid-stimulating hormone VF, ventricular fibrillation. Received 8 June 2017 Accepted 1 December 2017 February 2018 | Vol. 2, Iss. 2 First Published Online 6 December 2017 doi: 10.1210/js.2017-00276 | Journal of the Endocrine Society | 135–139 Downloaded from https://academic.oup.com/jes/article-abstract/2/2/135/4693882 by Ed 'DeepDyve' Gillespie user on 22 March 2018 136 | Journal of the Endocrine Society | doi: 10.1210/js.2017-00276 Figure 1. Electrocardiography. (A) Twelve-lead electrocardiogram recorded in the local hospital. (B) Dynamic J-wave changes associated with thyroid function. Arrow points to J wave. of 108 beats/minute, and body temperature of 36.3°C. He had no obvious thyroid swelling or exophthalmos. Laboratory data, including complete blood cell counts, and cardiac enzyme, renal function, and electrolyte levels were also within normal limits. The patient’s C-reactive protein level was 0.6 mg/dL. A thyroid function test showed the following levels: free tri- iodothyronine (FT3), 8.6 (range, 2.3 to 4.0) pg/mL; free thyroxine (FT4), 3.7 (1.0 to 1.8) ng/dL; thyroid-stimulating hormone (TSH), ,0.01 (0.27 to 4.20) mIU/L; TSH receptor antibody, 0.6 (,2) IU/L); thyroglobulin, 2.0 (3.5 to 77) ng/mL; TSH-stimulating receptor antibody, 105% (,120%); thyroperoxidase antibody, 354 (,16.0) IU/mL; and thyroglobulin antibody, 575 (,28.0) IU/mL. His serum thyroid hormone levels indicated thyrotoxicosis. Thyroid ultra- sonography and Tc-99m scintigraphy were performed and showed results compatible with silent thyroiditis. The clinical course of his thyroid function and ECG are shown in [Fig. 1(B)]. Compared with the 12-lead ECG recorded in the outpatient clinic, his ECG on day 11 after admission showed increased J-point elevation (.0.1 mV) in multiple leads (II, aVF, I, aVL, V2-V6). According to the Proposed Shanghai Score System for diagnosis of early repolarization syndrome (ERS), he had 4.5 points in total and was possible ERS was diagnosed [1]. Echocardiography and coronary angiography showed no unusual findings. A sodium-channel blocker infusion test did not result in the typical ECG pattern of Brugada syndrome (BS), and the test attenuated J-point elevation in the inferolateral leads. The patient was not treated with any antithyroid agents, thyroid hormone replacement, or b-blockers. He underwent cardioverter defibrillator implantation on day 11 and was Downloaded from https://academic.oup.com/jes/article-abstract/2/2/135/4693882 by Ed 'DeepDyve' Gillespie user on 22 March 2018 doi: 10.1210/js.2017-00276 | Journal of the Endocrine Society | 137 discharged on day 33. On day 54, FT3 and FT4 levels had changed to hypothyroid status (FT3, 2.69 pg/mL; FT4, 0.66 ng/dL; TSH, 9.73 mIU/L). J-point elevation in the ECG was decreased compared with his ECG after admission. On day 131, his serum thyroid hormone levels had returned to almost normal (FT3, 3.25 pg/mL; FT4, 1.08 ng/dL; TSH, 4.29 mIU/L), and there was no change in J-point elevation in the ECG between day 54 and day 131. There were also correlations between FT3 levels and the J-wave amplitudes in the lateral leads [Fig. 2(A)], but there were not important correlations in the inferior leads [Fig. 2(B)]. The J-wave amplitudes were measured by a previously reported method [2]. In the outpatient clinic, interrogation of the implanted cardioverter defibrillator showed no lethal arrhythmic events. 2. Discussion We report the case of a 45-year-old man with possible ERS who had an episode of unexplained VF and dynamic changes in J-point elevation in multiple ECG leads. Silent thyroiditis also was diagnosed, and there was a correlation between thyroid hormone levels and J-wave amplitudes. A J-wave, which is a positive deflection immediately following the QRS complex of the surface ECG or is, in part, buried inside the QRS as notching or slurring, is often found in the general population [1]. J waves are associated with the occurrence of lethal arrhythmic events in patients with BS, ischemic heart disease, hypertrophic cardiomyopathy, and long-QT syndrome [1, 3]. J-wave syndromes (JWS) are a spectrum of ECG manifestations of prominent J waves with a risk of VF. JWS consist of ERS and BS. This patient’s condition could be diagnosed as possible ERS by the Proposed Shanghai Score System and was classified as type 3 ERS based on the early repolarization (ER) in multiple ECG leads. Nam et al. [4] em- phasized there is high risk of sudden death in type 3 ERS compared with BS. Figure 2. Correlation between free triiodothyronine levels and the amplitudes of J waves in the (A) lateral leads and (B) inferior leads. Downloaded from https://academic.oup.com/jes/article-abstract/2/2/135/4693882 by Ed 'DeepDyve' Gillespie user on 22 March 2018 138 | Journal of the Endocrine Society | doi: 10.1210/js.2017-00276 Individuals with prominent J waves in multiple leads have a higher risk of lethal ar- rhythmias than those with low-amplitude J waves [1]. In this patient, thyrotoxicosis was thought to cause the increased J-wave amplitude and the occurrence of VF. Thyroid hormone has an important effect on cardiac muscle, particularly via the sympa- thetic nervous system [5]. Cardiac tissue contains b1- and b2-adrenergic receptor subtypes. b-blockers and parasympathetic stimulation augment the elevation of J-point and ST segment; b-stimulators and sympathetic stimulation cause them to decline [6]. Hyperthyroid status leads to an increased sensitivity of the sympathoadrenal system with more b-adrenergic re- ceptors, stimulatory guanine nucleotide-regulatory protein, and Gs proteins, so hyperthyroid status is considered to cause the decline of the J point. However, in the patient reported here, J-wave amplitudes were enhanced when the high thyroid hormone levels were increased. There are two mechanisms thought to enhance J-wave amplitudes in this patient. First, the transient outward current is influenced by triiodothyronine. Thyrotoxicosis increases the expression of KCND3, the gene that encodes the a subunit (K 4.3) of the transient outward current (I ) channel. Accentuation of I may cause an ER pattern in the ECG characterized to to by J-point elevation [7]. Second, the J wave was observed in circadian variations [8]. The J-wave amplitude increased at night and early morning and decreased during the day in patients with JWS by changing vagal activity. VF occurred at early morning; para- sympathetic stimulation might trigger enhanced J-wave amplitude. The change of J-wave amplitude is regulated by sympathetic and parasympathetic stimulation; therefore, the factors causing elevated J wave might have been dominant, as a result, in this patient. Furthermore, Vestergaard et al. [9] investigated thyroid histological images in 25 cases with an unknown cause of death and diagnosed silent thyroiditis in three cases. They might suggest silent thyroiditis is considered as a differential diagnosis of cardiac arrhythmias. Although the relationship between thyroid function abnormalities and J-point elevation was closely related, we have to consider other possibilities. The patient had been receiving verapamil before the event and the drug was stopped after the event. ER pattern was induced by adding the I agonist and the calcium channel blocker [10]. Thus, verapamil may play a to role in the development of augmented J-point elevation in the thyrotoxic phase. Alternatively, the elevation of the J point after the event may have been due to the event itself and not the hyperthyroidism, and the decrease in the J-point elevation over time may be a resolution of the acute ischemia caused by the VF as well as the discontinuation of the verapamil. The other known triggers might have influenced the elevation of J-wave amplitudes; additional in- vestigation is needed. In summary, the present case suggested that silent thyroiditis may contribute to the occurrence of VF in a patient with dynamic J-point elevation in multiple ECG leads. His clinical course showed that there was a close relationship between thyroid function and J-wave amplitude. A J wave is a common electrocardiographic finding. Physicians should pay attention to J-wave amplitude of the ECG in patients with thyrotoxicosis, which is clinically important because of the risk of life-threatening arrhythmias. Acknowledgments Correspondence: Takashi Yoneda, MD, PhD, Program Management Office for Paradigms Estab- lishing Center for Fostering Medical Researchers of the Future, Kanazawa University, Kanazawa 920-8691, Japan. E-mail: endocrin@med.kanazawa-u.ac.jp; or Kenshi Hayashi, MD, PhD, Division of Cardiovascular Medicine, Graduate School of Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa, Ishikawa 920-8691, Japan. E-mail address: kenshi@med.kanazawa-u.ac.jp. Disclosure Summary: The authors have nothing to disclose. References and Notes 1. Antzelevitch C, Yan GX, Ackerman MJ, Borggrefe M, Corrado D, Guo J, Gussak I, Hasdemir C, Horie M, Huikuri H, Ma C, Morita H, Nam GB, Sacher F, Shimizu W, Viskin S, Wilde AA. J-wave syndromes Downloaded from https://academic.oup.com/jes/article-abstract/2/2/135/4693882 by Ed 'DeepDyve' Gillespie user on 22 March 2018 doi: 10.1210/js.2017-00276 | Journal of the Endocrine Society | 139 expert consensus conference report: emerging concepts and gaps in knowledge. J Arrhythm. 2016;32(5): 315–339. 2. Brosnan MJ, Kumar S, LaGerche A, Brown A, Stewart S, Kalman JM, Prior DL. Early repolarization patterns associated with increased arrhythmic risk are common in young non-Caucasian Australian males and not influenced by athletic status. Heart Rhythm. 2015;12(7):1576–1583. 3. Tsuda T, Hayashi K, Konno T, Sakata K, Fujita T, Hodatsu A, Nagata Y, Teramoto R, Nomura A, Tanaka Y, Furusho H, Takamura M, Kawashiri MA, Fujino N, Yamagishi M. J waves for predicting cardiac events in hypertrophic cardiomyopathy [published online ahead of print June 2017]. JACC Clin Electrophysiol. DOI:10.1016/j.jacep.2017.03.010. 4. Nam GB, Ko KH, Kim J, Park KM, Rhee KS, Choi KJ, Kim YH, Antzelevitch C. Mode of onset of ventricular fibrillation in patients with early repolarization pattern vs. Brugada syndrome. Eur Heart J. 2010;31(3):330–339. 5. Kahaly GJ, Dillmann WH. Thyroid hormone action in the heart. Endocr Rev. 2005;26(5):704–728. 6. Ueno A, Yamamoto T, Sato N, Tanaka K. Ventricular fibrillation associated with early repolarization in a patient with thyroid storm. J Interv Card Electrophysiol. 2010;29(2):93–96. 7. Shimoni Y, Fiset C, Clark RB, Dixon JE, McKinnon D, Giles WR. Thyroid hormone regulates postnatal expression of transient K+ channel isoforms in rat ventricle. J Physiol. 1997;500(Pt 1):65–73. 8. Miyazaki H, Nakagawa M, Shin Y, Wakisaka O, Shinohara T, Ezaki K, Teshima Y, Yufu K, Takahashi N, Hara M, Saikawa T. Comparison of autonomic J-wave modulation in patients with idiopathic ventricular fibrillation and control subjects. Circ J. 2013;77(2):330–337. 9. Vestergaard V, Drostrup DH, Thomsen JL. Sudden unexpected death associated with lymphocytic thyroiditis. Med Sci Law. 2007;47(2):125–133. 10. Patocskai B, Barajas-Martinez H, Hu D, Gurabi Z, Koncz I, Antzelevitch C. Cellular and ionic mechanisms underlying the effects of cilostazol, milrinone, and isoproterenol to suppress arrhyth- mogenesis in an experimental model of early repolarization syndrome. Heart Rhythm. 2016;13(6): 1326–1334. Downloaded from https://academic.oup.com/jes/article-abstract/2/2/135/4693882 by Ed 'DeepDyve' Gillespie user on 22 March 2018

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Journal of the Endocrine SocietyOxford University Press

Published: Feb 1, 2018

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