CASE-LETTER
Acute Myocardial Infarction Associated With Painless Thyroiditis
T
hyrotoxicosis is a common endocrine disorder that can present with a variety of systemic symptoms and affect cardiac circulation. Thyrotoxicosis patients are susceptible to acute myocardial infarction (AMI), and especially if they have Grave’s disease. Painless thyroiditis, also termed “silent thyroiditis,” manifests as transient thyrotoxicosis, displays symptoms similar to those of Grave’s disease, but rarely causes AMI. Here, we report the case of a 26-year-old Chinese man with a normal coronary angiogram who experienced AMI secondary to painless thyroiditis. During the past 5 years, several reports have described AMI induced by Grave’s disease or a thyroidectomy1–3; however, few reports have described AMI related to thyroiditis,4–6 and only 2 cases were similar to the case described here.4,5 A 26-year-old Chinese man was admitted to our department on an emergency basis because of a sudden onset of chest pain lasting for 2 hours. The patient did not show symptoms of palpitation, tremor, cough, dyspnea, weight loss or recent upper respiratory infection. Also, the patient did not have any risk factors for coronary artery disease, except for a 10-year history of smoking. The chest pain started without
provocation and was characterized by a severe squeezing sensation in the anterior chest area, without radiation. One day before admission, the patient had experienced a similar but less severe chest pain without any inducement, and 10 days before admission, he had developed a fever after drinking. Several years earlier, the patient once found his thyroid function abnormal, but he did not receive treatment. On admission, the patient displayed mild tachycardia (100 beats per minute), but no pathological findings were detected on physical examination. An electrocardiogram showed a 1-mm ST-segment elevation in leads II, III and aVF (Figure 1). Initial laboratory tests showed markedly elevated levels of troponin I and CKMB. AMI was diagnosed based on typical chest pain, a typical AMI electrocardiogram and elevated levels of troponin I. The patient was treated with isosorbide dinitrate 15 minutes after hospital admission. Emergency coronary angiography was performed and showed normal coronary arteries but a coronary myocardial bridging over the left anterior descending artery. Cardiac magnetic resonance imaging also showed normal results. Later, laboratory findings revealed thyrotoxicosis: The TSH concentration was significantly reduced while the concentrations of fT3 and fT4 were markedly increased. Thyroid ultrasonography showed normal thyroid structure and echogenicity. A technetium-99m thyroid scan performed 11 days after hospital admission showed markedly reduced uptake by the thyroid gland, compatible with thyroiditis, and the patient was treated
FIGURE 1. (A) Electrocardiogram showing a 1-mm ST-segment elevation in leads II, III and aVF at the time of patient admission. (B) Electrocardiogram showing T wave in II, III and aVF inversion without Q-wave formation 3 days after admission.
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The American Journal of the Medical Sciences
Volume 348, Number 3, September 2014
Case-Letter
with aspirin, clopidogrel and isosorbide dinitrate. The patient’s chest pain nearly completely resolved 2 hours after hospitalization, and measurements of thyroid function and cardiac enzyme levels returned to normal 11 days after admission, without administration of antithyroid agents. During a 1-month follow-up visit, the patient did not complain of any chest pain. Thyrotoxicosis may manifest with a variety of cardiac symptoms including angina, myocardial infarction,7 cardiac arrest,3 ventricular tachyarrhythmia8 and cardiogenic shock.9 The patient described in this report was 1st diagnosed as acute inferior myocardial infarction. Coronary angiography results showed no signs of stenosis, occlusion or atherosclerotic changes, and we therefore excluded thrombolytic myocardial infarction and assumed that the symptoms were caused by a temporary coronary vasospasm, which induced a subsequent AMI. Moreover, results of thyroid function tests confirmed a diagnosis of painless thyroiditis (thyrotoxicosis stage). Because the diagnoses of both AMI and thyroiditis were confirmed, and no evidence of coronary artery stenosis or occlusion was found, we believed that the patient’s AMI was caused by thyrotoxicosis-induced coronary vasospasm. The patient’s family did not consent to the provocation test. AMI in a thyrotoxic patient may result from vasospasm, a temporary coronary arterial occlusion caused by in situ coronary thrombosis, or a thromboembolism with spontaneous lysis of the clot.10 Patients who experience AMI induced by thyrotoxicosis have an excellent prognosis. Once such patients become euthyroid, they can achieve complete resolution of cardiac symptoms. Additionally, only a single case of recurrent angina in euthyroid state has been reported.4 Painless thyroiditis manifests as transient thyrotoxicosis and does not require treatment with antithyroid agents. Treatment of coronary vasospasm due to thyrotoxicosis should include use of nitrates and calcium channel blockers.4 The patient described in this report remained free of angina chest pain after taking nitrates and achieved an euthyroid state as well as normal cardiac enzyme levels without the use of antithyroid agents. Additionally, the patient’s cardiac magnetic resonance imaging was normal 11 days after his first hospital admission. In conclusion, thyrotoxicosis should be suspected in AMI patients without the signs of coronary stenosis or occlusion. Also, painless thyroiditis may occur in the absence of obvious manifestations of thyrotoxicosis. We suggest that patients with typical AMI symptoms, but without coronary stenosis, have routine thyroid function tests, especially if they have a history of thyroid disease. The underlying pathological mechanism for thyrotoxicosis-induced AMI may be associated with coronary spasm, a hyperkinetic circulatory system, and abnormal coagulation system. We recommend treating these patients with nitrates and calcium channel blockers and avoiding antithyroid agents in cases of painless thyroiditis.
Ó 2014 Lippincott Williams & Wilkins
Li-Ping Zhang, MD Bo-Tao Shen, MD Yi-Meng Dai, MD *Xue-Zhong Zhao, MD, PhD Yang Zheng, MD, PhD Wei Zhao, MD The Department of Cardiology, The First Hospital Affiliated to Jilin University, Changchun, China Correspondence to: Xuezhong Zhao E-mail: [email protected] First 2 authors contributed equally to this work. The authors have no financial or other conflicts of interest to disclose.
ACKNOWLEDGMENTS The authors thank Medjaden Bioscience Limited for assisting in the preparation of this article.
REFERENCES 1. Pavlicek V, Zeif H, Widmer F. Thyrotoxicosis-induced Prinzmetal variant angina. Exp Clin Endocrinol Diabetes 2006;114:28–30. 2. Carey D, Hurst JW Jr, Silverman ME. Coronary spasm and cardiacarrest after coronary arteriography in unsuspected thyrotoxicosis. Am J Cardiol 1992;70:833–4. 3. Bassi S, Amersey R, Henderson R, et al. Thyrotoxicosis, sumatriptan and coronary artery spasm. J R Soc Med 2004;97:285–7. 4. Kim HJ, Jung TS, Hahm JR, et al. Thyrotoxicosis-induced acute myocardial infarction due to painless thyroiditis. Thyroid 2011;21: 1149–51. 5. Yasuda M, Takeuchi M, Kondo M, et al. Two cases of subendocardial infarction associated with subacute thyroiditis. Nihon Naika Gakkai Zasshi 1984;73:1347–52. 6. Gupta M, Pradhan D, Jian S, et al. Acute myocardial infarction associated with thyrotoxicosis. J Clin Case Rep 2013;3:270. 7. Lewandowski KC, Rechcinski T, Krzeminska-Pakula M, et al. Acute myocardial infarction as the first presentation of thyrotoxicosis in a 31-year old woman-case report. Thyroid Res 2010;3:1. 8. Wei JY, Genecin A, Greene HL, et al. Coronary spasm with ventricular fibrillation during thyrotoxicosis: response to attaining euthyroid state. Am J Cardiol 1979;43:335–9. 9. Lassnig E, Berent R, Auer J, et al. Cardiogenic shock due tomyocardial infarction caused by coronary vasospasm associatedwith hyperthyroidism. Int J Cardiol 2003;90:333–5. 10. Mustafa C, Ozgul U, Zehra GC, et al. Transient ST-segment elevation due to iatrogenic hyperthyroidism in a patient with normal coronary arteries. Intern Med 2011;50:1595–7.
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Acute Myocardial Infarction Associated With Painless Thyroiditis
T
hyrotoxicosis is a common endocrine disorder that can present with a variety of systemic symptoms and affect cardiac circulation. Thyrotoxicosis patients are susceptible to acute myocardial infarction (AMI), and especially if they have Grave’s disease. Painless thyroiditis, also termed “silent thyroiditis,” manifests as transient thyrotoxicosis, displays symptoms similar to those of Grave’s disease, but rarely causes AMI. Here, we report the case of a 26-year-old Chinese man with a normal coronary angiogram who experienced AMI secondary to painless thyroiditis. During the past 5 years, several reports have described AMI induced by Grave’s disease or a thyroidectomy1–3; however, few reports have described AMI related to thyroiditis,4–6 and only 2 cases were similar to the case described here.4,5 A 26-year-old Chinese man was admitted to our department on an emergency basis because of a sudden onset of chest pain lasting for 2 hours. The patient did not show symptoms of palpitation, tremor, cough, dyspnea, weight loss or recent upper respiratory infection. Also, the patient did not have any risk factors for coronary artery disease, except for a 10-year history of smoking. The chest pain started without
provocation and was characterized by a severe squeezing sensation in the anterior chest area, without radiation. One day before admission, the patient had experienced a similar but less severe chest pain without any inducement, and 10 days before admission, he had developed a fever after drinking. Several years earlier, the patient once found his thyroid function abnormal, but he did not receive treatment. On admission, the patient displayed mild tachycardia (100 beats per minute), but no pathological findings were detected on physical examination. An electrocardiogram showed a 1-mm ST-segment elevation in leads II, III and aVF (Figure 1). Initial laboratory tests showed markedly elevated levels of troponin I and CKMB. AMI was diagnosed based on typical chest pain, a typical AMI electrocardiogram and elevated levels of troponin I. The patient was treated with isosorbide dinitrate 15 minutes after hospital admission. Emergency coronary angiography was performed and showed normal coronary arteries but a coronary myocardial bridging over the left anterior descending artery. Cardiac magnetic resonance imaging also showed normal results. Later, laboratory findings revealed thyrotoxicosis: The TSH concentration was significantly reduced while the concentrations of fT3 and fT4 were markedly increased. Thyroid ultrasonography showed normal thyroid structure and echogenicity. A technetium-99m thyroid scan performed 11 days after hospital admission showed markedly reduced uptake by the thyroid gland, compatible with thyroiditis, and the patient was treated
FIGURE 1. (A) Electrocardiogram showing a 1-mm ST-segment elevation in leads II, III and aVF at the time of patient admission. (B) Electrocardiogram showing T wave in II, III and aVF inversion without Q-wave formation 3 days after admission.
266
The American Journal of the Medical Sciences
Volume 348, Number 3, September 2014
Case-Letter
with aspirin, clopidogrel and isosorbide dinitrate. The patient’s chest pain nearly completely resolved 2 hours after hospitalization, and measurements of thyroid function and cardiac enzyme levels returned to normal 11 days after admission, without administration of antithyroid agents. During a 1-month follow-up visit, the patient did not complain of any chest pain. Thyrotoxicosis may manifest with a variety of cardiac symptoms including angina, myocardial infarction,7 cardiac arrest,3 ventricular tachyarrhythmia8 and cardiogenic shock.9 The patient described in this report was 1st diagnosed as acute inferior myocardial infarction. Coronary angiography results showed no signs of stenosis, occlusion or atherosclerotic changes, and we therefore excluded thrombolytic myocardial infarction and assumed that the symptoms were caused by a temporary coronary vasospasm, which induced a subsequent AMI. Moreover, results of thyroid function tests confirmed a diagnosis of painless thyroiditis (thyrotoxicosis stage). Because the diagnoses of both AMI and thyroiditis were confirmed, and no evidence of coronary artery stenosis or occlusion was found, we believed that the patient’s AMI was caused by thyrotoxicosis-induced coronary vasospasm. The patient’s family did not consent to the provocation test. AMI in a thyrotoxic patient may result from vasospasm, a temporary coronary arterial occlusion caused by in situ coronary thrombosis, or a thromboembolism with spontaneous lysis of the clot.10 Patients who experience AMI induced by thyrotoxicosis have an excellent prognosis. Once such patients become euthyroid, they can achieve complete resolution of cardiac symptoms. Additionally, only a single case of recurrent angina in euthyroid state has been reported.4 Painless thyroiditis manifests as transient thyrotoxicosis and does not require treatment with antithyroid agents. Treatment of coronary vasospasm due to thyrotoxicosis should include use of nitrates and calcium channel blockers.4 The patient described in this report remained free of angina chest pain after taking nitrates and achieved an euthyroid state as well as normal cardiac enzyme levels without the use of antithyroid agents. Additionally, the patient’s cardiac magnetic resonance imaging was normal 11 days after his first hospital admission. In conclusion, thyrotoxicosis should be suspected in AMI patients without the signs of coronary stenosis or occlusion. Also, painless thyroiditis may occur in the absence of obvious manifestations of thyrotoxicosis. We suggest that patients with typical AMI symptoms, but without coronary stenosis, have routine thyroid function tests, especially if they have a history of thyroid disease. The underlying pathological mechanism for thyrotoxicosis-induced AMI may be associated with coronary spasm, a hyperkinetic circulatory system, and abnormal coagulation system. We recommend treating these patients with nitrates and calcium channel blockers and avoiding antithyroid agents in cases of painless thyroiditis.
Ó 2014 Lippincott Williams & Wilkins
Li-Ping Zhang, MD Bo-Tao Shen, MD Yi-Meng Dai, MD *Xue-Zhong Zhao, MD, PhD Yang Zheng, MD, PhD Wei Zhao, MD The Department of Cardiology, The First Hospital Affiliated to Jilin University, Changchun, China Correspondence to: Xuezhong Zhao E-mail: [email protected] First 2 authors contributed equally to this work. The authors have no financial or other conflicts of interest to disclose.
ACKNOWLEDGMENTS The authors thank Medjaden Bioscience Limited for assisting in the preparation of this article.
REFERENCES 1. Pavlicek V, Zeif H, Widmer F. Thyrotoxicosis-induced Prinzmetal variant angina. Exp Clin Endocrinol Diabetes 2006;114:28–30. 2. Carey D, Hurst JW Jr, Silverman ME. Coronary spasm and cardiacarrest after coronary arteriography in unsuspected thyrotoxicosis. Am J Cardiol 1992;70:833–4. 3. Bassi S, Amersey R, Henderson R, et al. Thyrotoxicosis, sumatriptan and coronary artery spasm. J R Soc Med 2004;97:285–7. 4. Kim HJ, Jung TS, Hahm JR, et al. Thyrotoxicosis-induced acute myocardial infarction due to painless thyroiditis. Thyroid 2011;21: 1149–51. 5. Yasuda M, Takeuchi M, Kondo M, et al. Two cases of subendocardial infarction associated with subacute thyroiditis. Nihon Naika Gakkai Zasshi 1984;73:1347–52. 6. Gupta M, Pradhan D, Jian S, et al. Acute myocardial infarction associated with thyrotoxicosis. J Clin Case Rep 2013;3:270. 7. Lewandowski KC, Rechcinski T, Krzeminska-Pakula M, et al. Acute myocardial infarction as the first presentation of thyrotoxicosis in a 31-year old woman-case report. Thyroid Res 2010;3:1. 8. Wei JY, Genecin A, Greene HL, et al. Coronary spasm with ventricular fibrillation during thyrotoxicosis: response to attaining euthyroid state. Am J Cardiol 1979;43:335–9. 9. Lassnig E, Berent R, Auer J, et al. Cardiogenic shock due tomyocardial infarction caused by coronary vasospasm associatedwith hyperthyroidism. Int J Cardiol 2003;90:333–5. 10. Mustafa C, Ozgul U, Zehra GC, et al. Transient ST-segment elevation due to iatrogenic hyperthyroidism in a patient with normal coronary arteries. Intern Med 2011;50:1595–7.
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