Chronic thyrotoxic myocarditis complicated by myocardial rupture in a patient with autoimmune thyroiditis

Причиной хронического аутоиммунного тиреоидита (ХАИТ) является генетически обусловленный дефект иммунной толерантности к антигенам щитовидной железы (ЩЖ) [1], ХАИТ чаще встречается у женщин в возрасте 40—50 лет и обнаруживается примерно у 20% женщин пожилого возраста [2, 3]. По анатомо-морфологическому признаку выделяют гипертрофическую и атрофическую форму ХАИТ. Главным цитои гистологическим признаком ХАИТ является диффузная или очаговая лимфоили плазмоцитарная инфильтрация ткани ЩЖ, хотя отмечается расплывчатость ее критериев [4, 5]. Гипертиреоз встречается у 5% больных гипертрофической формой ХАИТ [6]. У людей, перенесших тиреотоксикоз, даже при радикальном излечении повышена смертность по сравнению с остальной популяцией, в основном от сердечно-сосудистых причин [7—9]. Одним из осложнений ХАИТ является миокардит, возникающий вследствие токсического воздействия на миокард избытка тиреоидных гормонов Хронический тиреотоксический миокардит, осложненный разрывом миокарда у больной аутоиммунным тиреоидитом


Relevance
Chronic autoimmune thyroiditis (CAT) is caused by a genetically determined defect of immune tolerance to thyroid gland antigens (TG) [1]. CAT is more common in women aged 40-50 years and is found in about 20% of elderly women [2,3]. CAT is classifi ed as hypertrophic or atrophic based on the anatomy and morphology. The main cyto-and histological sign of CAT is diff use or focal lympho-or plasmacytic infi ltration of the thyroid tissue, although its criteria are vague [4,5]. Hyperthyroidism occurs in 5% of patients with hypertrophic form of CAT [6]. People who have had thyrotoxicosis, even after the radical cure, have increased mortality compared with the rest of the population, mainly from cardiovascular causes [7][8][9].
Myocarditis is one of the complications of CAT which is caused by toxic eff ects of an excess of thyroid hormones on the myocardium [10]. It also disrupts the energy-generating function of myocardiocytes and the contractile function of myofi brils [6,11,12]. There are cases of myocarditis occurring under the mask of acute coronary syndrome. An emergency coronary angiography is required to clarify the diagnosis [13][14][15].
The practice of management of patients with acute coronary syndrome involves emergency myocardial revascularization by percutaneous coronary intervention or thrombolytic therapy. This signifi cantly reduces the incidence of early complications of myocardial infarction, in particular, myocardial ruptures at the inpatient stage of treatment [16]. Myocardial rupture as a fatal complication of myocarditis is rare. Individual cases of myocardial rupture with fulminant, giant cell, bacterial myocarditis have been described [17][18][19]. Descriptions of cases of myocardial rupture in thyrotoxic myocarditis were not found in the available literature, which defi ned the interest in this clinical observation.

Description of the case
Patient N., 60 years old, medical record № 13787, was admitted to the intensive care unit for patients with myocardial infarction of the S.S. Yudin State Clinical Hospital, Moscow, on February 15, 2017, with complains of burning pain in the chest.
There was no history of coronary issues. During the last 5 years, she suff ered from arterial hypertension with elevations of blood pressure up to 180/100 mmHg and was taking amlodipine 5 mg in the mornings and, occasionally, captopril. She was adapted to blood pressure 140/80 mmHg. Over the past year, blood pressure was unstable despite antihypertensive drugs therapy, but the patient did not go to a doctor.
Medical history shows that she was diagnozed with thyrotoxicosis in 2005 and was prescribed tyrosol at a dose of 10 mg per day. Four years ago, the patient self-canceled the drug, and the level of thyroid hormones was not monitored. In the last year, she noted the appearance of unmotivated weakness not only in the evenings but also in the mornings. She had decreased exercise tolerance. She was bothered by palpitations. She visited an endocrinol-391 ogist, and three days before this hospitalization, blood was taken to study the level of thyroid hormones.
More than 20 years ago, she was diagnosed with duodenal ulcer, but she could not remember the last exacerbation. Periodically she experienced heartburn and discomfort in the epigastric region which occurred after a meal.
On the evening of February 15th, after returning home from work, she experienced burning and pressing chest pains radiating to the back at rest for the fi rst time in her life. The patient suff ered pain for 1.5 hours and did not try to manage it. Then she called the ambulance and, following a ECG registration she was hospitalized with a diagnosis of unstable angina. (Fig. 1).
The ambulance team prescribed the following treatment: ticagrelor 180 mg, acecardol 250 mg, 2 doses of isocet. The pain in the chest persisted.

Examination in the intensive care unit
The general condition of the patient was moderately severe. The skin with normal color, warm, normal humidity. No peripheral edema. RR: 20 per min. Auscultation revealed hard breathing without wheezing. The region of the heart was unmodifi ed, the borders of the heart were expanded to the left. Heart sounds were muffl ed rhythmic. A systolic murmur was heard over the projection of the apex of the heart. Strong pulse in the main and peripheral arteries. BP: 150/90 mmHg, HR: 120 bpm.
ECG did not identify a signifi cant increase in the ST segment, there was the oblique-ascending depression in ST-segment registered by V4-V6 leads.
Taking into account the clinical presentation, laboratory diagnostic data, ECG changes (see Results of the examination), the patient's condition was regarded as an "acute coronary syndrome" requiring emergency coronary angiography (CAG).
After obtaining the informed consent, administering neuroleptic algesia and pain relief, the patient was transferred to an X-ray room where she underwent CAG (see Results of the examination). No hemodynamically significant constriction of the coronary arteries was identifi ed.
The dynamical study of the cardiospecifi c enzymes revealed changes characteristic for focal myocardial damage (see Results of the examination).
After the relief of pain, the patient's condition did not worsen, chest pain did not recur, however, the complaints of palpitations persisted. With the prescribed treatment, blood pressure stabilized at a level of 120-130/70-80 mmHg.
Sinus tachycardia persisted on ECG, there was no convincing data for the presence of focal changes (Fig. 2). Chest X-ray revealed left-sided encapsulated pleurisy (see Results of the examination). No signs of hypokinesia and impaired global contractility of the left ventricle were noted in echoCG (see Results of the examination).
On 16.02.17, the patient was transferred to the cardiology department in a stable condition, where bisoprolol (5 mg of in the morning and 2.5 mg in the evening), as well as 5 mg torasemide in the morning on an empty stomach, were added to the treatment regimen.
At an outpatient blood test, the TSH level was 0 μMU/L (decreased), T4 concentration was 41 μg% (increased), and antithyroid antibodies were not detected. Endocrinologist diagnosis: Recurrent diff use toxic goiter. A complicated course of thyrotoxicosis, decompensation. Thyrotoxic heart. However, the genesis of chest pain remained unclear.
From February 16, 2017, the therapy with tyrosol in a daily dose of 30 mg was prescribed with monitoring of thyroid hormone levels. On treatment, the patient suff ered from general weakness and palpitations during the whole day. An abnormal Q wave appeared on the ECG in the posterior wall of the left ventricle. (Fig. 3). The cause of pain in the chest could be an exacerbation of peptic ulcer disease. Further examination was planned.
On February 20, 2017, the patient suddenly fainted, and breathing and cardiac activity ceased. Resuscitation for 30 minutes was ineff ective. Biological death was declared.

Final clinical diagnosis
Main disease: 1. Coronary heart disease: atherosclerosis of the heart vessels.
2. Recurrent diff use toxic goiter. A complicated course of thyrotoxicosis, decompensation.
Underlying disease: Hypertension stage III, grade 3, high risk of CVE.
Accompanying diseases: Duodenal ulcer, exacerbation. Chronic gastritis without exacerbation. Chronic bronchitis, exacerbation.  Conclusion: A 60-year-old patient who suff ered from autoimmune thyroiditis and developed thyrotoxic myocarditis died from a pericardial hemotamponade due to a rupture of the left ventricular myocardium (Fig. 4-8

Coronary angiography (radial access). Innova 3100 GE instrument
Through an introducer in the radial artery, a bolus of a solution of verapamil 5 mg and heparin 5 thousand U was injected. A contrast angiography of the left coronary artery and the right coronary artery was performed using a 6 Fr BLK catheter with Visipac 370 as a contrast agent (150 ml). The trunk of the left coronary artery without signifi cant narrowing. Left anterior descending coronary artery without hemodynamically signifi cant narrowing. The diagonal branch: 40-45% stenosis at the mouth, no hemodynamically signifi cant contractions further. The circumfl ex branch without hemodynamically signifi cant contractions. Obtuse marginal branch without hemodynamically significant contractions. Right coronary artery without hemodynamically signifi cant narrowing. Posterior-lateral branch without hemodynamically signifi cant narrowing. Right-handed type of blood supply to the heart. Conclusion: Coronary arteries without hemodynamically signifi cant narrowing.  the mid-clavicular line due to fl uid in the right pleural cavity. From the posterior, the darkened section is delimited by an interlobar pleura. Hyper-translucent lung fi elds. The lung pattern is deformed, the roots are compacted, not expanded. The diaphragm is contoured on both sides. The front sinus is darkened on the right. The median shadow is not shifted, not expanded. The heart is expanded to the left due to the left sections, the waist is smoothed, the aorta is indurated and sclerosed. Focal infi ltrative changes were not detected. X-ray picture of the left-sided encapsulated hydrothorax.

Discussion
There are cases of myocarditis developing under the guise of acute coronary syndrome described in the literature. Sometimes these patients undergo emergency coronary angiography [13][14][15]20].
Our patient is 60 years old, the clinical presentation of the disease which included burning and pressing chest pains radiating to the back at rest, and which developed for the fi rst time in her life and was accompanied by an increase in the level of cardiospecifi c enzymes is typical of acute coronary syndrome. Therefore, an emergency coronary angiography examination 2 hours after the onset of the painful attack was justifi ed.
Myocardial rupture, as a complication of myocarditis, is an extremely rare event. A clinical presentation similar to acute myocardial infarction (17,18) is possible.
At the time of CAG, our patient did not have blood test results for thyroid hormones made on an outpatient basis, but there was an evidence of a history of thyrotoxicosis.
Rapid administration of 150 ml of iodine-containing contrast during CAG could have caused an increase in the eff ects of hyperthyroidism with a sharp increase in the blood levels of thyroid hormones and catecholamines, which, in turn, could have contributed to myocardial damage with the development of its transmural damage. In addition, the eff ect of tachycardia that persisted in the following days on the expansion and deepening of the myocardial damage zone cannot be excluded.

Conclusion
In elderly patients with a long history of thyrotoxicosis, CAT may be the cause of the disease.
Thyrotoxic myocarditis may develop in case of CAT with the presentation similar to that of acute coronary syndrome.
In thyrotoxic myocarditis, administration of iodinecontaining contrast agents can lead to a deepening and expansion of the myocardial lesion and cause myocardial rupture.   Stained with hematoxylin and eosin (magn. ×100).