Acute myocarditis presenting as accelerated junctional rhythm in Graves’ disease: A case report

Table 1 Uniqueness of this case

Ref.	Setting	Main findings	Correlation and difference compared with this case
[6]	A 29-year-old male presents with hyperthyroidism and chest pain	The patient is diagnosed with new-onset of Graves’ disease combined with myocarditis	The manifestation in the study is similar to this case report. However, that patient has already known that he had hyperthyroidism, which reduces the difficulty of the diagnosis. That patient does not present with hypokalemic periodic paralysis. Withal, the patient presents with sinus tachycardia on the electrocardiograph instead of a junctional rhythm
[5]	A 40-year-old male presents with refractory hyperthyroidism and chest pain	The patient is diagnosed with Graves’ disease combined with myocarditis	The study is similar to the above research. The patient is finally diagnosed with refractory Graves’ disease combined with myocarditis. No other manifestations are observed
[7]	A 31-year-old woman with 2-mo pregnancy with hyperthyroidism complained of palpitation and excessive sweating	The patient is diagnosed with Graves’ disease combined with myocarditis	The patient has reduced ejection fraction in the study. Besides, the patient does not present with other combinations except for myocarditis, which is different from this case

Table 2 Diagnostic criteria for myocarditis[8]

Examinations and presentations	Features
ECG/Holter/stress test	Newly abnormal 12 lead ECG and/or Holter and/or stress testing, any of the following: I to III degree atrioventricular block, or bundle branch block, ST/T wave change (ST elevation or non-ST elevation, T wave inversion), sinus arrest, ventricular tachycardia or fibrillation and asystole, atrial fibrillation, reduced R wave height, intraventricular conduction delay (widened QRS complex), abnormal Q waves, low voltage, frequent premature beats, supraventricular tachycardia
Myocardiocytolysis markers	Elevated TnT/TnI
Functional and structural abnormalities on cardiac imaging (echo/angio/CMR)	New, otherwise unexplained LV and/or RV structure and function abnormality (including incidental finding in apparently asymptomatic subjects): regional wall motion or global systolic or diastolic function abnormality, with or without ventricular dilatation, with or without increased wall thickness, with or without pericardial effusion, with or without endocavitary thrombi
Tissue characterization by CMR	Oedema and/or LGE of classical myocarditic pattern
Clinical presentationsa	Acute chest pain, pericarditic, or pseudo-ischaemic (1) New-onset (days up to 3 mo) or worsening of: Dyspnea at rest or exercise, and/or fatigue, with or without left and/or right heart failure signs; (2) Subacute/chronic (> 3 mo) or worsening of: dyspnea at rest or exercise, and/or fatigue, with or without left and/or right heart failure signs; (3) Palpitation, and/or unexplained arrhythmia symptoms and/or syncope, and/or aborted sudden cardiac death; and (4) Unexplained cardiogenic shock

^aIf the patient is asymptomatic, ≥ 2 diagnostic criteria should be met. Clinically suspected myocarditis if ≥ 1 clinical presentation and ≥ 1 diagnostic criteron from different categories, in the absence of: (1) Angiographically detectable coronary artery disease (coronary stenosis ≥ 50%); (2) known pre-existing cardiovascular disease or extra-cardiac causes that could explain the syndrome (e.g., valve disease, congenital heart disease, and hyperthyroidism) (see text). Suspicion is higher with higher number of fulfilled criteria. ECG: Electrocardiography; CMR: Cardiac magnetic resonance; LV: Left ventricle; RV: Right ventricle; LGE: Late gadolinium enhancement; TNI: Troponin I; TNT: Troponin T.

Table 3 Diagnosis and treatment process of this case

Ref.	Findings	Correlation with this study
[10]	The revised Mayo Clinic Criteria: (1) Transient hypokinesis, akinesis, or dyskinesis of the left ventricular midsegments with or without apical involvement; the regional wall motion abnormalities extend beyond a single epicardial vascular distribution; a stressful trigger is often, but not always present; (2) absence of obstructive coronary disease or angiographic evidence of acute plaque rupture; (3) new electrocardiographic abnormalities (either ST-segment elevation and/or T-wave inversion) or modest elevation in cardiac troponin; and (4) absence of pheochromocytoma or myocarditis	CMR is a useful tool to confirm the diagnosis, and the pattern of DGE at CMR is useful to distinguish myocarditis from stress cardiomyopathy. The patient’s clinical presentation and CMR did not meet these criteria. Thus, stress cardiomyopathy was excluded in this patient
[11]	The clinical diagnosis of pericarditis can be made with two of the following criteria: (1) Chest pain (> 85%–90% of cases)—typically sharp and pleuritic, improved by sitting up and leaning forward; (2) pericardial friction rub (≤ 33% of cases)—a superficial scratchy or squeaking sound best heard with the diaphragm of the stethoscope over the left sternal border; (3) electrocardiogram changes (up to 60% of cases)—with new widespread ST elevation or PR depression in the acute phase; and (4) pericardial effusion (up to 60% of cases, generally mild). Additional signs and symptoms may be present according to the underlying etiology or systemic disease (i.e., signs and symptoms of systemic infection such as fever and leukocytosis, or systemic inflammatory disease or cancer). Diagnosis of predominant pericarditis with myocardial involvement, or “myopericarditis”, can be clinically established if patients with definite criteria for acute pericarditis show elevated biomarkers of myocardial injury (troponin I or T, CK-MB fraction) without newly developed focal or diffuse impairment of left ventricular function in echocardiography or CMR	The patient did not present with the manifestations in the diagnostic criteria. Thus, acute pericarditis and myopericarditis were excluded
[4]	The electrocardiography of a junctional rhythm shows a narrow complex QRS wave, along with retrograde P waves, sometimes are overlapped in the QRS waves. The RP interval is lower than 200 ms. Treatment of a junctional rhythm primarily depends on the underlying cause of the rhythm. If the heart rate is within 60 to 100 beats per min, accelerated junctional rhythm is considered. Aetiology-based treatment is recommended	The patient’s electrocardiography was consistent with accelerated junctional rhythm. Treatment of Graves’ disease is fundamental
[14]	Diagnosis of Graves’ disease is now usually based on anti-TSH-receptor antibody assays and thyroid ultrasonography.
[17]	TSHR-Ab is a specific biomarker for Graves’ disease. In addition to thyroid function and TSHR-Ab determination, most clinicians would request thyroid ultrasound and less often isotope scanning. A color-flow or power Doppler examination characterizes vascular patterns and quantifies thyroid vascularity. Beta-adrenergic blockade is recommended in all suitable patients with Graves’ hyperthyroidism	The patient’s positive TSHR-Ab and ultrasound examination results were consistent with Graves’ disease. Moreover, the patient’s thyroid static imaging further proved the diagnosis of Graves’ disease
[17]	Patients with newly diagnosed Graves’ hyperthyroidism should be treated with ATD. RAI therapy or thyroidectomy may be considered in patients who prefer this approach. Patients with side effects or recurrence after a course of ATD, cardiac arrhythmias, and thyrotoxic periodic paralysis are candidates for RAI	The patient was diagnosed with new-onset Graves’ disease. The ATD must be initiated. Thus, methimazole 20 mg/d was administered. The patient was combined with thyrotoxic periodic paralysis, which was suitable for RAI. However, he refused this treatment method. The patient was combined with acute myocarditis, beta-blocker was administered
[18]	Hypokalemia is present in most patients. Abnormal thyroid hormones like elevated T4, or elevated T3 and low TSH might be present. The thyroid uptake scan might show increased uptake. The goal for treatment is to supplement potassium quickly along with the reduction of thyroid hormones. Non-selective beta-blockers have been shown to improve neuromuscular symptoms by reducing the intracellular shift of phosphate and potassium	The patient was administered with potassium supplements, ATD and a beta-blocker, all of which met the treatment criteria
[8]	The core principles of treatment in myocarditis are optimal care of arrhythmia and heart failure and, where supported by evidence, aetiology-targeted therapy. For patients with autoimmune diseases, treatment of primary disease is of vital importance	The patient did not have heart failure, and a beta-blocker was administered to treat his arrhythmia. The treatment of Graves’ disease is significant for his myocarditis

CMR: Cardiac magnetic resonance; DGE: Delayed gadolinium enhancement; TSH: Thyroid stimulating hormone; TSHR-Ab: Thyroid-stimulating hormone receptor antibody; ATD: Antithyroid drug; RAI: Radioactive iodine.