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

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.