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

Abstract

BACKGROUND Acute myocarditis is an acute myocardium injury that manifests as arrhythmia, dyspnea, and elevated cardiac enzymes. Acute myocarditis is usually caused by a viral infection but can sometimes be caused by autoimmunity. Graves’ disease is an autoimmune disease that is a rare etiology of acute myocarditis. Accelerated junctional rhythm is also a rare manifestation of acute myocarditis in adults. CASE SUMMARY A rare case of new-onset Graves’ disease combined with acute myocarditis and thyrotoxic periodic paralysis is reported. The patient was a 25-year-old young man who suddenly became paralyzed and felt palpitations and dyspnea. He was then sent to our emergency department (ED). Upon arrival, electrocardiography revealed an accelerated junctional rhythm and ST-segment depression in all leads, and laboratory findings showed extreme hypokalemia and elevated troponin I, with the troponin I level being 0.32 ng/mL (reference range, 0-0.06 ng/mL). Coronary computer tomography angiography was performed, and there were no abnormal findings in the coronary arteries. Subsequently, the patient was admitted to the ED ward, where further testing revealed Graves’ disease, along with continued elevated cardiac enzyme levels and B-type natriuretic peptide (BNP) levels. The troponin I level was 0.24 ng/mL after admission. All of the echocardiography results were normal: Left atrium 35 mm, left ventricle 48 mm, end-diastolic volume 102 mL, right atrium 39 mm × 47 mm, right ventricle 25 mm, and ejection fraction 60%. Cardiac magnetic resonance was performed on the fifth day of admission, revealing myocardial edema in the lateral wall and intramyocardial and subepicardial late gadolinium enhancement in the lateral apex, anterior lateral, and inferior lateral segments of the ventricle. The patient refused to undergo an endomyocardial biopsy. After 6 d, the patient’s cardiac enzymes, BNP, potassium, and electrocardiography returned to normal. After the patient’s symptoms were relieved, he was discharged from the hospital. During a 6-mo follow-up, the patient was asymptomatic and subjected to thyroid function, liver function, kidney function, troponin I, and electrocardiograph routine tests for medicine adjustments. The hyperthyroid state was controlled. CONCLUSION Acute myocarditis is a rare manifestation of Graves’ disease. Accelerated junctional rhythm is also a rare manifestation of acute myocarditis in adults. When the reason for hypokalemia and elevated cardiac enzymes in patients is unknown, cardiologists should consider Graves’ disease and also pay attention to accelerated junctional rhythm.

Case report: acute myocarditis complicated with persistent complete heart block: a clinical dilemma when myocardial inflammation remains

“…This case is noteworthy for an unexpected persistent CHB after acute myocarditis complicated by cardiogenic shock and VF. Bradyarrhythmias are a rare and mostly transient manifestation in the setting of acute myocarditis, appearing mainly in children and seldomly in adults, 7 with reported rates of atrioventricular blocks ranging from 0.8 to 1.7–10%. 4 Persisting arrhythmias beyond the acute phase (>1 week) suggest myocardial fibrosis and chronic inflammation, anticipating a low likelihood of recovery.…”

Ritmo nodal: caso clínico

“…El ritmo nodal posoperatorio es probablemente el resultado de un traumatismo mecánico directo del tejido o estiramiento con hemorragias en la unión AV, como ha sido descrito previamente en un estudio post mortem de pacientes con esta arritmia Otras posibles condiciones que explican la aparición de un ritmo idionodal pudieran ser de origen metabólico. Li et al, (40) reportan la aparición de ritmo nodal acelerado, como manifestación de una miocarditis como debut de la enfermedad de Graves Basedow, en un hombre joven, que presentó palpitaciones y disnea de forma súbita. Los hallazgos electrocardiográficos indicaron un ritmo de la unión acelerado, con depresión del segmento ST en todas las derivaciones; mientras que los resultados de laboratorio indicaron un incremento en los niveles de Troponina I, con coronarias normales.…”