ANTIBODY-INDUCED PERIMYOCARDITIS MASQUERADING AS ACUTE CORONARY SYNDROME IN MYASTHENIA

TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Cardiac involvement in myasthenia gravis (MG) is extremely rare. Antibody (Ab) induced myocarditis MG patients can be difficult to distinguish from myasthenic crisis (MC). Both conditions lead dyspnea and orthopnea, especially with bulbar involvement. If clinicians are unaware, troponin (Tn) elevation electrocardiogram (EKG) changes may misdiagnosed as acute coronary syndrome (ACS). We present a case of Ab perimyocarditis patient presenting MC. CASE PRESENTATION: A 41-year-old female history recent onset MG, presented exertional dyspnea, leg weakness. She denied any preceding fevers, cough, rhinorrhea, or chest pain. Physical examination revealed tachycardia, lower extremity weakness, respiratory distress. Tn-T was elevated rising titers on recheck, EKG (figure-1) demonstrated new-onset anterior qs-waves. Acetylcholine receptor (AChR) anti-striated muscle (anti-Sm) were elevated. transthoracic echocardiogram (TTE) biventricular systolic dysfunction an ejection fraction (EF) 25%. The treated for exacerbation corticosteroids ACS protocol including beta-blockade therapy. Respiratory failure ensued requiring mechanical ventilation. computed tomography mediastinal mass measuring 7.9 x 5.2 6.9 cm (figure 2) suspicious thymoma. While telemetry, the developed ST-elevations premature ventricular complexes. repeat inferior lateral ST elevations T-wave inversions 3). However, asymptomatic unchanged but levels. TTE improved EF 50% global longitudinal strain -10.9%. Myopericarditis suspected stopped. Thymectomy performed pathology confirming Type B3 thymoma capsular invasion. DISCUSSION: Although orthopnea could caused by given leak, considered angina equivalent. Subsequently, myopericarditis lack symptoms despite levels, presence positive anti-Sm Ab. This confirmed improving corticosteroid CONCLUSIONS: Clinicians must consider patients, those concurrent disease course tends severe. both leak changes, risk factors carefully evaluated. has therapeutic implications worsen possibly precipitate REFERENCE #1: Aarli JA. Herzmyasthenie: Myasthenia Heart. Arch Neurol. 2009;66(11):1322–1323. doi:10.1001/archneurol.2009.23 #2: Suzuki S, Utsugisawa K, Yoshikawa H, et al. Autoimmune Targets Heart Skeletal Muscles Gravis. 2009;66(11):1334–1338. doi:10.1001/archneurol.2009.229 #3: Furlund Owe, J., Skulstad Davidsen, E., Eide, G.E. Left long-axis function gravis. J Neurol 255, 1777–1784 (2008). https://doi.org/10.1007/s00415-008-0049-x DISCLOSURES: No relevant relationships Devashish Desai, source=Web Response Sandeep Randhawa, Sachi Singhal,