Abstract
Myasthenia gravis (MG) primarily affects skeletal muscle through the production of autoantibodies against the nicotinic acetylcholine receptor in the motor endplates; in addition, heart muscle is an autoimmune target [1,2]. Although MG is believed to be relatively rare, 16% of patients with MG exhibit several types of cardiac involvement, ranging from asymptomatic electrocardiogram (ECG) changes to myocarditis, heart failure, and sudden death [2]. A persistent increase in cardiac troponins reportedly indicates ongoing myocardial damage during heart failure and a poor prognosis [3–6].
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