Clozapine is a Food and Drug Administration-approved, second-generation antipsychotic used to treat treatment-resistant schizophrenia. Known for its benefits in reducing extrapyramidal symptoms typically seen with antipsychotics, this drug carries a risk of agranulocytosis and, to a lesser-known extent, myocarditis. A 49-year-old patient, who was initially admitted to psychiatry with a primary diagnosis of schizophrenia, was started on clozapine. After three weeks of being on clozapine, the patient developed fevers and was admitted under internal medicine for further workup of presumed systemic inflammatory response syndrome due to noninfectious etiology. The patient was also asymptomatic. He was subsequently found to have elevated cardiac markers and C-reactive protein levels as well as decreased left ventricular ejection fraction and findings consistent with myocarditis using echocardiography. Clozapine was discontinued and the patient was transferred to the cardiology service for guideline-directed medical management of myocarditis and heart failure with reduced ejection fraction. The overall mechanism of clozapine cardiotoxicity is not well understood. Proposed hypotheses include IgE-mediated acute hypersensitivity and cardiac myocyte damage via the release of proinflammatory cytokines. However, when suspecting myocarditis after initiating clozapine, continuous monitoring and cessation of the medication are crucial in preventing permanent damage to the myocardium. Given the cardiac risk of medication and potential lethality of myocarditis via progression to heart failure, it is important to observe physical examination findings as well as symptoms of the condition when initiating a patient on clozapine.
Keywords: clozapine; drug-induced myocarditis; echocardiography; myocarditis; schizophrenia.
Copyright © 2021, Im et al.