Abstract Body (Do not enter title and authors here): Case Descripton
A 34-year-old male with Schizophrenia was transferred from inpatient Psychiatry unit for chest tightness, fevers andtachycardia after testing positive for COVID-19. Further history revealed antipsychotics had been recently adjusted with the addition of Clozapine 1 month prior to presentation.
On presentation, he was febrile (39.1°C) and tachycardic to the 146 in sinus tachycardiac on EKG and Telemetry. He was euvolemic on exam with tachycardia but no murmurs or discernable friction rub.
Labs revealed no leukocytosis but an elevated C-reactive protein (CRP) 168mg/L, high-sensitivity troponin (474ng/L) and brain-natriuretic peptide (BNP, 176 pg/mL, no baseline value). Otherwise, TSH, ANA and RF were normal. Repeat Respiratory Viral Panel, respiratory biofire and blood cultures were unrevealing. Imaging (CXR and Chest CTA) were normal. TTE showed normal function and small pericardial effusion. Cardiac MRI was limited by inability to tolerate the scan but reported preserved biventricular function. The home facility was contacted and reported initial COVID testing was expired and invalid. Psychiatry was consulted for suspected clozapine-induced myocarditis and recommending holding Clozapine while resuming Risperdione.
The patient reported subjective improvement in symptoms and return to baseline. Feversdefervesced and tachycardiac resolved.
Discussion
Rare (0.06%-3.88% reported incidence) and not well-described, Clozapine-induced myocarditis can be a challenging entity to identify. In the literature, it is defined as having elevated CRP or detectable troponin and at least 1 sign or symptom of myocarditis, in the absence of alternative plausible etiologies. Symtoms typically onset between 1-4 weeks of medication initiation. Mortality can range between 10-30%. The acute history of symptoms, elevation in CRP and troponin shortly after medication initiation suggested a diagnosis of clozapine-induced myocarditis. The absence of reduction in systolic function and indeterminant MRI are nocompelling against clozapine-induced myocarditis in lieu of other more plausible diagnoses. Early cessation and symtpomatic managemnt is standard therapy.
Conclusion
Clozapine-induced Myocarditis is an entity not well-described but carries a significant mortality risk. Perhaps cardiac-monitoring guidelines must be implemented in addition to the currently adopted montiroing for agranylocytosis with clozapine.