Objective: To report a case of a patient treated with clozapine who developed pericarditis with pericardial effusion that resolved when the drug was discontinued. Method: Case report of a 21-year-old man with psychotic disorder that had been stable on clozapine therapy for five months (after failure of atypical antipsyhotic agents) presented to the emergency department complaining of chest pain and progressive shortness of breath that had lasted for a few days. Echocardiography showed a pericardial effusion suggestive of a cardiac tamponade, and the fluid was removed by pericardiocentesis. All other possible causes of the pericardial effusion were ruled out and clozapine was suspected as the most likely explanation. Clozapine was discontinued and the patient's symptoms improved markedly. Discussion: According to the Naranjo probability scale, clozapine is a probable cause of pericarditis. Although clozapine is a known cause of myocarditis and cardiomyopathy, there are only several reports in the literature describing clozapine-induced pericarditis and pericardial effusion. In our patient, the pericardial effusion cleared within several days following clozapine discontinuation. Conclusion: There have been only a few cases of clozapine-induced pericarditis reported in the literature, however this adverse effect of clozapine can occur, as this case report clearly demonstrates. Cardiac adverse effects of clozapine are potentially life threatening, hence early recognition is essential to prevent serious outcomes.

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Introduction: Individuals with severe sleep related breathing disorders (SRBD) tend to experience intermittent hypoxia, sleep fragmentation and highly fluctuating intrathoracic pressures. Chronic exposure to these stressors sensitizes the parasympathetic system while suppressing the sympathetic system. Parasympathetic over-reactivity among patients with severe sleep related breathing disorders has been proposed as a predisposing factor for neurally mediated syncope. Goal: We sought to determine the relative risk for neurally mediated syncope in patients with severe SRBD compared to the general population. Methods: This is a retrospective cohort study of 228 cases selected from 2,598 patients who were referred for polysomnography on discharge from hospitalization. Incidence of neurally mediated syncope (NMS) was compared between patients with apneahypopnea-index (AHI) scores of 30 or greater and those with an AHI score below 5. Results: Approximately 32% of patients with severe SRBD had a history of neurally mediated syncope compared to only 14% in patients with normal sleep breathing patterns (OR = 3.09, 95% CI: 1.25 -7.62, p = 0.015). Conclusion: Our multi-center retrospective study supports an association between SRBD and NMS. Brief SummaryCurrent Knowledge/Study Rational. There are multiple reports that highlight a possible connection between sleep related breathing disorders and neurally mediated syncope. Deleterious effects on the autonomic and peripheral nervous system by severe sleep related breathing disorders have also been demonstrated. We sought to determine the association and relative risk of neurally mediated syncope in patients with severe sleep related breathing disorders.Study Impact. Patients with severe sleep related breathing disorders are at increased risk for neurally mediated syncope. Early identification and appropriate treatment in this Southwest Journal of Pulmonary and Critical Care/2019/Volume 18 77 patient population may reduce rates of syncope, improve quality of life and clinical outcomes.