Psychosomatics 43:248, June 2002
© 2002 The Academy of Psychosomatic Medicine
Clozapine-Associated Cardiomyopathy
K. Luan Dinh Phan, M.D., and
Stephan F. Taylor, M.D., Ann Arbor, Michigan
Key Words: Cardiomyopathy • Clozapine-Associated
TO THE EDITOR: Kilian et al.1 recently surveyed 8,000 patients treated with clozapine and found 8 cases with objective evidence of cardiomyopathy in previously healthy patients with schizophrenia. Only one previous case report had suggested this association.2 This prompted us to examine our own experience in a university-run clozapine clinic involving 195 patients (from February 1994 to August 2000) who received a minimum of 2 weeks of clozapine therapy. We report one well-documented case of cardiomyopathy following treatment with clozapine.
Case Report
Mr. A., a 29-year-old man with schizoaffective disorder, was initiated on clozapine therapy after failure of atypical antipsychotic agents. Clozapine was titrated to 125 mg over 3 weeks, limited by Mr. A.'s complaints of sedation and fatigue. One week after clozapine was initiated, he developed subjective fevers, dry cough, malaise, and pleuritic chest pain that became unresponsive to a 10-day trial of clarithromycin. Two weeks later, Mr. A. presented to the emergency department with worsening exercise-induced shortness of breath and dyspnea. His electrocardiogram showed sinus tachycardia and mild ST elevation in leads I and aVL, and a chest x-ray revealed pulmonary congestion. He was admitted for further workup.
On his second day of nebulizer and intravenous antibiotic treatments, Mr. A. developed severe respiratory distress with pulmonary edema, requiring transfer to the intensive care unit. A two-dimensional echocardiogram revealed dilated cardiomyopathy with diffuse hypokinesis and an ejection fraction of 35%. Extensive evaluation for infectious, metabolic, and ischemic causes did not reveal an etiology. On the fourth day of hospitalization, clozapine was discontinued. With continued aggressive diuresis and inotropic therapy, Mr. A.'s respiratory status began to improve, and he was extubated and transferred to the general floor. A follow-up echocardiogram 5 days after discontinuation of clozapine revealed significant improvement in kinetics and ejection fraction (50%), and the electrocardiogram had returned to its previous normal sinus rhythm without any ST abnormalities. Mr. A. was subsequently switched to an alternative antipsychotic medication and discharged from the hospital. He has since made a full recovery without reoccurrence of heart disease.
Discussion
Although our database is small (195 patients since its inception), we found one definitive and well-documented case of reversible cardiomyopathy after initiation of clozapine therapy. Mr. A. was taking a modest dose of clozapine and had no history of cardiac disease or alcoholism. Although a direct mechanism for his cardiac decompensation is uncertain, there was a close temporal relation between the onset of congestive symptoms and dose increases of clozapine (perhaps suggesting an immunoglobulin Emediated hypersensitivity reaction) as well as a dramatic reversal of cardiac dysfunction after discontinuation of clozapine.
Clozapine is typically well tolerated, but recent case reports have suggested some risk of serious cardiac complications with its use. Complaints of chest pain, dyspnea, and tachycardia at initiation of clozapine may not be fully attributable to side effects and should alert clinicians to potential early signs of cardiac failure. This potential association also may have treatment implications for those patients with known or significant risk factors for cardiac disease. Further studies are warranted to further delineate the association between clozapine and cardiomyopathy.
REFERENCES
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Kilian JG, Kerr K, Lawrence C, et al: Myocarditis and cardiomyopathy associated with clozapine. Lancet 1999; 354:1841-1845[CrossRef][Medline]
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Leo RJ, Kreeger JL, Kim KY: Cardiomyopathy associated with clozapine. Ann Pharmacother 1996; 30:603-605[Abstract]
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