[A Case of Dilated Cardiomyopathy after 17 Years of Clozapine Treatment].

Clozapine-induced cardiomyopathy is a rare but fatal complication with a reported incidence of 0.4% in Japan. Clozapine-induced cardiomyopathy develops at an average of 14.4 months after initiating clozapine, and to our knowledge, has a duration no longer than seven years. We present a patient who developed dilated cardiomyopathy after 17 years of clozapine treatment and made a full recovery of cardiac function at 40 weeks after clozapine treatment cessation. A 43-year-old male with a 24-year history of schizophrenia was treated with clozapine (600 mg/day) for 17 years. No abnormal findings were revealed at follow up until he pre- sented with dyspnea with no accompanying symptoms while walking. He was suspected of worsening asthma due to his past history and lack of abnormalities of ECG and CXR. However, as he experienced gradually worsening dyspnea accompanied by listlessness and lightheaded- ness, he was referred to a cardiologist. The echocardiogram revealed left ventricular dilatation and systolic dysfunction (left ventricular ejection fraction, LVEF=40%), which made a diagno- sis of dilated cardiomyopathy. We excluded cardiac ischemia and other possible causes of dilated cardiomyopathy with cardiac catheterization and endomyocardial biopsy. Clozapine treatment was stopped and switched to olanzapine along with standard heart failure medica- tions. The symptoms and left ventricular function improved following clozapine discontinua- tion. The symptoms resolved and echocardiogram showed a LVEF of 50% within 11 weeks after treatment with clozapine was ended. LVEF was reported at 59% 40weeks after cessation of clozapine. At the present time, 32 months since ceasing clozapine treatment, no worsening of symptoms has been presented. After ceasing clozapine and inducing standard heart failure medications, the patient presented the excellent recovery and the normalization of his echocar- diogram. Despite this outcome, there is currently insufficient evidence to conclusively establish a causal relationship between clozapine and cardiomyopathy in this case. In addition, this case demonstrates that we cannot exclude cardiomyopathy due to lack of abnormal findings of ECG and CXR. Therefore, we recommend that echocardiograms should be performed annually. The mortality associated with clozapine-induced cardiomyopathy is high, so if patients undergoing therapy with clozapine develop new symptoms or signs suggestive of cardiac dysfunction such as dyspnea, a focused cardiovascular examination should be considered.