Sanchez Asiel Yair Adan, Foster Jessica J, Plymen Carla M, Shergill Sukhi
, BBMed, Melbourne Medical School, Austin Hospital, The University of Melbourne, Melbourne, Australia.
, MB BCh, National Psychosis Unit, South London and Maudsley NHS Foundation Trust, London, UK.
BJPsych Open. 2016 Dec 14;2(6):390-393. doi: 10.1192/bjpo.bp.116.003723. eCollection 2016 Nov.
There is currently limited experience in the initiation and maintenance of clozapine for treatment-resistant psychosis in adults with established structural heart disease. These complex patients require close supervision and liaison between colleagues. Here we present the successful experience of treating one such patient within our service and describe a monitoring plan to ensure that these treatments can be provided both safely and effectively.
A 36-year-old man with treatment-resistant schizophrenia and known hypertrophic cardiomyopathy (HCM) was admitted to a specialist unit for a trial of clozapine. His psychiatric illness was characterised by multimodal hallucinations and delusions combined with low mood and poor motivation. The diagnosis of HCM was made 3 years previously following a routine electrocardiogram (ECG), and he had remained asymptomatic throughout this time; there were concerns about the risk of initiating clozapine given his pre-existing cardiac condition. Baseline investigations were performed as per local guidelines prior to commencing clozapine; these were within normal limits other than a mildly raised troponin level of 54 ng/L (normal <16 ng/L), which was attributed to the HCM. In addition, baseline transthoracic echocardiography (TTE) was performed which showed no change in the structural heart disease in comparison with previous TTEs. Clozapine was started at 12.5 mg daily and up-titrated to 150 mg twice daily over 14 days as per our institute's guidelines. The patient was monitored with regular testing of troponins, inflammatory markers and ECG. On day 18, the troponin level increased to 1371 ng/L. Creatine kinase and inflammatory markers remained stable. No changes in ECG or TTE were noted and the patient remained clinically asymptomatic. Cardiology opinion was sought and reported that the finding of an isolated elevated troponin was likely to reflect a 'troponin leak' in the context of increased cardiac muscle mass associated with HCM. In the absence of any clinical compromise, it was not felt to be of concern. Clozapine was continued with good effect on mental state. Troponin levels gradually reduced and the patient remained well.
While multiple cases of clozapine-induced cardiotoxicity have been reported in the literature, its implications for pre-existing structural disease are unclear. This case report suggests that clozapine can be safely introduced in pre-existing HCM, explores strategies for monitoring and highlights the importance of liaising with experienced cardiologists.
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© The Royal College of Psychiatrists 2016. This is an open access article distributed under the terms of the Creative Commons Non-Commercial, No Derivatives (CC BY-NC-ND) license.
目前，对于患有器质性心脏病的成年难治性精神病患者，在启动和维持氯氮平治疗方面经验有限。这些复杂的患者需要同事之间密切的监督和联络。在此，我们介绍了在我们的服务中治疗一名此类患者的成功经验，并描述了一项监测计划，以确保这些治疗能够安全有效地进行。
一名36岁患有难治性精神分裂症且已知患有肥厚型心肌病（HCM）的男性因氯氮平试验入住专科病房。他的精神疾病表现为多模态幻觉和妄想，伴有情绪低落和动力不足。HCM的诊断是在3年前通过常规心电图（ECG）做出的，在此期间他一直无症状；鉴于他已有的心脏疾病，人们担心启动氯氮平治疗的风险。在开始使用氯氮平之前，按照当地指南进行了基线检查；除肌钙蛋白水平轻度升高至54 ng/L（正常<16 ng/L）外，其他检查结果均在正常范围内，该升高归因于HCM。此外，进行了基线经胸超声心动图（TTE）检查，结果显示与之前的TTE相比，结构性心脏病无变化。根据我们研究所的指南，氯氮平开始时每日剂量为12.5 mg，并在14天内逐渐增加至每日两次，每次150 mg。通过定期检测肌钙蛋白、炎症标志物和ECG对患者进行监测。在第18天，肌钙蛋白水平升至1371 ng/L。肌酸激酶和炎症标志物保持稳定。ECG和TTE未发现变化，患者临床无症状。咨询了心脏病学专家的意见，专家报告称，在与HCM相关的心肌质量增加的情况下，孤立的肌钙蛋白升高可能反映了“肌钙蛋白泄漏”。在没有任何临床损害的情况下，认为无需担忧。继续使用氯氮平，对精神状态有良好效果。肌钙蛋白水平逐渐降低，患者情况良好。
虽然文献中已报道多例氯氮平引起的心脏毒性病例，但其对已有的结构性疾病的影响尚不清楚。本病例报告表明，在已有的HCM患者中可以安全地引入氯氮平，探讨了监测策略，并强调了与经验丰富的心脏病专家联络的重要性。
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©英国皇家精神科医学院2016年。本文是一篇开放获取文章，根据知识共享非商业性、无衍生作品（CC BY-NC-ND）许可条款发布。
