Attarian Shirin, Wang Cindy Y, Romero Jorge, Barta Stefan K, Aparo Santiago, Menegus Mark A
Department of Internal Medicine, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, USA.
Montefiore-Einstein Center for Heart and Vascular Care, Albert Einstein College of Medicine, Bronx, NY, USA.
J Cardiol Cases. 2014 Jul 28;10(5):176-179. doi: 10.1016/j.jccase.2014.07.004. eCollection 2014 Nov.
Cardiac toxicity as a side effect of chemotherapeutic agents has been well reported in the literature. Cardiac toxicity secondary to alemtuzumab has been reported, presenting as congestive heart failure and arrhythmias. Here we report a case of acute myocardial dysfunction after administration of a test dose of alemtuzumab. Our patient was a 66-year-old man with a history of small lymphocytic lymphoma/chronic lymphocytic lymphoma who received a test dose of alemtuzumab. Twenty minutes post administration, the patient developed nausea, vomiting, rigors, and tachycardia. Electrocardiography (ECG) showed acute ST-segment elevations in contiguous leads V2-V6, I, and AVL with no associated chest pain. Bedside echocardiogram showed akinesis of the anterior septum, apex, distal anterior wall, and decreased left ventricular ejection fraction. Cardiac catheterization showed non-critical occlusive disease and no intervention was undertaken. Post-catheterization ECG revealed resolution of ST segment elevations, TWI in V4-V6, and prolongation of corrected QT. Repeat echocardiogram 10 days after the event demonstrated no improvement in wall motion or ejection fraction. We discuss the possible mechanisms causing ST-elevations and acute myocardial dysfunction after treatment with alemtuzumab. < Alemtuzumab can cause acute myocardial dysfunction after administration of a test dose. Considering that this is a serious adverse effect, detailed cardiac evaluation and a high level of caution are recommended before administration of alemtuzumab. While no clear etiology could be identified for this side effect, excessive and acute cytokine release triggered by alemtuzumab administration is a possible explanation. This could be potentially attenuated by using anti-interleukin-6 or tumor necrosis factor inhibitors.>.
化疗药物的心脏毒性作为一种副作用在文献中已有充分报道。已报道阿仑单抗继发的心脏毒性，表现为充血性心力衰竭和心律失常。在此我们报告一例在给予阿仑单抗试验剂量后发生急性心肌功能障碍的病例。我们的患者是一名66岁男性，有小淋巴细胞淋巴瘤/慢性淋巴细胞性淋巴瘤病史，接受了阿仑单抗试验剂量。给药后20分钟，患者出现恶心、呕吐、寒战和心动过速。心电图（ECG）显示连续导联V2-V6、I和AVL出现急性ST段抬高，无相关胸痛。床旁超声心动图显示前间隔、心尖、远端前壁运动减弱，左心室射血分数降低。心脏导管检查显示非严重闭塞性疾病，未进行干预。导管检查后心电图显示ST段抬高、V4-V6导联T波倒置和校正QT间期延长消失。事件发生10天后复查超声心动图显示室壁运动或射血分数无改善。我们讨论了阿仑单抗治疗后导致ST段抬高和急性心肌功能障碍的可能机制。<阿仑单抗给予试验剂量后可导致急性心肌功能障碍。鉴于这是一种严重的不良反应，建议在给予阿仑单抗之前进行详细的心脏评估并高度谨慎。虽然这种副作用的明确病因尚无法确定，但阿仑单抗给药引发的过度和急性细胞因子释放是一种可能的解释。使用抗白细胞介素-6或肿瘤坏死因子抑制剂可能会减轻这种情况。>
