决定异体 CAR T 细胞排斥与扩增的细胞和分子机制
Cellular and molecular mechanisms determining allogeneic CAR T cell rejection and expansion.
我们评估了11例接受单一批次cemacabtagene ansegedleucel(cema-cel)治疗的大B细胞淋巴瘤患者,cemacabtagene ansegedleucel是一种异体抗CD19 CAR T产品。
英文原题:Case Report: A case of heart failure recovery after non-ischemic cardiomyopathy following chimeric antigen receptor T-cell therapy.
本病例展示了 CAR-T 疗法并发症后漫长的心脏恢复过程。
引言:CAR-T 细胞疗法已成为一种极有前景的癌症免疫治疗。研究者正积极关注输注CAR-T细胞后可能因细胞因子释放综合征(CRS)导致的不良反应。本报告介绍一例值得关注的病例:患者CAR-T治疗后发生CRS,继而出现急性非缺血性心肌病和室性心动过速;并详细讨论其后续住院及门诊管理。 病例介绍:一名78岁男性,既往有前列腺腺癌、高血压和2型糖尿病史,无心脏病史或心力衰竭,因弥漫性大B细胞淋巴瘤(DLBCL)接受CAR-T治疗。同次住院期间,患者发生1级CRS,并出现无症状非持续性室性心动过速,疑似束支折返性室性心动过速(BBRT-VT)。CAR-T输注后超声心动图发现左心室射血分数(LVEF)降至35%,明显低于两个月前基线的51%。发生室性快速性心律失常后,开始使用胺碘酮控制心律。但在接下来五个月内,患者多次因心力衰竭加重住院;此期间射血分数降至15%,之后转诊接受植入式心律转复除颤器(ICD)治疗,随后在继续胺碘酮和指南指导药物治疗后逐渐改善。此后18个月内,LVEF恢复至55%,凸显免疫治疗诱发的心肌病合并室性快速性心律失常后可能具有可逆性。 结论:本病例展现了CAR-T治疗并发症后的长期心脏恢复过程,也为临床成功管理CAR-T诱发心肌病及可能复杂室性心律失常提供了参考。
INTRODUCTION: Chimeric Antigen Receptor T-cell (CAR-T) therapy has emerged as a highly promising immunotherapy for cancer treatment. Intensive research is being conducted focusing on adverse effects that CAR-T infusions may have due to the development of cytokine release syndrome (CRS). We aim to highlight a noteworthy case of ventricular tachycardia presented in the setting of acute non-ischemic cardiomyopathy following CRS after CAR-T therapy, along with providing a detailed discussion of subsequent inpatient and outpatient management. CASE PRESENTATION: A 78-year-old man with a past medical history of prostate adenocarcinoma, hypertension, and type two diabetes mellitus, with no prior cardiac history or heart failure, underwent CAR-T therapy for diffuse large B-cell lymphoma (DLBCL). During the same hospitalization, he developed grade one CRS along with asymptomatic non-sustained ventricular tachycardia which was suspected to be bundle branch reentrant tachycardia (BBRT-VT). An echocardiogram performed after CAR-T infusion revealed a reduced left ventricular ejection fraction (LVEF) of 35%, a significant decline from his baseline LVEF of 51% two months prior. After the development of the ventricular tachyarrhythmia, amiodarone was initiated for rhythm control. However, over the subsequent five months, the patient had multiple hospital admissions for heart failure exacerbations. During this period, his EF declined to 15% when he was referred for implantable cardioverter defibrillator (ICD) implantation before gradually improving with continued amiodarone and guideline-directed medical therapy. Over the next 18 months, his LVEF recovered to 55%, highlighting the potential reversibility of immunotherapy-induced cardiomyopathy complicated by ventricular tachyarrhythmia. CONCLUSION: This case showcases a prolonged cardiac recovery following complications of CAR-T therapy. It also provides insight into the successful clinical management of a patient due to CAR-T-induced cardiomyopathy in the setting of potentially complex ventricular arrhythmias.
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