Endomyocardial biopsy in a patient with myositis and a negative cardiovascular magnetic resonance during immune checkpoint therapies
Endomyocardial biopsy in a patient with myositis and a negative cardiovascular magnetic resonance during immune checkpoint therapies
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免疫检查点治疗期间肌炎且心血管磁共振阴性患者的心内膜心肌活检
DOI：
10.1093/ehjci/jeac117
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发表时间：
2022
期刊：
影响因子：
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通讯作者：
Dohi Kaoru
中科院分区：
文献类型：
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作者：
Yamaguchi Kazuma;Ida Mizuki;Nakamori Shiro;Sugimoto Ryosuke;Dohi Kaoru
1例76岁男性晚期肝细胞癌患者在首次接受atezolizumab和贝伐珠单抗免疫治疗后出现疲乏和轻微肌痛。实验室检查结果如下：肌酸激酶（CK）：1926 U/L; CK-MB：69 U/L;肌钙蛋白I：79.7 pg/mL。心电图显示心前导联轻微T波异常，而超声心动图显示左心室（LV）收缩功能正常。总体纵向应变为− 19%，相对于基线值无≥ 12%的相对降低。电影心血管磁共振（CMR）也显示左心室腔大小、射血分数、质量指数正常，无心包积液。多参数标测（分别为1248 ms、46 ms和31.5%）上的整体心肌天然T1、T2和细胞外容积分数未增加，或LGE-CMR上T2加权短TI反转恢复无晚期钆增强（LGE）的高信号强度（图A-E）。冠状动脉造影显示无异常结果，并从中间室间隔取活检样本。组织学样本显示局灶性但强烈的淋巴细胞浸润和肌细胞坏死，诊断为免疫检查点抑制剂（ICI）心肌炎（图F）。先前的病理学研究报告，超过一半的ICI心肌炎病例显示出轻度的炎性细胞浸润。在不到30%的ICI心肌炎中存在LGE或T2加权短TI反转恢复升高。此外，使用临床参数标测的定量CMR的灵敏度受限于其不能覆盖整个心肌。这些数据表明，依赖基于CMR的方法排除ICI心肌炎时应谨慎。将伴随性肌炎视为心肌炎的“危险信号”，有助于提醒临床医生即使在CMR阴性后也要进行肌内膜活检。
A 76-year-old male with advanced hepatocellular carcinoma presented with fatigue and minor myalgias after his first immunotherapy with atezolizumab and bevacizumab. Laboratory tests were as follows: creatine kinase (CK), 1926 U/L; CK-MB, 69 U/L; and troponin I, 79.7 pg/mL. Electrocardiogram revealed slight T-wave abnormalities in the precordial leads, while echocardiography showed normal left ventricular (LV) systolic function. Global longitudinal strain was− 19% without≥ 12% relative reduction from the baseline value. Cine cardiovascular magnetic resonance (CMR) also demonstrated normal LV cavity size, ejection fraction, mass index, and no pericardial effusion. There was no increased global myocardial native T1, T2, and extracellular volume fraction on multiparametric mapping (1248 ms, 46 ms, and 31.5%, respectively) or high signal intensity on T2-weighted short-TI inversion recovery without late gadolinium enhancement (LGE) on LGE-CMR (Panels A–E). Coronary angiography revealed no abnormal findings, and biopsy samples were taken from the mid interventricular septum. Histological samples revealed a focal but intense lymphocytic infiltrate and myocyte necrosis, resulting in a diagnosis of immune checkpoint inhibitor (ICI) myocarditis (Panel F). A previous pathological study reported that more than half of ICI myocarditis cases showed a low degree of inflammatory cell infiltration. LGE or elevated T2-weighted short-TI inversion recovery was present in fewer than 30% of ICI myocarditis. Furthermore, the sensitivity of quantitative CMR using clinical parametric mapping is limited by its inability to cover the whole myocardium. These data suggest caution when relying on a CMR-based approach for the exclusion of ICI myocarditis. The identification of concomitant myositis being considered as a ‘red flag’for myocarditis should help alert the clinician to pursue endomyocardial biopsy even after negative CMR.