Sequential speckle tracking imaging to detect early stage of cancer therapeutics-related cardiac dysfunction in a patient with breast cancer
Sequential speckle tracking imaging to detect early stage of cancer therapeutics-related cardiac dysfunction in a patient with breast cancer
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序贯斑点追踪成像检测乳腺癌患者癌症治疗相关心脏功能障碍的早期阶段
DOI：
10.1007/s12574-019-00423-2
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发表时间：
2019
影响因子：
1.6
通讯作者：
Sata Masataka
中科院分区：
文献类型：
--
作者：
Saijo Yoshihito;Kusunose Kenya;Yamada Nao;Yamada Hirotsugu;Nishio Susumu;Hirata Yukina;Sata Masataka
一名69岁女性被诊断为右侧乳腺癌，为III期浸润性导管癌，具有高增殖活性（Ki-67表达：30%阳性染色细胞）、激素受体（雄激素受体）阳性和HER2过表达。初始化疗前超声心动图显示左心室 (LV) 大小和功能正常。初次超声心动图检查后，患者接受 4 个周期的表阿霉素和环磷酰胺治疗，随后接受 3 个周期的曲妥珠单抗和紫杉醇新辅助化疗。初次化疗 6 个月后，患者接受了右侧乳腺癌手术切除。初次化疗后，整体纵向应变（GLS）似乎较基线值有所下降；然而，在 15 个月的随访期间，左心室射血分数 (EF) 没有变化在正常范围内。初次化疗15个月后，虽然血清B型利钠肽为30 pg/ml，高敏肌钙蛋白I<5 mg/dl，但她有轻度劳力性呼吸困难。初次化疗15个月后经胸超声心动图显示LVEF下降33%（图1），诊断为化疗相关心功能不全（CTCRD）。我们停止化疗，并为患者提供心力衰竭药物治疗，包括依那普利 2.5 mg、卡维地洛 2.5 mg 和阿佐塞米 15 mg/天（补充材料 1）。随着药物缓慢上调，LVEF 和 GLS 已恢复正常。这个案例展示了两个重要的见解。首先是定期连续随访检查的重要性。通过定期随访检查，可以发现左室收缩功能障碍的微小变化。末次给药后 12 个月内接受化疗的患者中有 6-9% 发生 CTRCD [1]。然而，许多文献报道CTRCD也发生在远期[2]。我们应该进行序贯超声心动图检查、心脏磁共振成像或多门控采集扫描，因为 CTRCD 是由 LVEF 值定义的。第二是确认我们可以通过GLS而不是LVEF来检测化疗引起的左室收缩功能障碍的早期变化。既往文献报道化疗后ΔGLS下降11%的患者多发生CTRCD[3]。附录 1 显示了随访期间每 3 个月的 LVEF 和 GLS 测量值。初次化疗3个月后随访，ΔGLS下降14%，可能提示左心室心肌早期损伤。根据我们的病例，化疗后定期评估心脏收缩功能非常重要，GLS 比 LVEF 等常规值更有助于检测早期心肌损伤（如 CTRCD 前期）。
A 69-year-old woman was diagnosed with right breast cancer which was a stage III invasive ductal breast carcinoma with high proliferative activity (Ki-67 expression: 30% positively stained cell), positive hormone receptor (androgen receptor) and HER2 overexpressed. Echocardiography before initial chemotherapy showed normal left ventricular (LV) size and function. After the initial echocardiographic study, the patient was given 4 cycles of epirubicin and cyclophosphamide, followed by 3 cycles of trastuzumab and paclitaxel as neoadjuvant chemotherapy. The patient was performed surgical resection of right breast cancer at 6 months later from initial chemotherapy. After initial chemotherapy, global longitudinal strain (GLS) seemed to decrease from the baseline values; however, LV ejection fraction (EF) did not change within normal limit during 15 months follow-up. After 15 months from initial chemotherapy, although serum B-type natriuretic peptide is 30 pg/ml and high-sensitive troponin I is< 5 mg/dl, she had mild exertional breathlessness. Transthoracic echocardiography after 15 months from initial chemotherapy showed decreased LVEF of 33%(Fig. 1), then she was diagnosed chemotherapy-related cardiac dysfunction (CTCRD). We stopped chemotherapy, and patient was provided heart failure pharmacological treatment with enalapril 2.5 mg, carvedilol 2.5 mg, and azosemide 15 mg/day (SUPPLEMENT 1). With a slow pharmacological uptitration, LVEF and GLS had normalized. This case shows two important insights. The first is that importance of regular sequential follow-up examination. We can find the tiny change of LV systolic dysfunction by performing regular follow-up examinations. CTRCD occurred in 6–9% of the patients with chemotherapy within 12 months from the last administration [1]. However, many literatures reported that CTRCD also occurred in remote phase [2]. We should perform sequential echocardiographic examination, cardiac magnetic resonance imaging or multigated acquisition scan because CTRCD is defined by the value of LVEF. The second is to confirm that we can detect the early change of LV systolic dysfunction due to chemotherapy by GLS rather than LVEF. Previous literature reported that the patients with 11% decreased of ΔGLS after chemotherapy had more development of CTRCD [3]. SUPPLEMENT 1 shows the measurements of LVEF and GLS every 3 months during follow-up. The decrease of ΔGLS of 14% at followup study 3 months later from initial chemotherapy may indicate the early impairment of LV myocardium. According to our case, it is important to evaluate regularly cardiac systolic function after chemotherapy, and GLS is more useful than conventional values such as LVEF to detect early stage of myocardial impairment as pre-stage of CTRCD.