分享:
分享到微信朋友圈
X
综述
蒽环类药物所致心脏毒性的磁共振研究进展
田瑶天 王翠艳

Cite this article as: Tian YT, Wang CY. Research progress of cardiac magnetic resonance imaging in anthracycline-induced cardiotoxicity[J]. Chin J Magn Reson Imaging, 2022, 13(3): 147-150.本文引用格式:田瑶天, 王翠艳. 蒽环类药物所致心脏毒性的磁共振研究进展[J]. 磁共振成像, 2022, 13(3): 147-150. DOI:10.12015/issn.1674-8034.2022.03.036.


[摘要] 蒽环类药物(anthracycline,ATC)是常见的化疗药物,具有突出的心脏毒性。蒽环类药物所致心脏毒性(anthracycline-induced cardiotoxicity,AIC)是影响癌症患者生存质量的重要因素。准确检测及正确评估AIC能够为临床诊疗提供重要信息,降低癌症患者出现心血管并发症的风险。心脏磁共振(cardiac magnetic resonance,CMR)具有无创、可重复性好、空间分辨率高、多序列成像等优势,在AIC的基线评估及跟踪随访中起到了重要作用。近年来,包括特征追踪(feature-tracking,FT)技术及mapping技术在内的一系列CMR新技术的发展更是在AIC的早期检测方面发挥了重要的作用。本文将对CMR在检测和评估AIC中的应用及研究进展作一综述。
[Abstract] Anthracycline (ATC) is a commonly used chemotherapeutic drug with prominent cardiotoxic side effects. Anthracycline-induced cardiotoxicity (AIC) increases the cardiovascular morbidity and mortality of cancer survivors and seriously affects the quality of their life. Detecting and evaluating the AIC precisely can provide key information for clinical diagnosis and treatment, and reduce cardiovascular complications in cancer survivors. Cardiac magnetic resonance (CMR), as a noninvasive procedure, plays an important role in the baseline evaluation and follow-up of AIC due to its advantages of good repeatability, high spatial resolution, and multiple-parameter-imaging. Recently, series of new CMR technologies, including feature tracking (FT) and mapping, played an irreplaceable role in the early detection of AIC. Here we summarized the technical advantages and the progress of clinical application on CMR detecting and evaluating AIC.
[关键词] 心脏磁共振成像;蒽环类药物;心脏毒性;化学疗法;特征追踪;心肌应变;心肌组织特性
[Keywords] cardiac magnetic resonance imaging;anthracycline;cardiotoxicity;chemotherapy;feature tracking;myocardial strain;myocardial tissue characteristics

田瑶天 1   王翠艳 2*  

1 山东大学附属省立医院医学影像科,济南 250021

2 山东第一医科大学附属省立医院医学影像科,济南 250021

王翠艳,E-mail:wcyzhang@163.com

作者利益冲突声明:全体作者均声明无利益冲突。


基金项目: 山东省自然科学基金面上项目 ZR2019MH125
收稿日期:2021-08-05
接受日期:2022-02-17
中图分类号:R445.2  R595.4 
文献标识码:A
DOI: 10.12015/issn.1674-8034.2022.03.036
本文引用格式:田瑶天, 王翠艳. 蒽环类药物所致心脏毒性的磁共振研究进展[J]. 磁共振成像, 2022, 13(3): 147-150. DOI:10.12015/issn.1674-8034.2022.03.036.

       蒽环类药物(anthracycline, ATC)自1962年从链霉菌属中分离出来后被广泛应用于多种实体瘤及恶性血液系统肿瘤的治疗中,但突出的心脏毒性增加了人们的使用顾虑。最初的研究报道,蒽环类药物所致心脏毒性(anthracycline-induced cardiotoxicity,AIC)的发生率为16%~23%,通过后续的不断研究及改进,这一概率有所降低,但仍可达到6%~18%[1]。近年来随着癌症治疗方法的不断进步,癌症患者的无病生存期大大延长,心血管疾病已经成为癌症存活者远期发病率和死亡率的第二主要因素,仅次于癌症本身[2]。因此,早期检测并正确评估AIC对于临床决策具有重要意义。心脏磁共振(cardiac magnetic resonance,CMR)具有空间分辨率高,诊断一致性强,可重复性好等优点,CMR新技术还可以实现功能成像、应变分析、血流测速及心肌组织特性定量分析等功能,在AIC的早期检测、基线评估及跟踪随访中起到重要的作用。本文将对CMR在检测和评估AIC方面的技术优势、应用及研究进展作一综述。

1 AIC的损伤机制

       ATC可诱导具有剂量依赖性、渐进性及累积性的细胞层面上不可逆的心功能障碍,其原因可能和ATC导致的细胞坏死、凋亡有关[3]。AIC在ATC治疗后几分钟至1周内即可发生,主要表现为短暂的电生理异常,包括ST段和T波异常、Q-T间期延长和QRS低电压等;也可表现为急性短暂的心肌收缩功能下降[4]。由于心肌广泛的代偿机制,只有在心功能储备耗尽之后,这种损伤才可能转化为临床表现,因此临床表现可以在数年或者数十年之后才出现[3,5]。如果AIC表现为明显的慢性心力衰竭则预后很差,大多数患者在两年内死亡[6];而如果在检测到左室功能障碍的征象时立即开始心衰治疗,左室功能则部分可逆[3,5]。已有大量基础研究对AIC的损伤机制进行了探讨,尽管具体机制仍不清楚,但氧化应激、脂质过氧化、细胞凋亡和自噬的失调都参与其中[7]。除此之外,AIC的损伤机制还包括拓扑异构酶Ⅱ的参与。ATC可以与心肌细胞表达的拓扑异构酶Ⅱβ结合,诱导心肌细胞DNA双链的断裂与凋亡[3,8]

2 CMR常规技术在检测AIC中的应用

       常规CMR技术,包括电影序列及延迟钆强化(late gadolinium enhancement,LGE),可以从形态、功能和组织特征等多个方面为检测AIC提供信息,最常用的指标是左心室射血分数(left ventricular ejection fraction , LVEF)。2014年的一份专家共识中,AIC被定义为LVEF下降幅度>10%,并最终<53%,且在初次异常后2~3周进行影像学复查结果依然异常[3]。CMR评估LVEF具有良好的组间和组内可重复性[9],因而被视作金标准[10]。应用LVEF对AIC进行评估较为便捷直观,缺点是不能反映AIC早期心功能的细微变化。诸多研究显示,在应用ATC后的早期,LVEF往往并无明显的变化,或虽然存在变化,但仍在正常范围内(>53%)[11, 12, 13, 14, 15, 16]。一旦检测到LVEF急剧下降,则心功能的改变无法逆转,影响患者预后[5]。因此,有必要使用更灵敏的指标来及早地检测AIC。

       除了LVEF,左室质量的降低也是AIC的表现之一。大量研究显示接受ATC治疗后,患者的左室质量降低,此时LVEF可表现为下降或无明显变化[12,17, 18, 19]。对ATC治疗后出现LVEF下降的患者进行研究发现,左室质量和ATC剂量成反比,且左室质量的减少和ATC剂量的增加都与心血管不良事件的高发生率有关[19]。另一项研究认为左室质量的降低可能与ATC治疗后心肌细胞的萎缩有关[12]。此外,部分研究显示,在接受ATC治疗后,患者会出现右心室射血分数(right ventricular ejection fraction,RVEF)的降低及左心房容积的增大[17,20]。总的来说,对ATC治疗后右心室和左心房结构及功能的CMR研究目前相对较少,还需要进一步的研究为我们提供更多的信息。

       除了对常规形态及功能的评估外,CMR还可以评估心肌纤维化及瘢痕。LGE是目前应用最广泛的评估局灶性纤维化的技术,其位置及分布模式有助于鉴别缺血性及非缺血性心肌病。在接受ATC治疗的患者中,研究报道的LGE发生率并不一致,为0%~30%。在所有接受癌症治疗(无论是ATC还是非ATC)的患者中,LGE存在与否、位置及分布模式都不具有统计学意义的差异[21]。因此,目前认为LGE与AIC并不具有相关性,但LGE可能有助于鉴别AIC与其他心肌疾病。

3 CMR新技术在检测AIC中的应用

       尽管常规MRI检查为AIC的检测和评估提供了诸多信息,但对AIC的早期改变不够敏感,无法检测到亚临床AIC的存在。近年随着CMR新技术的发展,包括心肌应变、mapping技术等逐步应用于临床后均表现出特有的优势,为检测亚临床AIC的存在提供了更多的选择。

3.1 磁共振网格标记(tigging)技术及特征追踪(feature-tracking,FT)技术

       心肌力学研究的相关量化参数,如应变和应变率,被认为可以用来检测早期AIC的存在。常用的指标包括整体周向应变(global circumferential strain,GCS)、整体纵向应变(global longitudinal strain,GLS)及整体径向应变(global radial strain,GRS),其中GLS较GCS及GRS更稳定,具有更好的可重复性[22]。这些参数可以通过tigging技术及FT技术获得。tigging技术被认为是非侵入性测量心肌应变及相关参数的金标准,所测得的参数准确性高,但需要特定的扫描序列,繁杂的后处理也限制了其临床应用[23]。FT技术则是通过算法,在常规电影序列上跟踪和测量心肌组织的位移,获取相关量化参数。FT技术简化了扫描流程,但无法很好地识别心肌内部均匀组织的运动特征,所获取的心内膜参数有效性也远远高于心外膜[24]

       在接受ATC治疗的患者中,GCS、GLS及GRS的变化与患者AIC的发生风险相关[25]。相较于GLS正常的患者,GLS受损的患者发生AIC的风险增加4.9倍[26]。Lunning等[27]研究发现,在ATC治疗后早期(3个月),患者的GCS及GLS即发生显著降低,此时患者的LVEF并无显著性变化。对ATC治疗后早期AIC的研究普遍证实GLS的降低会先于LVEF,且认为GLS可以预测AIC的未来发展[3,13,25, 26,28, 29]。一项系统评价表明,在ATC治疗期间或之后,GLS会出现9%~19%的下降,其中早期GLS降低10%~15%被认为是预测癌症化疗患者心脏毒性的最有用参数[29]。因此,在2014年的专家共识及2016年欧洲心脏病学会的指南中认为GLS较治疗前基线下降>15%提示了AIC的存在[3,28]

3.2 mapping技术

       在电镜下,AIC的组织病理学变化首先表现为心肌细胞变性和炎性细胞浸润,随后出现水肿和弥漫性心肌纤维化[30]。这些病理变化会引起心肌组织T1、T2及细胞外容积(extracellular volume,ECV)的改变。mapping序列可以基于T1、T2及ECV的变化对心肌组织特性的变化进行像素级别的量化及可视化,为在体检测这些变化提供了解决方案[31]

3.2.1 Native T1 mapping及ECV

       Native T1 mapping反映的是心肌细胞和细胞外间质水的组成或局部分子环境,可以量化组织的T1弛豫信号。心肌组织水肿、纤维化、铁沉积及细胞外异常物质的积聚都会导致心肌组织Native T1的变化。这些病理变化也会导致强化后T1的变化,但强化后T1容易受到对比剂剂量、对比后图像采集时间、肾功能和红细胞压积的干扰,因而较少应用于临床实践中[31]。ECV反映了细胞外间质容积占整个心肌容积的百分比,相较于Native T1及强化后T1,ECV与心肌纤维化相关性最强,在没有浸润性心肌病及细胞外水肿的状况下,可作为心肌纤维化的生物标记物[32]

       研究显示,Native T1及ECV对AIC的检测往往早于LVEF的变化,并可以预测损伤的恢复情况及AIC的远期不良结果[11, 12,18,20,33]。在接受ATC治疗时或治疗后,患者的Native T1及ECV显著性增高,此时LVEF往往仍保持在正常范围内[11,16,18,20,33]。这种升高与LVEF及左室质量的降低相一致,独立于癌症本身及因年龄、性别导致的潜在心血管风险[18]。Muehlberg等[20]对30位接受ATC治疗的肉瘤患者进行了研究,发现在ATC初次应用后的48 h内,Native T1的显著升高可以预测化疗结束后AIC的发展。Ferreira等[12]的研究则表明,ATC治疗结束后3个月,ECV的显著升高与AIC所致的心肌细胞萎缩有关。

3.2.2 T2 mapping

       心肌水肿及铁沉积导致的局部磁敏感效应会引起组织T2弛豫时间的改变,引起组织T2的变化。常规T2WI可以监测心肌水肿,但线圈引起的信号强度变化、运动伪影、快心律/心律失常时的信号丢失以及慢血流区域的不完全血液抑制会干扰图像的最终成像质量[34]。T2 mapping序列具有很好的可重复性,可以快速、准确地量化心肌细胞内及细胞外水肿,因而被应用于多种心脏疾病的水肿检测及评估中。

       多项研究证实,在ATC治疗后的早期,心肌T2会出现显著性升高[11,14,15,35]。心肌T2的显著性增高在初次用药后的48 h内即可发生[15],但在ATC治疗后一年以上的患者中,仅观察到心肌Native T1及ECV的增高,T2并无显著性变化[14,16,20]。Haslbauer等[14]的研究说明了这一点,他们发现ATC治疗后的早期阶段(1个月)心肌T2显著性增高,但随着时间的推移,T2值出现稳步下降。这可能是由于在ATC治疗早期,炎性浸润导致的心肌水肿引起心肌T2增高,随着治疗结束水肿逐渐消退,T2值开始下降,而由于细胞坏死、凋亡导致的间质纤维化及细胞外容积扩大,Native T1及ECV升高。

3.2.3 联合Native T1 mapping、ECV及T2 mapping对AIC进行评估

       最新的关于AIC的动物模型研究,联合应用了Native T1 mapping、ECV及T2 mapping序列,将ATC治疗后心肌病理生理学变化与CMR图像表现结合起来[35, 36]。Farhad等[36]对45只小鼠AIC模型进行了研究,发现心肌T2及ECV的增加分别与心肌水肿及纤维化具有显著相关性,并可以预测AIC导致的小鼠远期死亡率;而LVEF则没有这个功能。Galan-Arriola等[35]对构建的猪AIC模型进行每两周一次的CMR检查,随访至16周并与组织病理学变化相对照。他们发现,最早发生的变化是T2的增高,随后才是Native T1及ECV的增高和LVEF的下降;最初T2的显著性增高仅与细胞内水肿相关;如果在T2显著升高时立刻停止ATC的使用,T2及心肌组织学的变化可以恢复。

       总之,CMR在监测及评估AIC方面具有独特的价值。部分CMR新技术,如FT技术及mapping技术为监测和评估早期AIC的存在提供了新的选择。目前还需要更进一步的研究,以确定mapping技术检测AIC的阈值,并解决其在不同机器中存在标准化差异的问题。相信随着研究的不断深入,我们可以找到临床干预及治疗AIC的最佳靶点,从而大大降低癌症存活者心血管不良事件的发生风险。

[1]
Lotrionte M, Biondi-Zoccai G, Abbate A, et al. Review and meta-analysis of incidence and clinical predictors of anthracycline cardiotoxicity[J]. Am J Cardiol, 2013, 112(12): 1980-1984. DOI: 10.1016/j.amjcard.2013.08.026.
[2]
Bodai BI, Tuso P. Breast cancer survivorship: a comprehensive review of long-term medical issues and lifestyle recommendations[J]. Perm J, 2015, 19(2): 48-79. DOI: 10.7812/TPP/14-241.
[3]
Plana JC, Galderisi M, Barac A, et al. Expert consensus for multimodality imaging evaluation of adult patients during and after cancer therapy: a report from the American Society of Echocardiography and the European Association of Cardiovascular Imaging[J]. J Am Soc Echocardiogr, 2014, 27(9): 911-939. DOI: 10.1016/j.echo.2014.07.012.
[4]
左洋萍, 刘柳, 曹礼庭. 超声心动图评估蒽环类化疗药物对乳腺癌患者心脏毒性作用的新进展[J]. 中华医学超声杂志(电子版), 2019, 16(12): 976-980. DOI: 10.3877/cma.j.issn.1672-6448.2019.12.018.
Zuo YP, Liu L, Cao LT. New advances in ultrasound evaluation of cardiotoxicities of anthracyclines in breast cancer patients. Chin J Med Ultrasound (Electronic Edition), 2019, 16(12): 976-980. DOI: 10.3877/cma.j.issn.1672-6448.2019.12.018.
[5]
Curigliano G, Cardinale D, Dent S, et al. Cardiotoxicity of anticancer treatments: Epidemiology, detection, and management[J]. CA Cancer J Clin, 2016, 66(4): 309-325. DOI: 10.3322/caac.21341.
[6]
Cardinale D, Colombo A, Lamantia G, et al. Anthracycline-induced cardiomyopathy: clinical relevance and response to pharmacologic therapy[J]. J Am Coll Cardiol, 2010, 55(3): 213-220. DOI: 10.1016/j.jacc.2009.03.095.
[7]
Renu K, Abilash VG, Tirupathi P, et al. Molecular mechanism of doxorubicin-induced cardiomyopathy-An update[J]. Eur J Pharmacol, 2018, 818: 241-253. DOI: 10.1016/j.ejphar.2017.10.043.
[8]
Murabito A, Hirsch E, Ghigo A. Mechanisms of anthracycline-induced cardiotoxicity: Is mitochondrial dysfunction the answer?[J]. Front Cardiovasc Med, 2020, 7: 35. DOI: 10.3389/fcvm.2020.00035.
[9]
Lambert J, Lamacie M, Thampinathan B, et al. Variability in echocardiography and MRI for detection of cancer therapy cardiotoxicity[J]. Heart, 2020, 106(11): 817-823. DOI: 10.1136/heartjnl-2019-316297.
[10]
Halliday BP, Senior R, Pennell DJ. Assessing left ventricular systolic function: from ejection fraction to strain analysis[J]. Eur Heart J, 2020. DOI: 10.1093/eurheartj/ehaa587.
[11]
Melendez GC, Jordan JH, D'agostino RB, et al. Progressive 3-month increase in LV myocardial ECV after anthracycline-based chemotherapy[J]. JACC Cardiovasc Imaging, 2017, 10(6): 708-709. DOI: 10.1016/j.jcmg.2016.06.006.
[12]
Ferreira De Souza T, Quinaglia ACST, Osorio Costa F, et al. Anthracycline therapy is associated with cardiomyocyte atrophy and preclinical manifestations of heart disease[J]. JACC Cardiovasc Imaging, 2018, 11(8): 1045-1055. DOI: 10.1016/j.jcmg.2018.05.012.
[13]
Gripp EA, Oliveira GE, Feijo LA, et al. Global longitudinal strain accuracy for cardiotoxicity prediction in a cohort of breast cancer patients during anthracycline and/or trastuzumab treatment[J]. Arq Bras Cardiol, 2018, 110(2): 140-150. DOI: 10.5935/abc.20180021.
[14]
Haslbauer JD, Lindner S, Valbuena-Lopez S, et al. CMR imaging biosignature of cardiac involvement due to cancer-related treatment by T1 and T2 mapping[J]. Int J Cardiol, 2019, 275: 179-186. DOI: 10.1016/j.ijcard.2018.10.023.
[15]
Lustberg MB, Reinbolt R, Addison D, et al. Early Detection of anthracycline-induced cardiotoxicity in breast cancer survivors with T2 cardiac magnetic resonance[J]. Circ Cardiovasc Imaging, 2019, 12(5): e008777. DOI: 10.1161/CIRCIMAGING.118.008777.
[16]
Tong X, Li VW, Liu AP, et al. Cardiac magnetic resonance T1 mapping in adolescent and young adult survivors of childhood cancers[J]. Circ Cardiovasc Imaging, 2019, 12(4): e008453. DOI: 10.1161/CIRCIMAGING.118.008453.
[17]
De Ville De Goyet M, Brichard B, Robert A, et al. Prospective cardiac MRI for the analysis of biventricular function in children undergoing cancer treatments[J]. Pediatr Blood Cancer, 2015, 62(5): 867-874. DOI: 10.1002/pbc.25381.
[18]
Jordan JH, Vasu S, Morgan TM, et al. Anthracycline-associated T1 mapping characteristics are elevated independent of the presence of cardiovascular comorbidities in cancer survivors[J]. Circ Cardiovasc Imaging, 2016, 9(8). DOI: 10.1161/CIRCIMAGING.115.004325.
[19]
Neilan TG, Coelho-Filho OR, Pena-Herrera D, et al. Left ventricular mass in patients with a cardiomyopathy after treatment with anthracyclines[J]. Am J Cardiol, 2012, 110(11): 1679-1686. DOI: 10.1016/j.amjcard.2012.07.040.
[20]
Muehlberg F, Funk S, Zange L, et al. Native myocardial T1 time can predict development of subsequent anthracycline-induced cardiomyopathy[J]. ESC Heart Fail, 2018, 5(4): 620-629. DOI: 10.1002/ehf2.12277.
[21]
Modi K, Joppa S, Chen KA, et al. Myocardial damage assessed by late gadolinium enhancement on cardiovascular magnetic resonance imaging in cancer patients treated with anthracyclines and/or trastuzumab[J]. Eur Heart J Cardiovasc Imaging, 2020. DOI: 10.1093/ehjci/jeaa279.
[22]
Claus P, Omar AMS, Pedrizzetti G, et al. Tissue tacking technology for assessing cardiac mechanics: pinciples, normal values, and clinical applications[J]. JACC Cardiovasc Imaging, 2015, 8(12): 1444-1460. DOI: 10.1016/j.jcmg.2015.11.001.
[23]
Ibrahim El SH. Myocardial tagging by cardiovascular magnetic resonance: evolution of techniques--pulse sequences, analysis algorithms, and applications[J]. J Cardiovasc Magn Reson, 2011, 13: 36. DOI: 10.1186/1532-429X-13-36.
[24]
Almutairi HM, Boubertakh R, Miquel ME, et al. Myocardial deformation assessment using cardiovascular magnetic resonance-feature tracking technique[J]. Br J Radiol, 2017, 90(1080): 20170072. DOI: 10.1259/bjr.20170072.
[25]
Narayan HK, French B, Khan AM, et al. Noninvasive measures of ventricular-arterial coupling and circumferential strain predict cancer therapeutics-related cardiac dysfunction[J]. JACC Cardiovasc Imaging, 2016, 9(10): 1131-1141. DOI: 10.1016/j.jcmg.2015.11.024.
[26]
Portugal G, Moura Branco L, Galrinho A, et al. Global and regional patterns of longitudinal strain in screening for chemotherapy-induced cardiotoxicity[J]. Rev Port Cardiol, 2017, 36 (1): 9-15. DOI: 10.1016/j.repc.2016.06.009.
[27]
Lunning MA, Kutty S, Rome ET, et al. Cardiac magnetic resonance imaging for the assessment of the myocardium after doxorubicin-based chemotherapy[J]. Am J Clin Oncol, 2015, 38(4): 377-381. DOI: 10.1097/COC.0b013e31829e19be.
[28]
Zamorano JL, Lancellotti P, Rodriguez Munoz D, et al. 2016 ESC position paper on cancer treatments and cardiovascular toxicity developed under the auspices of the ESC committee for practice guidelines: the task force for cancer treatments and cardiovascular toxicity of the European Society of Cardiology (ESC)[J]. Eur Heart J, 2016, 37(36): 2768-2801. DOI: 10.1093/eurheartj/ehw211.
[29]
Thavendiranathan P, Poulin F, Lim KD, et al. Use of myocardial strain imaging by echocardiography for the early detection of cardiotoxicity in patients during and after cancer chemotherapy: a systematic review[J]. J Am Coll Cardiol, 2014, 63 (25Pt A): 2751-2768. DOI: 10.1016/j.jacc.2014.01.073.
[30]
Park CJ, Branch ME, Vasu S, et al. The role of cardiac MRI in animal models of cardiotoxicity: hopes and challenges[J]. J Cardiovasc Transl Res, 2020, 13(3): 367-376. DOI: 10.1007/s12265-020-09981-8.
[31]
Messroghli DR, Moon JC, Ferreira VM, et al. Clinical recommendations for cardiovascular magnetic resonance mapping of T1, T2, T2* and extracellular volume: a consensus statement by the Society for Cardiovascular Magnetic Resonance (SCMR) endorsed by the European Association for Cardiovascular Imaging (EACVI)[J]. J Cardiovasc Magn Reson, 2017, 19(1): 75. DOI: 10.1186/s12968-017-0389-8.
[32]
Treibel TA, Fridman Y, Bering P, et al. Extracellular volume associates with outcomes more strongly than native or post-contrast myocardial T1[J]. JACC Cardiovasc Imaging, 2020, 13(1Pt 1): 44-54. DOI: 10.1016/j.jcmg.2019.03.017.
[33]
Tham EB, Haykowsky MJ, Chow K, et al. Diffuse myocardial fibrosis by T1-mapping in children with subclinical anthracycline cardiotoxicity: relationship to exercise capacity, cumulative dose and remodeling[J]. J Cardiovasc Magn Reson, 2013, 15: 48. DOI: 10.1186/1532-429X-15-48.
[34]
Yu AF, Chan AT, Steingart RM. Cardiac magnetic resonance and cardio-oncology: does T2 signal the end of anthracycline cardiotoxicity?[J]. J Am Coll Cardiol, 2019, 73(7): 792-794. DOI: 10.1016/j.jacc.2018.11.045.
[35]
Galan-Arriola C, Lobo M, Vilchez-Tschischke JP, et al. Serial magnetic resonance imaging to identify early stages of anthracycline-induced cardiotoxicity[J]. J Am Coll Cardiol, 2019, 73(7): 779-791. DOI: 10.1016/j.jacc.2018.11.046.
[36]
Farhad H, Staziaki PV, Addison D, et al. Characterization of the changes in cardiac structure and function in mice treated with anthracyclines using serial cardiac magnetic resonance imaging[J]. Circ Cardiovasc Imaging, 2016, 9(12). DOI: 10.1161/CIRCIMAGING.115.003584.

上一篇 重度抑郁症患者治疗前后脑功能及结构的MRI研究进展
下一篇 T1 mapping技术原理及其在心肌定量的研究进展
  
诚聘英才 | 广告合作 | 免责声明 | 版权声明
联系电话:010-67113815
京ICP备19028836号-2