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Article(id=1200024245423140873, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1200024241572770746, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.1570.2023.0413, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1658160000000, receivedDateStr=2022-07-19, revisedDate=null, revisedDateStr=null, acceptedDate=1665763200000, acceptedDateStr=2022-10-15, onlineDate=1764037675480, onlineDateStr=2025-11-25, pubDate=1695830400000, pubDateStr=2023-09-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1764037675480, onlineIssueDateStr=2025-11-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1764037675480, creator=13701087609, updateTime=1764037675480, updator=13701087609, issue=Issue{id=1200024241572770746, tenantId=1146029695717560320, journalId=1189873630562394117, year='2023', volume='48', issue='9', pageStart='993', pageEnd='1112', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1764037674563, creator=13701087609, updateTime=1764038723302, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1200028640353288193, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1200024241572770746, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1200028640353288194, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1200024241572770746, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=1100, endPage=1106, ext={EN=ArticleExt(id=1200024245699964954, articleId=1200024245423140873, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Advances in the research of cardiovascular diseases related to treatment of hematological malignancies, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Advances in the treatment of haematological malignancies have improved the long-term prognosis of patients to some extent, but have also highlighted the importance of tumour progression and cardiovascular events caused by anti-tumour therapy. A significant proportion of patients with haematological malignancies receiving existing and emerging oncological treatment regimens such as anthracyclines, proteasome inhibitors, targeted therapies and immunotherapy experience cardiovascular events at some point after disease remission, which seriously affects the survival and quality of life of the patients. This article reviews the mechanisms, clinical manifestations and interventions of cardiotoxicity induced by therapeutic agents for haematological malignancies, with the aim of providing a reference to protect patients with haematological malignancies from cardiovascular complications.

, correspAuthors=Xue-Chun Lu, authorNote=null, correspAuthorsNote=
E-mail:
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血液系统恶性肿瘤诊疗的持续进步改善了患者的长期预后，同时也凸显了肿瘤进展及抗肿瘤治疗引起的心血管事件的重要性。血液系统恶性肿瘤患者在接受现有及新兴的肿瘤治疗方案如蒽环类药物、蛋白酶体抑制剂、靶向治疗、免疫治疗后，部分患者在疾病缓解后可能出现心血管事件，严重影响其生存率及生存质量。本文从血液系统恶性肿瘤治疗药物引起的心脏毒性的机制、临床表现和干预治疗三方面进行综述，旨在为血液系统恶性肿瘤治疗相关心血管事件的预防和治疗提供参考。

, correspAuthors=卢学春, authorNote=null, correspAuthorsNote=
卢学春，E-mail：
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王紫宁，硕士研究生，主要从事血液系统疾病诊断、治疗及预防等方面的研究

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王紫宁，硕士研究生，主要从事血液系统疾病诊断、治疗及预防等方面的研究

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血液系统恶性肿瘤治疗相关的心血管疾病研究进展
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王紫宁 1, 2 , 王益民 3 , 卢学春 2, *
解放军医学杂志 | 综述 2023,48(9): 1100-1106
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解放军医学杂志 | 综述 2023, 48(9): 1100-1106
血液系统恶性肿瘤治疗相关的心血管疾病研究进展
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王紫宁1, 2, 王益民3, 卢学春2, *
作者信息
  • 1解放军医学院，北京 100853
  • 2解放军总医院第二医学中心血液病科/国家老年疾病临床医学研究中心，北京 100853
  • 3山西医科大学附属临汾医院/临汾市人民医院心内科，山西临汾 041000

    • 王紫宁，硕士研究生，主要从事血液系统疾病诊断、治疗及预防等方面的研究

通讯作者:

卢学春，E-mail：
Advances in the research of cardiovascular diseases related to treatment of hematological malignancies
Zi-Ning Wang1, 2, Yi-Min Wang3, Xue-Chun Lu2, *
Affiliations
  • 1Medical School of Chinese PLA, Beijing 100853, China
  • 2Department of Hematology, the Second Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Geriatric Diseases, Beijing 100853, China
  • 3Department of Cardiovascular Medicine, Linfen People's Hospital, Affiliated Linfen Hospital of Shanxi Medical University, Linfen, Shanxi 041000, China
出版时间: 2023-09-28 doi: 10.11855/j.issn.0577-7402.1570.2023.0413
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摘要
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血液系统恶性肿瘤诊疗的持续进步改善了患者的长期预后，同时也凸显了肿瘤进展及抗肿瘤治疗引起的心血管事件的重要性。血液系统恶性肿瘤患者在接受现有及新兴的肿瘤治疗方案如蒽环类药物、蛋白酶体抑制剂、靶向治疗、免疫治疗后，部分患者在疾病缓解后可能出现心血管事件，严重影响其生存率及生存质量。本文从血液系统恶性肿瘤治疗药物引起的心脏毒性的机制、临床表现和干预治疗三方面进行综述，旨在为血液系统恶性肿瘤治疗相关心血管事件的预防和治疗提供参考。

肿瘤心脏病学  /  抗肿瘤药物  /  血液系统恶性肿瘤  /  心血管疾病

Advances in the treatment of haematological malignancies have improved the long-term prognosis of patients to some extent, but have also highlighted the importance of tumour progression and cardiovascular events caused by anti-tumour therapy. A significant proportion of patients with haematological malignancies receiving existing and emerging oncological treatment regimens such as anthracyclines, proteasome inhibitors, targeted therapies and immunotherapy experience cardiovascular events at some point after disease remission, which seriously affects the survival and quality of life of the patients. This article reviews the mechanisms, clinical manifestations and interventions of cardiotoxicity induced by therapeutic agents for haematological malignancies, with the aim of providing a reference to protect patients with haematological malignancies from cardiovascular complications.

oncologic cardiology  /  antineoplastic drug  /  hematological malignancy  /  cardiovascular disease
王紫宁, 王益民, 卢学春. 血液系统恶性肿瘤治疗相关的心血管疾病研究进展. 解放军医学杂志, 2023 , 48 (9) : 1100 -1106 . DOI: 10.11855/j.issn.0577-7402.1570.2023.0413
Zi-Ning Wang, Yi-Min Wang, Xue-Chun Lu. Advances in the research of cardiovascular diseases related to treatment of hematological malignancies[J]. Medical Journal of Chinese People’s Liberation Army, 2023 , 48 (9) : 1100 -1106 . DOI: 10.11855/j.issn.0577-7402.1570.2023.0413
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当前随着多模式治疗的发展，血液系统恶性肿瘤患者预后得到显著改善，但随之出现的急性、长期药物不良反应影响了患者的生存质量。除了现有的常规化疗、造血干细胞移植、免疫疗法和靶向治疗外，每年有多达30余种新疗法获批，但其不良反应尚不清楚。作为肿瘤治疗中常见的不良反应，心脏毒性限制了抗肿瘤治疗药物的使用剂量与疗程，影响了患者的预后。为降低肿瘤患者合并心血管疾病的病死率，改善其预后，逐渐出现肿瘤心脏病学这一新兴学科。既往研究显示，肿瘤患者10年罹患动脉粥样硬化性心脏病的风险是无肿瘤患者的3.42倍，约9%的肿瘤患者最终因出现心血管疾病而死亡[1]。本文综述了血液系统恶性肿瘤治疗相关心血管疾病的国内外研究进展及专家共识，旨在为相关的心血管损伤机制和防治研究提供参考。
1 血液系统恶性肿瘤治疗药物的心脏毒性反应机制
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心脏毒性是多种抗肿瘤药物的常见不良反应[2]，其发生风险取决于化疗药物的类型、剂量、输注速率，患者年龄、性别及既往基础疾病等因素，不同药物引起的临床症状也不尽相同，应在治疗前谨慎评估，以兼顾抗肿瘤治疗与患者的心血管系统保护。
1.1 蒽环类药物
蒽环类化疗药物已广泛应用于血液系统恶性肿瘤及实体瘤的治疗，主要包括阿霉素、脂质体多柔比星、米托蒽醌、伊达比星和表柔比星等，可用于急性髓系白血病、急性粒系白血病、淋巴瘤等多种血液系统肿瘤的治疗[3]。蒽环类药物导致的心脏毒性可在治疗后数天至数年发生，潜伏期较长[4]，主要表现为左心室射血分数(left ventricular ejection fractions，LVEF)降低、室壁厚度增加、心律失常及心力衰竭等。蒽环类药物剂量不存在适用安全范围，导致心脏毒性出现的机制包括DNA损伤、线粒体功能障碍及氧化应激等[5]。心肌细胞较其他组织更易受到自由基的永久性损伤，蒽环类药物可促进铁介导的活性氧自由基生成，从而导致心脏组织脂质过氧化及钙超载。促炎症细胞因子如组胺、肿瘤坏死因子(tumor necrosis factor，TNF)-α及白细胞介素-2(interleukin-2，IL-2)的释放也与心脏毒性相关。蒽环类药物可通过拓扑异构酶Ⅱ(topoisomerase Ⅱ，TOP2)结构与DNA结合形成复合物，从而导致DNA双链断裂，触发细胞死亡。敲除Top2β基因可使心肌细胞免于发生阿霉素诱导的DNA双链断裂导致的线粒体功能缺陷[6]。在阿霉素诱导的心脏毒性动物模型中，Top2抑制反应中DNA损伤调节剂GTP酶Rac1是还原型烟酰胺腺嘌呤二核苷酸磷酸(nicotinamide adenine dinucleotide phosphate，NADPH)氧化激活及活性氧(reactive oxygen species，ROS)产生所必需的；若特异性敲除Rac1可减少ROS的生成，改善心脏功能。蒽环类药物也可通过钙调蛋白依赖性蛋白激酶肌联蛋白水解，引起肌丝降解及心肌细胞凋亡，从而导致心脏舒张功能受限。研究显示，阿霉素可同时触发不同的细胞死亡调节途径，如自噬、铁死亡、坏死性凋亡等[7]，影响线粒体中GATA-4基因的表达，抑制线粒体合成及代谢，从而诱导细胞凋亡[8]。蒽环类药物引发的心脏毒性具有剂量依赖性，当阿霉素剂量为200 mg/m2时，可导致左心室舒张功能障碍，随着剂量的增高，可逐渐演变为心室收缩功能障碍；当阿霉素剂量累计达到400 mg/m2、550 mg/m2、700 mg/m2时，心肌损伤的发生风险分别为3%~5%、7%~26%、18%~48%[9]。血液肿瘤患者在使用蒽环类药物期间，对于心脏并发症高风险患者可加用血管紧张素转化酶抑制剂(angiotensin converting enzyme inhibitors，ACEI)、血管紧张素Ⅱ受体拮抗剂(angiotensin receptor blocker，ARB)或β-受体阻滞药物以达到预防及治疗的目的。此外，右雷佐生作为铁螯合剂可降低蒽环类药物相关心脏毒性的发生率。
1.2 烷化剂类药物
烷化剂作为在临床中应用较早的细胞毒性药物，可用于恶性淋巴瘤、慢性淋巴细胞白血病、骨髓移植及恶性肿瘤的诱导化疗。常用的烷化剂包括环磷酰胺、氮芥、顺铂、甲基苄肼等。高剂量环磷酰胺[>1.5 g/(m2.d)]心脏毒性明显，心血管事件发生率为7%~28%[10]。烷化剂类药物导致心脏毒性的主要机制包括血管内皮细胞氧化应激及功能障碍、血栓形成和直接DNA损伤等[11]。环磷酰胺仅在体内活化后发挥作用，具体过程为药物在肝脏中被细胞色素P450氧化酶氧化生成4-羟基环磷酰胺后分解为磷酰氮芥和丙烯醛，后者是一种对心肌细胞高度敏感的毒性代谢物，可诱导心肌细胞中ROS积累及炎性因子释放[12]，并参与心肌细胞的凋亡。研究显示，环磷酰胺代谢产物丙烯醛可减少内皮型一氧化氮合酶(endothelial nitric oxide synthase，eNOS)的生成，导致eNOS偶联，通过亚硝化应激反应造成心脏毒性；环磷酰胺还可通过Nrf2/ARE、Akt/GSK-3β/NFAT/钙调神经磷酸酶、P53/P38MAPK、NF-κB/TLR-4等信号通路间的串扰作用触发心脏毒性[13]。此外，环磷酰胺还可直接损伤血管内皮，引起毛细血管微血栓形成和内皮通透性升高，导致间质出血和水肿。另有研究显示，环磷酰胺及异环磷酰胺可抑制心型脂肪酸结合蛋白和CPT1A蛋白的表达，导致血液中乳酸脱氢酶、肌酸激酶同工酶、丙二酰CoA浓度增加，对心肌组织产生病理性损伤，导致心脏毒性的发生[14]。环磷酰胺相关的心脏毒性通常在用药后2~3周出现，其病死率为11%~43%[15]。烷化剂类药物联合蒽环类药物或放疗时心脏毒性的发生风险可进一步增高。
1.3 靶向治疗相关药物
近年来，分子靶向药物在血液系统恶性疾病治疗中的应用逐渐增多，其引起的心脏毒性多与药物剂量无关，表现为无症状性LVEF降低及可逆性心肌损伤。分子靶向药物主要包括酪氨酸激酶抑制剂(如伊马替尼、芦可替尼、吉非替尼等)、蛋白酶体抑制剂(如硼替佐米、卡非佐米等)、血管内皮生长因子(vascular endothelial growth factor，VEGF)及其受体(VEGF receptor，VEGFR)的抑制剂等[16-17]。
伊马替尼是一种BCR-ABL酪氨酸激酶抑制剂，已被批准用于治疗慢性粒细胞白细胞，可通过抑制BCL-ABL融合基因及其编码的P210蛋白等小分子表达降低酪氨酸激酶活性。伊马替尼引起的心血管事件包括心肌梗死、QT间期延长及血管性疾病。研究显示，伊马替尼引起心脏毒性的主要机制在于MAPK相关信号通路激活所诱导的内质网应激反应，进而导致线粒体功能障碍及心肌细胞坏死[18]。van Hasselt等[19]的研究显示，接受第三代BCR-ABL抑制剂Ponatinib治疗的患者，约20%会出现心力衰竭、缺血性心脏病等不良事件。Ponatinib是一种多靶点激酶抑制剂，可用于慢性髓细胞白血病(chronic myelocytic leukemia，CML)、急性淋巴细胞白血病(acute lymphoblastic leukemia，ALL)等多种类型白血病的治疗，但Ponatinib也可通过激活炎性因子如TNF-α、γ干扰素(interferon-γ，IFN-γ)、IL-6等促进微血管病的发生及血栓形成，当与激素或蛋白酶体抑制剂联合使用时，会进一步增加心血管事件的发生风险。
蛋白酶体可降解细胞内损坏或错误折叠的多肽，并作为真核细胞组调节器降解调节蛋白，其抑制剂在临床中用于治疗多发性骨髓瘤(multiple myeloma，MM)和套细胞淋巴瘤等疾病。Cornell等[20]对蛋白酶体抑制剂治疗复发性MM的前瞻性研究显示，约65%的患者出现心血管不良事件，其中超过55%的患者严重程度≥3级。药物卡非佐米可在心脏中积聚，不可逆地降低心肌细胞中20S蛋白酶体的糜蛋白酶样活性，导致泛素化与非泛素化蛋白失衡、线粒体功能障碍、ATP合成减少等，依次形成更高阶蛋白质聚集物，产生不溶性包涵体，致使细胞损伤，最终导致心功能不全[21]。除直接作用于心肌细胞外，蛋白酶体抑制剂还可影响血管内皮细胞相关信号通路，导致血管收缩、血管痉挛增加，降低对血管扩张剂的敏感性，从而间接影响心功能[22]。
VEGF或VEGFR的抑制剂可通过血管内皮生长因子配体及其受体相结合的细胞内外结构域抑制血管生成和肿瘤细胞生长。VEGF和VEGFR抑制剂可根据作用位点的不同分为抑制胞外结构域的VEGF单抗(如贝伐珠单抗)，以及抑制胞内结构域的VEGFR酪氨酸激酶抑制剂(VEGFR-TKI)，如舒尼替尼、索拉菲尼、帕唑替尼、瑞戈非尼等[23]。具有心脏毒性的VEGF单抗和VEGFR-TKI分别以贝伐珠单抗和舒尼替尼为代表，可引发左心室内径(left ventricular dimension，LVD)异常、心力衰竭、QT间期延长等Ⅱ型心脏毒性，其机制主要包括药物影响PI3K和MAPK通路活化，导致血管收缩和外周血管阻力增加、外周毛细血管密度降低等。Abdel-Qadir等[24]纳入77种VEGF或VEGFR抑制剂治疗恶性肿瘤的心脏毒性反应的荟萃分析结果显示，应用VEGF或VEGFR抑制剂后出现中重度高血压、左心功能障碍、心肌缺血或动脉血栓栓塞的风险增高。
1.4 免疫疗法
免疫治疗作为一种创新性的癌症治疗方法已取得重大进展[25]，目前相关的免疫疗法主要涉及免疫检查点抑制剂(immune checkpoint inhibitor，ICI)[26]、基于新抗原的肿瘤疫苗、嵌合抗原受体T细胞(chimeric antigen receptor T-cell immunotherapy，CAR-T)[27]等。ICI是指阻断表达免疫检查点的肿瘤细胞与免疫细胞之间作用的药物，可解除肿瘤细胞的免疫逃逸，维持机体自身的免疫应答过程。现有的ICIs包括细胞毒性T淋巴细胞相关蛋白4(cytotoxic T-lymphocyte-associated protein 4，CTLA-4)抑制剂、程序性细胞死亡蛋白-1(programmed death-1，PD-1)抑制剂等[28]。CTLA-4是一种下调T淋巴细胞功能的蛋白受体，可降低人体免疫应答；PD-1是机体不可或缺的免疫抑制因子，PD-1及其配体PD-L1的抑制剂可阻断抑制性信号传递，活化T细胞，从而增强免疫应答。ICIs致免疫性心肌炎的具体机制尚不明确，可能与肿瘤及健康组织内存在的抗原T细胞活性、预先存在的自身抗体水平、炎性细胞因子及其介导的炎症增强有关，上述过程均可使CTLA-4抗体直接作用于正常组织中表达的CTLA-4。有研究对应用ICIs患者的心内膜下心肌进行活检，结果显示心肌组织中CD3+ T淋巴细胞大量浸润，部分患者存在CD68+巨噬细胞、嗜酸性粒细胞及CD56+细胞浸润，并伴有一定程度的心肌纤维化[29]。Reuben等[30]的研究显示，CTLA-4、PD-1及PD-L1对应激后免疫介导的心脏损伤具有保护作用。因此，应用ICIs可导致心肌细胞更易受到损伤。另有研究在该类患者的心肌和原发肿瘤组织内发现相同高频T淋巴细胞受体序列，推测ICIs活化的T淋巴细胞可能是肿瘤细胞和心肌细胞共同的靶向抗原，可引起心肌淋巴细胞浸润，诱导自身免疫性心肌炎的发生[31]。
CAR-T是一种可用于实体瘤及血液系统疾病的新兴精准疗法，在复发与难治性MM、B细胞ALL、霍奇金淋巴瘤等的治疗中取得了良好效果[32]。CAR-T可通过基因工程技术大量扩增具有高效抗肿瘤活性的免疫效应细胞，使T细胞直接与肿瘤细胞表面的特异性抗原相结合后激活，从而达到抗肿瘤的目的[33]。CAR-T的不良反应主要为细胞因子释放综合征，可引起包括IL-6、IFN-γ、TNF-α和IL-1在内的炎性因子大量释放，而IL-6升高与炎症介导的心肌损伤有关，可激活补体及凝血级联反应，导致血管内皮细胞损伤、凝血功能异常及心肌受损等[34]。CAR-T细胞激活后的脱靶效应可能是导致心肌损伤的潜在机制。Lefebvre等[35]对145例接受 CAR-T细胞治疗的患者进行回顾性研究发现，其中7.5%出现心律失常，15%出现心力衰竭。Alvi等[36]的研究显示，在发生细胞因子释放综合征和应用IL-6抑制剂托珠单抗之间延迟12 h，心血管不良事件的发生风险会显著增加。上述研究提示，CAR-T细胞治疗与心血管不良事件之间高度相关，但其引起心脏毒性的具体机制及相关危险因素仍有待进一步研究。
免疫细胞治疗还包括自然杀伤细胞、巨噬细胞、与DC细胞等非特异性免疫细胞培养的CIK/DC细胞、T细胞受体嵌合型T细胞等，其心血管毒性的主要原因与CAR-T疗法相似，均为通过诱发细胞因子释放综合征而引起，主要表现为心动过速、血压降低、心肌酶谱升高、QT间期延长、左心室功能障碍和心跳骤停等。
2 血液系统恶性肿瘤治疗相关心血管疾病的临床表现
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2.1 心力衰竭
心力衰竭是血液系统恶性肿瘤治疗中常见和危害最大的心血管并发症之一。肿瘤治疗相关心功能不全(cancer therapy related cardiac dysfunction，CTRCD)是指LVEF<50%，且降低幅度大于10%[37]。不同化疗药物所致左心室功能障碍的发生率不尽相同，其中蒽环类药物所致心力衰竭较为常见且严重。Oliva等[38]对霍奇金淋巴瘤和弥漫性大B细胞淋巴瘤患者的长期随访显示，患者在治疗后出现多种心血管疾病事件的概率显著增高，接受放疗和蒽环类药物治疗的患者在25年期间心力衰竭和心肌病的发生风险增加29%。阿霉素累积用量达700 mg/m2时，充血性心力衰竭的发生率可高达48%[39]。此外，伴有糖尿病或冠状动脉粥样硬化性心脏病等危险因素的患者再发心力衰竭的风险也会显著增加。依据病理学及临床特征可将CTRCD分为Ⅰ型和Ⅱ型。Ⅰ型CTRCD呈剂量累积型，可逆程度低，主要由蒽环类药物引起；Ⅱ型CTRCD不受药物剂量的影响，心肌功能受损为可逆性的，多为单克隆抗体或小分子TKI药物引起[40]。因此，对患者的各项心功能指标进行早期和持续监测，对于改善预后、提高生存率有较大帮助。
2.2 心律失常
血液系统恶性肿瘤患者在化疗过程中会出现不同类型和严重程度的心律失常，如窦性心动过缓、心动过速、QT间期延长、心房纤颤等，可影响治疗方案的选择及患者预后。研究显示，抗肿瘤治疗过程中约40%的患者会出现不同程度的心律失常[41]。QT间期延长和三氧化二砷的使用相关性较强，如出现QTc>500 ms、ΔQTc>60 ms或其他类型心律失常时，应考虑停止治疗或更换药物类型[42]。心房纤颤是常见的室上性心律失常，室上性心动过速次之[43]。Hu等[44]的研究显示，患有恶性肿瘤的患者新发心房颤动的发生率显著升高，反之，心房颤动患者合并恶性肿瘤的概率也明显增高。电解质及代谢紊乱、炎症、自主神经功能障碍等均可诱发心房颤动，而细胞毒性药物、靶向药物等均可导致心肌损伤，诱发心房颤动的发生。室性心律失常的发生还与放、化疗导致的左心功能障碍和心肌缺血相关。因此，血液系统恶性肿瘤合并心律失常的患者应进行个体化管理，兼顾心血管疾病相关的预期寿命、生活质量和并发症发生风险等；同时，严密监测心电图也是肿瘤治疗过程中检出心律失常不可缺少的手段。
2.3 血栓形成
静脉血栓栓塞(venous thrombo-embolism，VTE)是肿瘤患者常见且危及生命的并发症之一。血液系统疾病可损害血液系统的稳定性，导致栓塞事件，而合并VTE使患者的病情更为复杂，影响其原发病的治疗效果及预后。研究显示，血液系统恶性疾病患者VTE的发生风险接近实体肿瘤[45]，但目前尚无临床循证指南对此类患者进行研究。不同类型血液系统恶性肿瘤的VTE发生率为1%~12%；其中急性早幼粒细胞白血病、ALL和侵袭性淋巴瘤的VTE发生率较高，危险因素包括年龄、基础疾病、大静脉置管、左旋天冬酰胺酶、蒽环类药物、大剂量激素及免疫抑制剂等[46]。Hunault-Berger等[47]对214例ALL及淋巴母细胞淋巴瘤成年患者的研究显示，第一次注射左旋天冬酰胺酶后2~35 d，共发生20起(9.3%)血栓事件。此外，造血干细胞移植后出现移植物抗宿主病(graft versus-host disease，GVHD)的患者发生VTE的风险明显增加，其中急性GVHD发生VTE的风险为45%，慢性GVHD为35%[48]。美国临床肿瘤学会(ASCO)和美国国立综合癌症网络(National Comprehensive Cancer Network，NCCN)的相关指南建议，应首选低分子肝素预防VTE，因为其出血事件的概率和VTE复发率较低；也可选用口服抗凝剂如利伐沙班、阿哌沙班等作为替代治疗[49]。因此，在面对血液系统恶性肿瘤患者VTE的预防及治疗时，应综合考虑诸多因素而进行个体化评估。
3 血液系统恶性肿瘤治疗相关心血管疾病的风险监测
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3.1 危险因素管理
接受抗肿瘤治疗的患者需积极识别危险因素并进行基线评估，尤其是接受已知具有心脏毒性药物治疗的患者。ASCO[50]、加拿大心血管学会(CCS)[51]的循证指南均建议，对血液系统恶性肿瘤患者的个体化基线风险评估及危险因素管理应在治疗前进行。血液系统恶性肿瘤合并心血管疾病的潜在危险因素包括年龄、性别、肥胖、糖尿病、吸烟及血脂异常等。除了需对共同危险因素进行评估外，2020版欧洲心脏病学会肿瘤治疗指南[52]指出，恶性肿瘤患者的心血管危险因素包括：现合并心力衰竭，无症状左心室功能障碍，冠状动脉粥样硬化性心脏病，心肌病，心律失常等；65岁以后使用蒽环类药物，50岁以下有心血管疾病家族史、糖尿病、高胆固醇血症等；先前接受过具有心脏毒性的治疗方案，如蒽环类药物及放射治疗等；生活习惯不佳，如吸烟、嗜酒、肥胖、久坐等。如果不能很好地识别及控制风险因素，可改变的风险因素将加速治疗相关心血管事件的发生。因此，应加强多学科专家的沟通，对血液系统恶性肿瘤患者的心脏状况进行评估，选择适当的治疗方案。
3.2 影像学检查
2016年CCS肿瘤治疗相关心血管毒性防治指南提出，心脏毒性的筛查和检测策略包括心脏成像检查、生物标志物及心电图检查等，同时需根据疾病亚型、治疗方案、药物累积剂量及患者的基线心血管风险确定监测的时间和频次[53]。研究显示，监测心脏毒性的主要指标之一是LVEF是否降低。建议所有患者在治疗前完善超声心动图检查，评估左心室功能，以便后期进行对比分析。超声心动图、X线检查和磁共振成像等技术均可用于测量LVEF。超声心动图是在整个治疗期间和长期随访中较为方便的检查方法，若LVEF下降幅度>10%或低于正常值下限，左心室收缩期整体纵向应变较基线降低幅度>15%时，提示出现治疗相关心血管事件的风险显著增高。心电图检查可用于发现各种心脏毒性迹象，如静息性心动过速、ST-T改变、QT间期延长及心房纤颤等；但仍需对其特异性进行鉴别。心脏磁共振成像可用于确定左心室功能障碍的原因和心包周围情况；监测心肌瘢痕或纤维化时可采用钆对比剂延迟强化磁共振成像技术，可作为左心室功能受损时的预后判断标准之一。生物标志物检测的确切作用和时机尚无定论。2020年欧洲肿瘤内科学会发布的ESMO专家共识指南[54]建议，高危或接受抗肿瘤治疗的患者可长期监测肌钙蛋白、脑钠肽(brain natriuretic peptide，BNP)和N末端前脑钠肽(N-terminal brain natriuretic peptide，NT-proBNP)等指标的变化。一项对703例肿瘤患者超过3年的随访研究显示，对于接受以蒽环类药物为基础的化疗方案的患者，高敏肌钙蛋白水平可作为判断心脏毒性的预后标志物。C反应蛋白作为非特异性的炎症指标，在CAR-T细胞疗法中可间接反映心肌损害情况，但在常规放、化疗中是否可作为生物标志物仍需进一步研究。
除改变生活方式外，心脏保护的时机需根据患者的临床表现及指标决定。基线风险较高的患者，须对危险因素进行严格控制，并应考虑预防性给予心脏保护药物治疗。低基线风险的血液系统恶性肿瘤患者若计划使用高累积剂量的蒽环类药物，可考虑预防性应用心脏保护药物。
4 总结与展望
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化疗或靶向药物引起的心脏毒性正逐渐发展为抗肿瘤治疗中普遍存在且具有挑战性的并发症。临床医师须意识到抗肿瘤治疗可引起多种心血管事件，并应及时评估，制定个体化的治疗方案。此外，在对血液系统恶性肿瘤及心血管疾病的常见危险因素进行控制、探讨心血管安全性能更高的抗肿瘤治疗方法、及早发现不良事件、提高治疗手段等方面，还有待通过更多大规模、多中心临床试验探索制定出专家指南，以推动肿瘤心脏病学的进步，使更多的血液系统恶性肿瘤患者受益。
基金
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  • 国家重点研发计划(2020YFC2002706)
  • 解放军总医院新技术新业务扶持项目(XYW-202107)
文献
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2023年第48卷第9期
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doi: 10.11855/j.issn.0577-7402.1570.2023.0413
  • 接收时间：2022-07-19
  • 首发时间：2025-11-25
  • 出版时间：2023-09-28
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  • 收稿日期：2022-07-19
  • 录用日期：2022-10-15
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Key Research and Development Program of China(2020YFC2002706)
国家重点研发计划(2020YFC2002706)
New Technology and Business Support Project of Chinese PLA General Hospital(XYW-202107)
解放军总医院新技术新业务扶持项目(XYW-202107)
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    1解放军医学院，北京 100853
    2解放军总医院第二医学中心血液病科/国家老年疾病临床医学研究中心，北京 100853
    3山西医科大学附属临汾医院/临汾市人民医院心内科，山西临汾 041000

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2种不同金属材料的力学参数
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Family		 属数
Number of
genus		 种数
Number of
species		 占总种数比例
Percentage of
total species (%)		 属
Genus		 种数
Number of
species		 占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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