蒽环类抗肿瘤药物的心脏毒性及其防治分析
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摘要
目的:研究在肿瘤治疗中使用蒽环类药物的心脏毒性及其防治措施。方法:选择2014年1月-2015年1月在我院进行抗肿瘤治疗的患者160例作为研究对象。根据使用的蒽环类抗肿瘤药物累积量(ANTH),患者被分为高ANTH组(ANTH>100mg/m~2,110例)和低ANTH组(ANTH≤100mg/m~2, 50例),两组均治疗24个月。比较两组患者治疗前后的心肌肌钙蛋白I(cTnI)、肌酐激酶同工酶(CK-MB)、脑钠肽(BNP)、左室射血分数(LVEF)、左室短轴缩短率(LVFS)、左室舒张末期内径(LVEDd)、左室收缩末期内径(LVESd)。结果:两组患者的cTnI和CK-MB水平的变化无显著差异,P均>0.05。与低ANTH组相比,高ANTH组治疗24个月后的BNP水平[(41.2±15.1)ng/ml比(46.9±15.2)ng/ml]、LVEDd [(32.8±4.3)mm比(34.6±4.6)mm]及LVESd[(21.4±2.6)mm比(22.7±3.4)mm]显著升高,而LVEF[(71.5±5.7)%比(65.7±7.1)%]及LVFS[(38.9±4.6)%比(37.2±4.2)%]均显著降低,P<0.05或<0.01。治疗前后BNP水平与LVEF、LVFS不存在显著相关性(P均>0.05)。结论:蒽环类抗肿瘤药物会引起患者心脏毒性的产生或发展,使患者的BNP水平显著升高,LVEF水平显著降低,因此,应采取一定的防治措施减少其对患者心脏产生的不良影响。
Objective: To study cardiac toxicity of anthracycline antineoplastic drugs and its preventive and therapeutic measures. Methods:A total of 160 patients undergoing anti-tumor treatment in our hospital from Jan 2014 to Jan 2015 were enrolled. According to accumulated dose of anthracycline(ANTH), patients were divided into high ANTH group(ANTH>100 mg/m~2, n=110) and low ANTH group(ANTH≤100 mg/m~2, n=50), both groups were treated for 24 months. Levels of cardiac troponin I(cTnI), creatine kinase isoenzyme MB(CK-MB), brain natriuretic peptide(BNP), left ventricular ejection fraction(LVEF), left ventricular fractional shortening(LVFS), left ventricular end-diastolic diameter(LVEDd) and left ventricular end-systolic diameter(LVESd) were measured and compared between two groups before and after treatment. Results:There were no significant differences in levels of cTnI and CK-MB between the two groups, P>0.05 both. Compared with low ANTH group after 24-month treatment, there were significant rise in BNP level [(41.2±15.1)ng/ml vs.(46.9±15.2)ng/ml], LVEDd [(32.8±4.3)mm vs.(34.6±4.6)mm] and LVESd [(21.4±2.6) mm vs.(22.7±3.4)mm], and significant reductions in LVEF[(71.5±5.7)% vs.(65.7±7.1)%] and LVFS [(38.9±4.6)% vs.(37.2±4.2)%] in high ANTH group, P<0.05 or <0.01. There was no significant correlation among BNP level, LVEF and LVFS before and after treatment(P>0.05 all). Conclusion:Anthracycline antineoplastic drugs can induce cardiac toxicity or make it develop, so significantly increase BNP level and reduce LVEF in patients. Therefore, certain preventive measures should be performed to reduce its adverse effects on heart.
Objective: To study cardiac toxicity of anthracycline antineoplastic drugs and its preventive and therapeutic measures. Methods:A total of 160 patients undergoing anti-tumor treatment in our hospital from Jan 2014 to Jan 2015 were enrolled. According to accumulated dose of anthracycline(ANTH), patients were divided into high ANTH group(ANTH>100 mg/m~2, n=110) and low ANTH group(ANTH≤100 mg/m~2, n=50), both groups were treated for 24 months. Levels of cardiac troponin I(cTnI), creatine kinase isoenzyme MB(CK-MB), brain natriuretic peptide(BNP), left ventricular ejection fraction(LVEF), left ventricular fractional shortening(LVFS), left ventricular end-diastolic diameter(LVEDd) and left ventricular end-systolic diameter(LVESd) were measured and compared between two groups before and after treatment. Results:There were no significant differences in levels of cTnI and CK-MB between the two groups, P>0.05 both. Compared with low ANTH group after 24-month treatment, there were significant rise in BNP level [(41.2±15.1)ng/ml vs.(46.9±15.2)ng/ml], LVEDd [(32.8±4.3)mm vs.(34.6±4.6)mm] and LVESd [(21.4±2.6) mm vs.(22.7±3.4)mm], and significant reductions in LVEF[(71.5±5.7)% vs.(65.7±7.1)%] and LVFS [(38.9±4.6)% vs.(37.2±4.2)%] in high ANTH group, P<0.05 or <0.01. There was no significant correlation among BNP level, LVEF and LVFS before and after treatment(P>0.05 all). Conclusion:Anthracycline antineoplastic drugs can induce cardiac toxicity or make it develop, so significantly increase BNP level and reduce LVEF in patients. Therefore, certain preventive measures should be performed to reduce its adverse effects on heart.
引文
[1]杜天幸,杨继元.蒽环类抗肿瘤药物对心脏毒性防治的研究进展[J].华南国防医学杂志,2015,29(1):80-82.
[2]吴周贵,李金国.超声心动图对蒽环类化疗药物心脏毒性的评价进展[J].医学综述,2015,21(8):1452-1454.
[3]林莹,李彦华,郭新红,等.蒽环类抗肿瘤药诱发心肌病1例及文献复习[J].中华老年多器官疾病杂志,2017,16(1):61-63.
[4]赵越,李怀业,袁兰,等.蒽环类化合物的结构修饰及抗肿瘤活性研究进展[J].中国药学杂志,2016,51(12):953-961.
[5]王琳,杨雪,肖玲芳,等.蒽环类药物心脏毒性分析及临床使用建议[J].中国现代医学杂志,2017,27(12):101-105.
[6]胡慧敏,张伟令,黄东生,等.儿童蒽环类药物心脏毒性研究进展[J].国际儿科学杂志,2016,43(1):1-4.
[7]张楚婕,程蕾蕾.蒽环类药物致心脏毒性的预防与治疗现状[J].中国临床医学,2016,23(1):110-113.
[8]慕万颖,刘伶.蒽环类药物治疗儿童白血病致心脏损害的评价及对策[J].医学综述,2016,22(6):1145-1148.
[9]金之湲,胡燕华.超声心动图评估蒽环类化疗药物心脏毒性的临床研究进展[J].内蒙古医科大学学报,2016,38(3):255-258.
[10]Mele D,Nardozza M,Spallarossa P,et al.Current views on anthracycline cardiotoxicity[J].Heart Fail Rev,2016,21(5):621-634.
[11]Cardinale D,Colombo A,Bacchiani G,et al.Early Detection of Anthracycline Cardiotoxicity and Improvement With Heart Failure Therapy[J].Circulation,2015,131(22):1981-1988.
[12]罗霞,程黎明.抗癌药物引起心脏毒性的生物标志物研究进展[J].内科急危重症杂志,2017,23(1):65-69.
[13]姚亮,张晓娟,田富国.小剂量卡维地洛联合坎地沙坦与右丙亚胺对接受蒽环类药物化疗乳腺癌患者的心脏保护作用的对比研究[J].中国药物与临床,2016,16(11):1634-1637.
[14]Adamcova M,Lencova Popelova O,Jirkovsky E,et al.Experimental determination of diagnostic window of cardiac troponins in the development of chronic anthracycline cardiotoxicity and estimation of its predictive value[J].Int J Cardiol,2015,201(2):358-367.
[15]覃业语,苏素文.抗肿瘤药物心脏毒性作用机制研究进展[J].海南医学,2015,26(24):3661-3664.
[16]汪羚利,陈少敏,李昭屏.超声心动图评价抗肿瘤药物心脏毒性的研究进展[J].心血管病学进展,2016,37(5):516-521.
[17]Jirkovská-Vávrová A,Roh á O,et al.Synthesis and analysis of novel analogues of dexrazoxane and its open-ring hydrolysis product for protection against anthracycline cardiotoxicity in vitro and in vivo[J].Toxicol Res,2015,4(4):1098-1114.
[18]卢少玲,张烁.病毒性心肌炎演变为扩张型心肌病的机制[J].心血管康复医学杂志,2016,25(3):341-343.
[19]吴红,韩薇.mTOR信号通路在心血管系统中作用研究的进展[J].心血管康复医学杂志,2016,25(2):225-228.
[20]Quyam S,Steeden J,Muthurangu V,et al.Characterisation of anthracycline cardiotoxicity in long-term childhood cancer survivors using conventional and novel CMR techniques:probing the pathology[J].J Cardiovasc Magn Reson,2015,17(1):1-3.
[2]吴周贵,李金国.超声心动图对蒽环类化疗药物心脏毒性的评价进展[J].医学综述,2015,21(8):1452-1454.
[3]林莹,李彦华,郭新红,等.蒽环类抗肿瘤药诱发心肌病1例及文献复习[J].中华老年多器官疾病杂志,2017,16(1):61-63.
[4]赵越,李怀业,袁兰,等.蒽环类化合物的结构修饰及抗肿瘤活性研究进展[J].中国药学杂志,2016,51(12):953-961.
[5]王琳,杨雪,肖玲芳,等.蒽环类药物心脏毒性分析及临床使用建议[J].中国现代医学杂志,2017,27(12):101-105.
[6]胡慧敏,张伟令,黄东生,等.儿童蒽环类药物心脏毒性研究进展[J].国际儿科学杂志,2016,43(1):1-4.
[7]张楚婕,程蕾蕾.蒽环类药物致心脏毒性的预防与治疗现状[J].中国临床医学,2016,23(1):110-113.
[8]慕万颖,刘伶.蒽环类药物治疗儿童白血病致心脏损害的评价及对策[J].医学综述,2016,22(6):1145-1148.
[9]金之湲,胡燕华.超声心动图评估蒽环类化疗药物心脏毒性的临床研究进展[J].内蒙古医科大学学报,2016,38(3):255-258.
[10]Mele D,Nardozza M,Spallarossa P,et al.Current views on anthracycline cardiotoxicity[J].Heart Fail Rev,2016,21(5):621-634.
[11]Cardinale D,Colombo A,Bacchiani G,et al.Early Detection of Anthracycline Cardiotoxicity and Improvement With Heart Failure Therapy[J].Circulation,2015,131(22):1981-1988.
[12]罗霞,程黎明.抗癌药物引起心脏毒性的生物标志物研究进展[J].内科急危重症杂志,2017,23(1):65-69.
[13]姚亮,张晓娟,田富国.小剂量卡维地洛联合坎地沙坦与右丙亚胺对接受蒽环类药物化疗乳腺癌患者的心脏保护作用的对比研究[J].中国药物与临床,2016,16(11):1634-1637.
[14]Adamcova M,Lencova Popelova O,Jirkovsky E,et al.Experimental determination of diagnostic window of cardiac troponins in the development of chronic anthracycline cardiotoxicity and estimation of its predictive value[J].Int J Cardiol,2015,201(2):358-367.
[15]覃业语,苏素文.抗肿瘤药物心脏毒性作用机制研究进展[J].海南医学,2015,26(24):3661-3664.
[16]汪羚利,陈少敏,李昭屏.超声心动图评价抗肿瘤药物心脏毒性的研究进展[J].心血管病学进展,2016,37(5):516-521.
[17]Jirkovská-Vávrová A,Roh á O,et al.Synthesis and analysis of novel analogues of dexrazoxane and its open-ring hydrolysis product for protection against anthracycline cardiotoxicity in vitro and in vivo[J].Toxicol Res,2015,4(4):1098-1114.
[18]卢少玲,张烁.病毒性心肌炎演变为扩张型心肌病的机制[J].心血管康复医学杂志,2016,25(3):341-343.
[19]吴红,韩薇.mTOR信号通路在心血管系统中作用研究的进展[J].心血管康复医学杂志,2016,25(2):225-228.
[20]Quyam S,Steeden J,Muthurangu V,et al.Characterisation of anthracycline cardiotoxicity in long-term childhood cancer survivors using conventional and novel CMR techniques:probing the pathology[J].J Cardiovasc Magn Reson,2015,17(1):1-3.