Anthracycline-Associated T1 Mapping Characteristics Are Elevated Independent of the Presence of Cardiovascular Comorbidities in Cancer Survivors.

Anthracycline-Associated T1 Mapping Characteristics Are Elevated Independent of the Presence of Cardiovascular Comorbidities in Cancer Survivors.
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DOI:
10.1161/circimaging.115.004325
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发表时间:
2016-08
期刊:
Circulation. Cardiovascular imaging
影响因子:
--
通讯作者:
Hundley WG
Hundley WG
中科院分区:
其他
文献类型:
--
作者:
Jordan JH;Vasu S;Morgan TM;D'Agostino RB Jr;Meléndez GC;Hamilton CA;Arai AE;Liu S;Liu CY;Lima JA;Bluemke DA;Burke GL;Hundley WG

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成年癌症幸存者的心血管磁共振(CMR)T1标测特征升高;然而,尚不清楚这些升高是否与年龄或同时存在的心血管合并症有关。我们对327例受试者(65%为女性,年龄64±12岁)的左心室(LV)T1和细胞外容积分数(ECV)进行了盲态CMR分析。37名患有乳腺癌或血液恶性肿瘤但尚未开始治疗的患者,以及54名在2.8±1.3年前接受基于蒽环类药物(n=37)或非基于蒽环类药物(n=17)化疗的癌症幸存者与236名无癌症参与者进行了比较。进行多变量分析,以确定T1/ECV指标与心肌纤维化相关变量之间的相关性。与对照药物相比,蒽环类药物化疗前(1058±7 ms)和化疗后(1040±7 ms),经X线校正的天然T1升高(均为965±3 ms,p<0.0001)。蒽环类药物治疗的癌症受试者中,心肌纤维化的标志物--非蒽环类药物存活者的T1和ECV与治疗前存活者无差异(分别为p=0.17和p=0.16)。在考虑了人口统计学(包括年龄)、心肌纤维化风险因素和LV射血分数或心肌质量指数后,癌症幸存者的天然T1和ECV仍然升高(所有p<0.0001)。蒽环类药物化疗3年后,心肌T1和ECV升高与潜在癌症或心血管合并症无关,表明癌症幸存者间质纤维化的影像学生物标志物与既往接受潜在心脏毒性癌症治疗方案有关。
Cardiovascular magnetic resonance (CMR) T1 mapping characteristics are elevated in adult cancer survivors; however, it remains unknown whether these elevations are related to age or presence of coincident cardiovascular comorbidities. We performed blinded CMR analyses of left ventricular (LV) T1 and extracellular volume fraction (ECV) in 327 individuals (65% women, aged 64±12 years). Thirty-seven (37) individuals had breast cancer or a hematologic malignancy but had not yet initiated their treatment, and 54 cancer survivors that received either anthracycline-based (n=37) or non-anthracycline-based (n=17) chemotherapy 2.8±1.3 years earlier were compared to 236 cancer-free participants. Multivariable analyses were performed to determine the association between T1/ECV measures and variables associated with myocardial fibrosis. Age-adjusted native T1 was elevated pre- (1058±7 ms) and post- (1040±7 ms) receipt of anthracycline chemotherapy versus comparators (965±3 ms, p<0.0001 for both). Age-adjusted ECV, a marker of myocardial fibrosis, was elevated in anthracycline-treated cancer participants (30.4±0.7%) compared with either pre-treatment cancer (27.8±0.7%, p<0.01) or cancer-free comparators (26.9±0.2%, p<0.0001). T1 and ECV of non-anthracycline survivors was no different than pre-treatment survivors (p=0.17 and p=0.16, respectively). Native T1 and ECV remained elevated in cancer survivors after accounting for demographics (including age), myocardial fibrosis risk factors, and LV ejection fraction or myocardial mass index (p<0.0001 for all). Three years after anthracycline-based chemotherapy, elevations in myocardial T1 and ECV occur independent of underlying cancer or cardiovascular comorbidities suggesting that imaging biomarkers of interstitial fibrosis in cancer survivors are related to prior receipt of a potentially cardiotoxic cancer treatment regimen.