On T2* magnetic resonance and cardiac iron.
On T2* magnetic resonance and cardiac iron.
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DOI：
10.1161/circulationaha.110.007641
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发表时间：
2011-04-12
期刊：
影响因子：
37.8
通讯作者：
Pennell DJ
中科院分区：
文献类型：
--
作者：
Carpenter JP;He T;Kirk P;Roughton M;Anderson LJ;de Noronha SV;Sheppard MN;Porter JB;Walker JM;Wood JC;Galanello R;Forni G;Catani G;Matta G;Fucharoen S;Fleming A;House MJ;Black G;Firmin DN;St Pierre TG;Pennell DJ
心肌铁的测量是有侧情色性心肌病风险患者临床管理的关键。在室间隔测量的心血管磁共振（CMR）松弛参数R2*（通过其倒数T2*在临床上评估）用于评估心脏铁，但铁在人类中的校准和分布数据有限。研究了12例输血依赖患者的心脏，这些患者要么死亡（心力衰竭n=7，中风n=1），要么因终末期心力衰竭移植（n=4）。在CMR R2*测量后，使用电感耦合等离子体原子发射光谱测量每个心脏的多个样品中的组织铁浓度。铁在心脏各节段间的分布无系统性变化，但心外膜铁浓度高于心内膜铁浓度。10例患者心肌铁致严重心力衰竭的平均值（±SD）为5.98±2.42mg/g dw（范围3.19-9.50），但1例心力衰竭的异常值为25.9mg/g dw。心肌ln[R2*]与ln[Fe]呈强线性相关（R2=0.910, p<0.001），导致[Fe]=45.0•(T2*)−1.22（临床校准方程中[Fe]单位为mg/g dw， T2*单位为ms）。室间隔中铁浓度和R2*均高度代表整体平均心肌铁。这些数据详细说明了铁过载时整个心脏的铁分布，并为人类CMR R2*对心肌铁浓度的校准提供了依据。铁值对与铁相关死亡相关的心脏铁水平有相当大的兴趣，并表明心脏对铁负荷比肝脏更敏感。该结果也验证了目前临床应用中隔CMR监测体内心脏铁的可行性。
Measurement of myocardial iron is key to the clinical management of patients at risk of siderotic cardiomyopathy. The cardiovascular magnetic resonance (CMR) relaxation parameter R2* (assessed clinically via its reciprocal T2*) measured in the ventricular septum is used to assess cardiac iron, but iron calibration and distribution data in humans is limited. Twelve human hearts were studied from transfusion dependent patients following either death (heart failure n=7, stroke n=1) or transplantation for end-stage heart failure (n=4). After CMR R2* measurement, tissue iron concentration was measured in multiple samples of each heart using inductively coupled plasma atomic emission spectroscopy. Iron distribution throughout the heart showed no systematic variation between segments, but epicardial iron concentration was higher than in the endocardium. The mean (±SD) global myocardial iron causing severe heart failure in 10 patients was 5.98 ±2.42mg/g dw (range 3.19–9.50), but in 1 outlier case of heart failure was 25.9mg/g dw. Myocardial ln[R2*] was strongly linearly correlated with ln[Fe] (R2=0.910, p<0.001) leading to [Fe]=45.0•(T2*)−1.22 for the clinical calibration equation with [Fe] in mg/g dw and T2* in ms. Mid-ventricular septal iron concentration and R2* were both highly representative of mean global myocardial iron. These data detail the iron distribution throughout the heart in iron overload and provide calibration in humans for CMR R2* against myocardial iron concentration. The iron values are of considerable interest with regard to the level of cardiac iron associated with iron-related death and indicate that the heart is more sensitive to iron loading than the liver. The results also validate the current clinical practice of monitoring cardiac iron in-vivo by CMR of the mid septum.