Role of transcytolemmal water-exchange in magnetic resonance measurements of diffuse myocardial fibrosis in hypertensive heart disease.
Role of transcytolemmal water-exchange in magnetic resonance measurements of diffuse myocardial fibrosis in hypertensive heart disease.
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DOI：
10.1161/circimaging.112.979815
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发表时间：
2013-01-01
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影响因子：
--
通讯作者：
Jerosch-Herold M
中科院分区：
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作者：
Coelho-Filho OR;Mongeon FP;Mitchell R;Moreno H Jr;Nadruz W Jr;Kwong R;Jerosch-Herold M
心肌细胞外容积分数（MECVF）已被用于检测弥漫性纤维化。MECVF的估计依赖于对比增强后T1弛豫时间的定量，这对平衡的跨细胞膜水交换敏感。我们假设，MECVF，量化与简约的2空间水交换模型，与结缔组织体积分数（CTVF）在啮齿动物模型的高血压心脏病，而广泛使用的分析的基础上假设快速transytolemmal水交换可能会导致一个显着低估的MECVF。分别对22只和15只野生型小鼠给予Nω-硝基-L-精氨酸甲酯（L-NAME）或安慰剂。在基线和7周随访时，使用双空间水交换模型，在4.7 T下通过对比前后T1 CMR成像测量MECVF。使用Masson三色染色定量CTVF。与对照组相比，L-NAME诱导肥大（体重指数LV质量2.2±0.3 vs. 4.1±0.4 µg/g，p<0.001），并增加CTVF（8.6%±1.5 vs. 2.58%±0.6，p<0.001）。L-NAME治疗组的MECVF更高（0.43±0.09 vs，0.26±0.03，p<0.001），并与CTVF和重量指数LV质量相关（分别为r=0.842和r=0.737，均P<0.0001）。忽略跨细胞膜水交换造成了显着低估的MECVF的变化。10例有高血压病史的患者的MECVF（0.446±0.063）显著高于健康对照组（0.307±0.030，p<0.001）。CMR允许在小鼠模型和有高血压病史的患者中检测心肌细胞外基质扩张。与假设快速的细胞膜水交换相比，考虑细胞膜水交换的影响可能导致MECVF的实质性差异。
The myocardial extracellular volume fraction (MECVF) has been used to detect diffuse fibrosis. Estimation of MECVF relies quantification of the T1 relaxation time after contrast enhancement, which can be sensitive to equilibrium transcytolemmal water exchange. We hypothesized that MECVF, quantified with a parsimonious 2-space water-exchange model, correlates positively with the connective tissue volume fraction (CTVF) in a rodent model of hypertensive heart disease, while the widely used analysis based on assuming fast transcytolemmal water exchange could result in a significant underestimate of MECVF. Nω–nitro-L-arginine-metyl-ester (L-NAME) or placebo was administered to 22 and 15 wild-type mice, respectively. MECVF was measured at baseline and 7-week follow-up by pre- and post-contrast T1 CMR imaging at 4.7 T, using a 2-space water-exchange model. CTVF was quantified, using Masson’s trichrome stain. L-NAME induced hypertrophy (weight-indexed LV mass 2.2±0.3 vs. 4.1±0.4 µg/g, p<0.001), and increased CTVF (8.6%±1.5 vs. 2.58%±0.6, p<0.001), compared to controls. MECVF was higher in L-NAME-treated animals (0.43±0.09 vs, 0.26±0.03, p<0.001), and correlated with CTVF and weight-indexed LV mass (r=0.842 and r=0.737 respectively, both P<0.0001). Neglecting transcytolemmal water-exchange caused a significant underestimate of MECVF changes. Ten patients with history of hypertension had significantly higher MECVF (0.446±0.063) compared to healthy controls 0.307±0.030, p<0.001). CMR allowed detection of myocardial extracellular matrix expansion in a mouse model, and in patients with a history of hypertension. Accounting for the effects of transcytolemmal water exchange can result in a substantial difference of MECVF, compared to assuming fast transcytolemmal water exchange.