Institute of Diagnostic and Interventional Radiology, University Hospital Zurich, Switzerland; Institute of Forensic Medicine, University of Zurich, Switzerland.
NMR Biomed. 2014 Jul;27(7):795-801. doi: 10.1002/nbm.3119. Epub 2014 Apr 16.
The aim of this study was to quantify the response of the myocardial transverse relaxation times (ΔT2*) to hyperoxic respiratory challenge (HRC) at different field strengths in an intra-individual comparison of healthy volunteers and in a patient with coronary artery disease. Blood oxygenation level-dependent (BOLD) cardiovascular MR (CMR) data were acquired in 10 healthy volunteers (five women, five men; mean age, 29 ± 3 years; range, 22-35 years) at 1.5 and 3.0 T. Medical air (21% O2 ), pure oxygen and carbogen (95% O2 , 5% CO2 ) were administered in a block-design temporal pattern to induce normoxia, hyperoxia and hyperoxic hypercapnia, respectively. Average T2* times were derived from measurements by two independent and blind readers in 16 standard myocardial segments on three short-axis slices per patient. Inter- and intra-reader correlations of T2* measurements were good [intra-class correlation coefficient (ICC) = 0.75 and ICC = 0.79, both p < 0.001]. During normoxia, the mean T2* times were 29.9 ± 6.1 ms at 1.5 T and 27.1 ± 6.6 ms at 3.0 T. Both hyperoxic gases induced significant (all p < 0.01) T2* increases (∆T2* hyperoxia: 1.5 T, 12.7%; 3.0 T, 11.2%; hyperoxic hypercapnia: 1.5 T, 13.1%; 3.0 T, 17.7%). Analysis of variance (ANOVA) results indicated a significant (both p < 0.001) effect of the inhaled gases on the T2* times at both 1.5 T (F = 17.74) and 3.0 T (F = 39.99). With regard to the patient imaged at 1.5 T, HRC induced significant T2* increases during hyperoxia and hyperoxic hypercapnia in normal myocardial segments, whereas the T2* response was not significant in ischemic segments (p > 0.23). The myocardial ∆T2* response to HRC can reliably be imaged and quantified with BOLD CMR at both 1.5 and 3.0 T. During HRC, hyperoxia and hyperoxic hypercapnia induce a significant increase in T2*, with ∆T2* being largest at 3.0 T and during hyperoxic hypercapnia in normal myocardial segments.
这项研究的目的是在健康志愿者的个体内比较和冠心病患者中，定量测量心肌横向弛豫时间（ΔT2*）对高氧呼吸挑战（HRC）的反应，比较在不同场强下的变化。在 10 名健康志愿者（5 名女性，5 名男性；平均年龄 29 ± 3 岁；范围 22-35 岁）中，在 1.5 和 3.0 T 进行了基于血氧水平依赖（BOLD）的心血管磁共振（CMR）数据采集。采用块设计时间模式分别给予医用空气（21% O2）、纯氧和碳化氧（95% O2，5% CO2），以分别诱导正常氧合、高氧合和高氧合高碳酸血症。在每个患者的三个短轴切片上的 16 个标准心肌节段中，由两位独立和盲法读者进行测量得出平均 T2时间。T2测量的组内和组间相关性良好[组内相关系数（ICC）= 0.75 和 ICC = 0.79，均 p < 0.001]。在正常氧合时，1.5 T 时的平均 T2时间为 29.9 ± 6.1 ms，3.0 T 时为 27.1 ± 6.6 ms。两种高氧气体均引起显著（均 p < 0.01）的 T2增加（1.5 T 时的 ∆T2高氧：12.7%；3.0 T 时为 11.2%；高氧合高碳酸血症：1.5 T 时为 13.1%；3.0 T 时为 17.7%）。方差分析（ANOVA）结果表明，吸入气体对 1.5 T（F = 17.74）和 3.0 T（F = 39.99）的 T2时间均有显著影响（均 p < 0.001）。对于在 1.5 T 成像的患者，在正常心肌节段中，HRC 在高氧合和高氧合高碳酸血症期间诱导显著的 T2增加，而在缺血节段中 T2*的反应不显著（p > 0.23）。BOLD CMR 可在 1.5 和 3.0 T 可靠地成像和定量测量 HRC 引起的心肌 ∆T2反应。在 HRC 期间，高氧合和高氧合高碳酸血症引起 T2显著增加，在 3.0 T 时和正常心肌节段中的高氧合高碳酸血症时，ΔT2最大。
