BACKGROUND Both ischemic and non-ischemic heart disease can cause disturbances in the myocardial blood volume (MBV), myocardial perfusion and the myocardial extracellular volume fraction (ECV). Recent studies suggest that native myocardial T1 mapping can detect changes in MBV during adenosine stress without the use of contrast agents. Furthermore, native T2 mapping could also potentially be used to quantify changes in myocardial perfusion and/or MBV. Therefore, the aim of this study was to explore the relative contributions of myocardial perfusion, MBV and ECV to native T1 and native T2 at rest and during adenosine stress in normal physiology. METHODS Healthy subjects (n = 41, 26 ± 5 years, 51% females) underwent 1.5 T cardiovascular magnetic resonance (CMR) scanning. Quantitative myocardial perfusion [ml/min/g] and MBV [%] maps were computed from first pass perfusion imaging at adenosine stress (140 microg/kg/min infusion) and rest following an intravenous contrast bolus (0.05 mmol/kg, gadobutrol). Native T1 and T2 maps were acquired before and during adenosine stress. T1 maps at rest and stress were also acquired following a 0.2 mmol/kg cumulative intravenous contrast dose, rendering rest and stress ECV maps [%]. Myocardial T1, T2, perfusion, MBV and ECV values were measured by delineating a region of interest in the midmural third of the myocardium. RESULTS During adenosine stress, there was an increase in myocardial native T1, native T2, perfusion, MBV, and ECV (p ≤ 0.001 for all). Myocardial perfusion, MBV and ECV all correlated with both native T1 and native T2, respectively (R2 = 0.35 to 0.61, p < 0.001 for all). Multivariate linear regression revealed that ECV and perfusion together best explained the change in native T2 (ECV beta 0.21, p = 0.02, perfusion beta 0.66, p < 0.001, model R2 = 0.64, p < 0.001), and native T1 (ECV beta 0.50, p < 0.001, perfusion beta 0.43, p < 0.001, model R2 = 0.69, p < 0.001). CONCLUSIONS Myocardial native T1, native T2, perfusion, MBV, and ECV all increase during adenosine stress. Changes in myocardial native T1 and T2 during adenosine stress in normal physiology can largely be explained by the combined changes in myocardial perfusion and ECV. TRIAL REGISTRATION Clinicaltrials.gov identifier NCT02723747. Registered March 16, 2016.

中文翻译：

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正常生理状态下静息时和腺苷应激期间心肌灌注、血容量和细胞外容量对天然 T1 和天然 T2 的相对贡献。


背景技术缺血性和非缺血性心脏病均可引起心肌血容量(MBV)、心肌灌注和心肌细胞外体积分数(ECV)的紊乱。最近的研究表明，天然心肌 T1 标测可以在不使用造影剂的情况下检测腺苷应激期间 MBV 的变化。此外，天然 T2 映射也可能用于量化心肌灌注和/或 MBV 的变化。因此，本研究的目的是探讨正常生理中休息时和腺苷应激期间心肌灌注、MBV 和 ECV 对天然 T1 和天然 T2 的相对贡献。方法 健康受试者（n = 41，26 ± 5 岁，51% 女性）接受 1.5 T 心血管磁共振 (CMR) 扫描。定量心肌灌注 [ml/min/g] 和 MBV [%] 图根据腺苷应激（140 µg/kg/min 输注）和静脉注射造影剂（0.05 mmol/kg，钆布醇）后休息时的首过灌注成像计算得出。天然 T1 和 T2 图是在腺苷应激之前和期间获得的。 0.2 mmol/kg 累积静脉造影剂剂量后还获得了静息和应激时的 T1 图，绘制了静息和应激 ECV 图 [%]。通过在心肌的中壁三分之一处描绘感兴趣区域来测量心肌 T1、T2、灌注、MBV 和 ECV 值。结果 在腺苷应激期间，心肌天然 T1、天然 T2、灌注、MBV 和 ECV 均增加（全部 p ≤ 0.001）。心肌灌注、MBV 和 ECV 均分别与天然 T1 和天然 T2 相关（R2 = 0.35 至 0.61，p < 0.001）。多元线性回归显示，ECV 和灌注共同最好地解释了天然 T2 的变化（ECV beta 0.21，p = 0.02，灌注 beta 0.66，p < 0.001，模型 R2 = 0.64，p < 0.001）和天然 T1（ECV beta 0.50，p < 0.001，灌注 beta 0.43，p < 0.001，模型 R2 = 0.69，p < 0.001）。结论 在腺苷应激期间，心肌天然 T1、天然 T2、灌注、MBV 和 ECV 均增加。正常生理中腺苷应激期间心肌天然 T1 和 T2 的变化在很大程度上可以通过心肌灌注和 ECV 的综合变化来解释。试验注册 ClinicalTrials.gov 标识符 NCT02723747。 2016 年 3 月 16 日注册。