Objective In a proof-of-concept study, to quantify myocardial viability in patients with acute myocardial infarction using manganese-enhanced MRI (MEMRI), a measure of intracellular calcium handling. Methods Healthy volunteers (n=20) and patients with ST-elevation myocardial infarction (n=20) underwent late gadolinium enhancement (LGE) using gadobutrol and MEMRI using manganese dipyridoxyl diphosphate. Patients were scanned ≤7 days after reperfusion and rescanned after 3 months. Differential manganese uptake was described using a two-compartment model. Results After manganese administration, healthy control and remote non-infarcted myocardium showed a sustained 25% reduction in T1 values (mean reductions, 288±34 and 281±12 ms). Infarcted myocardium demonstrated less T1 shortening than healthy control or remote myocardium (1157±74 vs 859±36 and 835±28 ms; both p<0.0001) with intermediate T1 values (1007±31 ms) in peri-infarct regions. Compared with LGE, MEMRI was more sensitive in detecting dysfunctional myocardium (dysfunctional fraction 40.5±11.9 vs 34.9%±13.9%; p=0.02) and tracked more closely with abnormal wall motion (r2=0.72 vs 0.55; p<0.0001). Kinetic modelling showed reduced myocardial manganese influx between remote, peri-infarct and infarct regions, enabling absolute discrimination of infarcted myocardium. After 3 months, manganese uptake increased in peri-infarct regions (16.5±3.5 vs 22.8±3.5 mL/100 g/min, p<0.0001), but not the remote (23.3±2.8 vs 23.0±3.2 mL/100 g/min, p=0.8) or infarcted (11.5±3.7 vs 14.0±1.2 mL/100 g/min, p>0.1) myocardium. Conclusions Through visualisation of intracellular calcium handling, MEMRI accurately differentiates infarcted, stunned and viable myocardium, and correlates with myocardial dysfunction better than LGE. MEMRI holds major promise in directly assessing myocardial viability, function and calcium handling across a range of cardiac diseases. Trial registration numbers [NCT03607669][1]; EudraCT number 2016-003782-25. All data relevant to the study are included in the article or uploaded as online supplemental information. [1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT03607669&atom=%2Fopenhrt%2F8%2F1%2Fe001646.atom

中文翻译：

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使用锰增强 MRI 评估顿抑和存活的心肌

目的 在一项概念验证研究中，使用锰增强 MRI (MEMRI) 量化急性心肌梗死患者的心肌活力，MEMRI 是细胞内钙处理的一种测量方法。方法 健康志愿者 (n=20) 和 ST 段抬高型心肌梗死患者 (n=20) 使用钆布醇进行晚期钆增强 (LGE)，使用二吡哆醇二磷酸锰进行 MEMRI。患者在再灌注后 ≤ 7 天接受扫描，并在 3 个月后重新扫描。使用二室模型描述不同的锰吸收。结果 锰给药后，健康对照和远处未梗死的心肌显示 T1 值持续降低 25%（平均降低，288±34 和 281±12 ms）。梗塞心肌表现出比健康对照或远端心肌更少的 T1 缩短（1157±74 vs 859±36 和 835±28 ms；两者 p < 0.0001），在梗塞周围区域具有中间 T1 值（1007±31 ms）。与 LGE 相比，MEMRI 在检测功能障碍心肌方面更敏感（功能障碍分数 40.5±11.9 vs 34.9%±13.9%；p=0.02）并且更密切地跟踪异常室壁运动（r2=0.72 vs 0.55；p<0.0001）。动力学模型显示远程、梗塞周围和梗塞区域之间的心肌锰流入减少，从而能够绝对区分梗塞心肌。3 个月后，梗死周围区域的锰摄取增加（16.5±3.5 vs 22.8±3.5 mL/100 g/min，p<0.0001），但远端区域（23.3±2.8 vs 23.0±3.2 mL/100 g/min）没有增加, p=0.8) 或梗塞 (11.5±3.7 vs 14.0±1.2 mL/100 g/min, p>0.1) 心肌。结论 MEMRI 通过细胞内钙处理的可视化，准确地区分梗死心肌、顿抑心肌和存活心肌，并且与心肌功能障碍的相关性优于 LGE。MEMRI 在直接评估一系列心脏病的心肌活力、功能和钙处理方面具有重要前景。试用注册号[NCT03607669][1]；EudraCT 编号 2016-003782-25。与研究相关的所有数据都包含在文章中或作为在线补充信息上传。[1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT03607669&atom=%2Fopenhrt%2F8%2F1%2Fe001646.atom MEMRI 在直接评估一系列心脏病的心肌活力、功能和钙处理方面具有重要前景。试用注册号[NCT03607669][1]；EudraCT 编号 2016-003782-25。与研究相关的所有数据都包含在文章中或作为在线补充信息上传。[1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT03607669&atom=%2Fopenhrt%2F8%2F1%2Fe001646.atom MEMRI 在直接评估一系列心脏病的心肌活力、功能和钙处理方面具有重要前景。试用注册号[NCT03607669][1]；EudraCT 编号 2016-003782-25。与研究相关的所有数据都包含在文章中或作为在线补充信息上传。[1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT03607669&atom=%2Fopenhrt%2F8%2F1%2Fe001646.atom