SODIUM IMAGING IS ISCHEMIC HEART DISEASE

细胞内和细胞外钠离子和钾离子的交换对细胞的功能和完整性至关重要。在心脏中，来自动物和人类钾和钾类似物的放射性核素成像研究，以及动物模型的生化和磁共振波谱（MRS）研究的证据表明，钠-钾泵功能在心肌缺血期间受到损害，并且随着细胞内和细胞外池的平衡，它在无活力的梗死组织中丢失。钠（23Na）磁共振成像（MRI）是唯一能够成像和测量体内自然丰富的内源性钠的非侵入性。动物模型在b> 2.7特斯拉(T)磁场下的23Na MRI显示，在无活力、组织学证实的急性再灌注性心肌梗死（MI）中，23Na信号水平增加了2倍。23Na MRI具有较高的组织浓度和灵敏度，弛豫时间短，与磷（31P） MRI检测高能磷酸盐代谢物相比，具有巨大的灵敏度优势（约80倍）。因此，23Na MRI是通过改变缺血性心脏病和/或心肌梗死患者的钠水平来评估细胞代谢和离子功能的潜在独特而重要的工具。然而，目前在临床1.5T MRI扫描仪上还不能常规使用23Na。此外，人体23Na MRI从未受益于新的MRI硬件和软件技术。在初步研究中，我们在临床MRI扫描仪上实施了23Na MRI，并证明了心肌梗死中23Na MRI水平的改变。我们展示了通过31P MRS代谢检测应激性缺血患者的初步应力-23Na MRI数据。这里，我们建议在临床1.5 T MRI/MRS系统上开发和优化人类心脏23Na MRI，通过实施高速MRI， 23Na相控阵检测，利用先验解剖信息增强分辨率。以及抑制心室血23Na信号的方法。我们将使用优化的23Na MRI来表征正常和梗死的人类心肌，并验证23Na MRI可以通过放射性核素成像检测区分正常和非活性再灌注心肌的假设，并与对比增强MRI进行比较。此外，优化的23Na MRI可以检测能量受损心肌中应力诱导的钠变化的假设将在应力-23Na/ 31p联合代谢研究中得到验证。成千上万的临床MRI扫描仪的可用性为推进23Na MRI作为评估人类心脏病钠泵功能的工具提供了一个很好的机会。

The exchange of intra- and extra-cellular sodium and potassium ions is essential to cell function and integrity. In the heart, evidence from animal and human radionuclide imaging studies of potassium and potassium analogs, and from biochemical and magnetic resonance spectroscopy (MRS) studies of animal models, indicates that sodium- potassium pump function is compromised during periods of myocardial ischemia and that it is lost in non-viable, infarcted tissue as intra- and extra-cellular pools equilibrate. Sodium (23Na) magnetic resonance imaging (MRI) is uniquely able to image and measure noninvasively naturally abundant, endogenous sodium in the body. 23Na MRI at magnetic fields of > 2.7 Tesla (T) in animal models demonstrate a 2-fold increase in 23Na signal levels in nonviable, histologically-confirmed, acute reperfused myocardial infarction (MI). Owing to its higher tissue concentration and sensitivity and its short relaxation time, 23Na MRI has an enormous sensitivity advantage compared, for example, with the detection of high-energy phosphate metabolites by phosphorus (31P) MRI (approximately 80- fold). Thus 23Na MRI is a potentially unique and important tool for assessing cellular metabolic and ionic function through altered sodium levels in patients with ischemic heart disease and/or MI. Yet 23Na is not now routinely possible on clinical 1.5T MRI scanners. Moreover, human 23Na MRI has never benefitted from new MRI hardware and software technology. In preliminary studies we implemented 23Na MRI on a clinical MRI scanner, and demonstrate altered 23Na MRI levels in MI. We show preliminary stress-23Na MRI data from patients with stress-induced ischemia detected metabolically by 31P MRS. Here we propose to develop and optimize human cardiac 23Na MRI on a clinical 1.5 T MRI/MRS system, by implementing high-speed MRI, 23Na phased-array detection, resolution-enhancement using a priori anatomic information, and methods of suppressing 23Na signals from ventricular blood. We will use optimized 23Na MRI to characterize normal and infarcted human myocardium, and to test the hypotheses that 23Na MRI can differentiate normal from non-viable reperfused MI in patients as detected by radionuclide imaging, and compared with contrast- enhanced MRI. Further, the hypothesis that optimized 23Na MRI can detect stress-induced changes in sodium in energetically- compromised myocardium will be tested in combined stress-23Na/3 1P metabolic studies. The availability of thousands of clinical MRI scanners offers a great opportunity for advancing 23Na MRI as a tool for assessing sodium pump function in human heart disease.