SODIUM IMAGING IS ISCHEMIC HEART DISEASE

细胞内外钠和钾离子的交换对细胞的功能和完整性是必不可少的。在心脏方面，来自动物和人类对钾和钾类似物的放射性核素成像研究，以及来自动物模型的生化和磁共振波谱(MRS)研究的证据表明，在心肌缺血期间，钠钾泵功能受到损害，随着细胞内和细胞外池的平衡，钠钾泵功能在不能存活的梗塞组织中丢失。钠(23Na)磁共振成像(MRI)是唯一能够非侵入性地成像和测量体内自然丰富的内源性钠的设备。在动物模型中，~GT；2.7特斯拉(T)磁场下的~(23)Na磁共振显示，在无法存活的、经组织学证实的急性再灌流性心肌梗死(MI)中，~(23)Na信号水平增加了2倍。由于其更高的组织浓度和灵敏度以及其较短的弛豫时间，23Na MRI具有巨大的敏感性优势，例如，与磷(31P)MRI检测高能磷酸盐代谢物相比(约80倍)。因此，~(23)Na磁共振成像是一种潜在的独特而重要的工具，可以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。然而，现在临床1.5T核磁共振扫描仪上常规使用23Na是不可能的。此外，人类23Na核磁共振从未受益于新的核磁共振硬件和软件技术。在初步研究中，我们在临床MRI扫描仪上进行了~(23)Na磁共振成像，并展示了心肌梗死患者~(23)Na磁共振成像水平的改变。我们展示了由~(31)P-MRS代谢检测的应激性心肌缺血患者的初步~(23)Na MRI数据。在此，我们提出在临床1.5T MRI/MRS系统上开发和优化人的心脏~(23)Na MRI，通过实施高速MRI、~(23)Na相控阵检测、利用先验解剖信息的分辨率增强以及抑制来自脑室血的~(23)Na信号的方法。我们将使用优化的~(23)Na MRI来表征正常和梗死的人体心肌，并检验~(23)Na MRI能够区分放射性核素成像检测的正常和死亡再灌注性心肌梗死的假设，并与增强MRI进行比较。此外，优化的~(23)Na核磁共振可以检测到能量受损心肌中钠的变化的假设将在联合的压力-~(23)Na/3~1P代谢研究中得到验证。数以千计的临床MRI扫描仪的出现为推动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.