IMAGING MYOCARDIAL PERFUSION WITH NMR

描述(改编自申请者摘要)：本研究的目标 是开发和验证新的磁共振成像方法来量化变化 在不使用外源性磁共振造影剂的情况下进行局部心肌灌注 媒体。我们提出了理论模型和实验协议来检测， 描述和利用由以下因素引起的本征核磁共振信号的变化 心肌潜在生理学的改变。这些信号， 它们产生于物理、化学、生物和 当心脏受到干扰时，生理变量会发生微妙的变化。 例如，观察到的纵向松弛时间(T1)可以是 对心肌灌注的变化敏感，从而适当地 T1加权图像可以制作成定量的血流灌注图。在……里面 此外，由于氧-和-的潜在磁性 脱氧血红蛋白，横向弛豫时间(T2*，T2)是固有的 对血液含氧量的变化敏感。初步结果表明， 本征核磁共振成像方法可以测量心肌血流储备。 动物和人类。 在这项拟议的研究中，研究人员首先试图证明 这些变化的幅度可以在血液灌流时预测，例如 活体，犬心脏模型在4.7T，其中重要的潜在基础 生理参数(血流量和血容量、血氧和 红细胞压积)可以控制或测量。跟随图像的优化 在1.5吨的质量，他们寻求利用这些变化来生产量化 完整猪血管扩张性(腺苷)应激的结果图 包括通过冠状动脉狭窄进行流量限制的模型。他们 假设他们可以使用以下任一方法测量局部心肌血流储备 血管扩张挑战下的T1或T2/T2*效应：T1的变化可能是 直接解释为流量变化，而T2变化是结果 由于最低限度的血流量增加而增加的血氧含量 耗氧量增加。申请者将优化成像 方法，确定哪种方法更有力地检测到 冠心病组动物模型的灌流储备 在正常人身上证明其可行性，以供后续研究 在疑似冠心病的患者中。

DESCRIPTION (Adapted from Applicant's Abstract): The goal of this research is to develop and validate novel MR imaging approaches to quantify changes in local myocardial perfusion without the use of exogenous MR contrast media. We propose theoretical models and experimental protocols to detect, characterize and exploit changes in the intrinsic NMR signals caused by changes in the underlying physiology of the myocardium. These signals, which arise from the interaction of physical, chemical, biological and physiological variables, are subtly altered when the heart is perturbed. For example, the observed longitudinal relaxation time (T1) can be sensitized to changes in myocardial perfusion, and thus appropriately T1-weighted images can be made into quantitative perfusion maps. In addition, due to the underlying magnetic properties of oxy- and deoxyhemoglobin, the transverse relaxation times (T2*, T2) are inherently sensitive to changes in blood oxygenation. Preliminary results suggest that intrinsic NMR imaging approaches can measure myocardial flow reserve in animals and in man. In the proposed research, the investigators seek first to demonstrate that the amplitude of these changes can be predicted in a blood-perfused, ex vivo, canine heart model at 4.7 T, in which the important underlying physiological parameters (blood flow and volume, blood oxygenation, and hematocrit) can be controlled or measured. Following optimization of image quality at 1.5 T, they seek to exploit these changes to produce quantitative maps of the results of vasodilatory (adenosine) stress, in an intact porcine model that includes flow limitation via coronary artery stenosis. They hypothesize that they can measure local myocardial flow reserve using either T1 or T2/T2* effects under vasodilatory challenge: T1 changes can be directly interpreted as flow changes, whereas the T2 changes are the result of an increase in blood oxygenation due to the increased flow with minimal increased oxygen consumption. The applicants will optimize the imaging methodologies, determine which method more robustly detects deficits in perfusion reserve in animal models of coronary artery disease and demonstrate its feasibility in normal human subjects for subsequent studies in patients with suspected coronary artery disease.