POSITRON TOMOGRAPHY IN ISCHEMIC HEART DISEASE
POSITRON TOMOGRAPHY IN ISCHEMIC HEART DISEASE
批准号:
3344787
负责人:
HEINRICH R SCHELBERT
金额:
$43.78万
依托单位国家:
美国
项目类别:
财政年份:
1984
资助国家:
美国
项目状态:
已结题
起止时间:
1984-12-01 至 1994-11-30
关键词:
acyl carrier protein blood pressure carbon cardiovascular disorder chemotherapy chronic disease /disorder coronary bypass coronary sinus disease /disorder model edema extracellular matrix fluorine glucose metabolism glucose transport heart contraction heart rate human subject hypertension intraluminal angioplasty muscle necrosis myocardial infarction myocardial ischemia /hypoxia nitrogen positron emission tomography radionuclides radiotracer scars vascular endothelium permeability ventricular hypertrophy
中文摘要
拟议研究的统一主题是血流代谢
用正电子发射断层扫描观察到的不匹配作为
缺血性心脏病患者的心肌存活性。 最初
根据我们实验室的报告,这种模式的存在已经被
已被其他调查人员证实,并正在被其他调查人员雇用。 然而,在这方面,
关于保存葡萄糖的潜在病理生理学的问题
功能障碍心肌的代谢及其临床相关性仍然存在。
拟议的研究将采用新开发的非侵入性方法,
定量局部血流速度、葡萄糖利用率、氧气
消耗,蛋白质合成和脂肪酸代谢的评价
并绘制这些过程的空间分布图,
确定异常的地理范围和严重程度。 这将是
通过高时间和空间分辨率的正电子发射
动脉输入功能和心肌摄取的断层成像
N-13氨、F-18 2-脱氧葡萄糖、C-11棕榈酸酯、C-11乙酸酯和C-11
标记的氨基酸。 新型PET扫描仪的多切片功能
将进一步用于定义这些的空间分布
在左心室心肌的功能过程。 有了这些工具,
这项研究将探索和定义可能
解释了观察到的血流代谢不匹配模式,
“冬眠”与“昏迷”的例子描述了相关的异常
在血流中,氧化代谢和脂肪酸氧化及其
与局部和整体左心室功能的关系。 研究
将进一步研究这些代谢性疾病的预后意义,
冠状动脉疾病患者的异常,
慢性乙型肝炎患者代谢异常及其时空变化
缺血性心脏病或急性心肌梗死后,
介入恢复血流后恢复。 这项研究将
还可以确定缺血、缺血后和缺血后蛋白质合成的速率,
冠心病患者治疗前后正常心肌的变化
冠状动脉介入治疗和急性心肌梗死后。 结果
很可能为人类的病理生理学提供新的见解。
心肌缺血,并应证明在临床上同样适用于改善
更准确地描述缺血性脑血管病的严重程度和范围,
受损心肌以及患者的治疗决策
冠状动脉疾病和局部和整体左心室
功能障碍
英文摘要
The unifying theme of the proposed research is the blood flow metabolism
mismatch as observed with position emission tomography as a sign of
myocardial viability in patients with ischemic heart disease. Initially
reported from our laboratory, the existence of this pattern has been
confirmed by and is now being employed by other investigators. However,
questions regarding the underlying pathophysiology of preserved glucose
metabolism in dysfunctional myocardium and its clinical relevance remain.
The proposed research will employ newly developed noninvasive methods for
quantifying regional rates of blood flow, glucose utilization, oxygen
consumption, protein synthesis and for evaluation of fatty acid metabolism
and for mapping the spatial distribution of these processes and to
determine geographic extent and severity of abnormalities. This will be
accomplished by high temporal and spatial resolution positron emission
tomographic imaging of the arterial input function and myocardial uptake of
N-13 ammonia, F-18 2-deoxyglucose, C-11 palmitate, C-11 acetate and C-11
labeled amino acids. The multi-slice capability of the new PET scanner
will further be used for defining the spatial distribution of these
functional process in the left ventricular myocardium. With these tools,
the research will explore and define different mechanisms that might
account for the observed blood flow metabolism mismatch pattern as for
example "hibernation" versus "stunning" delineate associated abnormalities
in blood flow, oxidative metabolism and fatty acid oxidation and their
relation to regional and global left ventricular function. The research
will further examine the prognostic significance of these metabolic
abnormalities in patients with coronary artery disease who are of these
metabolic abnormalities and their temporal and spatial changes in chronic
ischemic heart disease or after an acute myocardial infarction and their
recovery after interventional restoration of blood flow. The research will
also determine rates of protein synthesis in ischemic, post-ischemic and
normal myocardium in patients with coronary artery disease before and after
coronary interventions and after acute myocardial infarction. The results
are likely to provide new insights into the pathophysiology of human
myocardial ischemia and should prove clinically equally useful for improved
and more accurate delineation of severity and extent of ischemically
compromised myocardium as well as for therapeutic decisions in patients
with coronary artery disease and regional and global left ventricular
dysfunction.
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POSITRON TOMOGRAPHY IN ISCHEMIC HEART DISEASE
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资助金额:$7.34万
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依托单位:
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批准号:6200200
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依托单位:
海外基金