CORONARY MICROCIRCULATION-ACUTE MYOCARDIAL INFARCTION

描述（申请人的描述逐字）：尽管改善了管理 对于AMI的治疗策略，为这些策略正确选择患者仍然是 在它的幼年期。其中一个主要原因是使用不敏感的标记物， 急性冠状动脉闭塞、再灌注和临床环境中的梗死。 常规使用心电图和心肌酶的AMI患者，虽然 廉价和易于执行，限制了我们选择个人的能力， 患者进行个性化治疗。例如，我们仍然使用心电图来诊断 尽管只有三分之一到五分之二的AMI患者 诊断性心电图我们用心肌酶 但这些在几小时后变成阳性， 冠状动脉闭塞，在确定立即管理方面价值不大 AMI患者的治疗策略。梗死面积不能大于 危险区域（冠状动脉闭塞后灌注不足的区域）。 如果风险区域较小，溶栓可能不值得冒险， 血管成形术可能不值得花费。如果有足够的抵押品， 在维持心肌存活的风险区域内， 甚至可能不需要干预。另一方面，如果溶栓 无法实现组织再灌注，使用或不使用药物进行补救血管成形术 限制微血管损伤。最后，跨壁 梗死范围可能决定哪种患者将从ACE中获益最多 抑制剂.目前，我们没有以优化的方式对患者进行分层， 他们的待遇。 我们假设，通过对心肌微血管成像， 对于疑似AMI，我们可以：1）检测AMI并确定最终梗死面积 尽管冠状动脉持续闭塞2)确定组织的成功 再灌注和腺苷静脉给药的影响， 冠状动脉微血管灌注和梗死面积。3)确定影响的 AMI后微血管异常程度对左室重构的影响， 引起血管生成的ACE抑制剂对这种重塑的影响;以及4） 确定正常和异常微血管的长期预后价值 急性心肌梗死初始治疗后的灌注模式。 我们将用心肌造影剂研究心肌微血管 超声心动图，一种新开发的技术，可以提供一个非侵入性的 评估人类心肌微血管。研究的目的是 在疑似AMI患者中检验上述4个假设。

DESCRIPTION (The applicant's description verbatim): Despite improved management strategies for AMI, proper selection of patients for these strategies is still in its infancy. One of the main reasons is the use of insensitive markers of acute coronary occlusion, reperfusion, and infarction in the clinical setting. Routine use of the EKG and cardiac enzymes in patients with AMI, although inexpensive and easy to perform, has limited our ability to select individual patients for customized treatment. For instance, we still use EKG to diagnose AMI despite the fact that only one-third to two-fifth of all AMI patients have a diagnostic EKG at the time of hospital presentation. We use cardiac enzymes for the confirmation of AMI, but these become positive several hours after coronary occlusion, and are of little value in determining immediate management strategies for patients with AMI. The infarct size can be no larger than the risk area (the region with hypoperfusion after a coronary artery is occluded). If the risk area is small, thrombolysis may not be worth the risk and angioplasty may not be worth the cost. If there is adequate collateral MBF within the risk area that will maintain myocardial viability, immediate intervention may not even be necessary. On the other hand, if thrombolysis fails to achieve tissue reperfusion, rescue angioplasty with or without a drug that limits microvascular injury may be indicated. Finally, the transmural extent of infarction may determine which patient will most benefit from an ACE inhibitor. At present, we do not stratify patients in a manner to optimize their treatment. We hypothesize that by imaging the myocardial microvasculature in patients with suspected AMI we can: 1) detect AMI and determine the ultimate infarct size despite persistent coronary occlusion. 2) Determine the success of tissue reperfusion and the effect of intravenous administration of adenosine on coronary microvascular perfusion and infarct size. 3) Determine the effect of the extent of microvascular abnormalities after AMI on LV remodeling and the effect of an ACE inhibitor that causes angiogenesis on this remodeling; and 4) Determine the long-term prognostic value of normal and abnormal microvascular perfusion patterns after the initial management of AMI. We will study the myocardial microvascular using myocardial contrast echocardiography, a newly developed technique that can provide a noninvasive assessment of the myocardial microvasculature in humans. The study aims will be to test the 4 above-mentioned hypotheses in patients with suspected AMI.