CORONARY MICROCIRCULATION-ACUTE MYOCARDIAL INFARCTION

描述(申请人的逐字描述)：尽管管理有所改善 治疗急性心肌梗死的策略，仍然是正确选择这些策略的患者 在它的初级阶段。其中一个主要原因是使用了不敏感的标记 临床环境中的急性冠脉闭塞、再灌注和梗塞。 急性心肌梗死患者常规应用EKG和心肌酶 价格低廉且易于执行，限制了我们选择个人的能力 为患者量身定做治疗。例如，我们仍然使用EKG来诊断 尽管只有三分之一到五分之二的急性心肌梗死患者有 入院时的诊断性EKG。我们使用的是心肌酶 用于确认急性心肌梗死，但这些在几个小时后转为阳性 冠状动脉闭塞，在确定立即处理方面价值不大 急性心肌梗死患者的治疗策略。梗塞面积不能大于 危险区域(冠状动脉闭塞后低灌注区)。 如果风险区域很小，溶栓治疗可能不值得冒险， 血管成形术可能不值得这样做。如果有足够的抵押品MBF 在将维持心肌存活的危险区域内，立即 干预甚至可能没有必要。另一方面，如果溶栓治疗 未能实现组织再灌注，用或不用药物抢救血管成形术 这可能表明限制了微血管损伤。最后，跨壁画 脑梗塞的范围可能决定哪位患者将从ACE中获益最多 抑制剂。目前，我们没有对患者进行分层优化 他们的待遇。 我们假设，通过对慢性心肌梗死患者的心肌微血管成像 疑似急性心肌梗死我们可以：1)检测急性心肌梗死并确定最终的梗塞范围 尽管有持续性的冠状动脉闭塞。2)决定组织的成败 再灌流及静脉注射腺苷对心肌梗死的影响 冠状动脉微血管灌注量和梗塞面积。3)确定 急性心肌梗死后微血管异常程度对左心室重构的影响 血管紧张素转换酶抑制剂对血管重塑的影响；4) 确定正常和异常微血管的长期预后价值 急性心肌梗死首次治疗后的血流灌注模式。 我们将使用心肌造影剂来研究心肌微血管。 超声心动图，一种新开发的技术，可以提供无创的 人类心肌微血管系统的评估。这项研究的目标是 在疑似急性心肌梗死患者中验证上述4种假说。

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.