CAUSES OF TRANSIENT ISCHEMIA IN ANGINAL PATIENTS WITH CD

冠状动脉疾病可导致心绞痛、脑梗塞和猝死 短暂性脑缺血是这些症状的基础，可能预示着 脑室受损。动态心电图监测缺血性ST段压低的临床意义 仔细描述的患者最近表明，短暂性脑缺血 活动并不表现为疼痛，它比症状更频繁 大多数情况下都没有明显的心率增加， 这表明，传统的触发机制，如运动，并不 在日常生活中频繁操作。这项研究有三个短期目标：1) 我们计划在医院外研究短暂性脑缺血。 心绞痛和阻塞性冠状动脉疾病患者的定量研究 外在刺激因素的相对重要性(例如，心理唤醒， 运动，寒冷)来对抗心肌缺血的内在触发因素，即， 与任何外部环境无关的事件。2)具有以下特点 在每个患者的相关触发机制中，我们计划使用定量 血管造影术和血流动力学监测以描述这些影响 导致缺血和血管狭窄的触发机制 描述导致缺血反应的事件顺序。3)在 特征相似的患者，我们计划测试某些特定的细胞 动脉粥样硬化性冠状动脉病变的机制，例如， 评估内皮依赖性血管运动的丧失，并寻找 对某些生理性血管收缩药的敏感性异常增加 药物作为心肌缺血的可能原因。在寻找 短暂性脑缺血的原因，长期目标包括： 确定内部触发和外部触发的相对重要性 确定是否需要操纵外部机制的机制 有利于短暂性脑缺血。此外，更重要的是，我们寻求 认识动脉粥样硬化与细胞活性的关系 冠状动脉病变和血管运动功能障碍导致 缺血症。这项研究寻求完整的病理生理机制 患有不能在动物实验室复制的疾病的患者。 另一方面，我们计划使用从基本 实验室(如内皮依赖性血管运动)以便在人体内进行测试 动脉粥样硬化病变活动性与功能性的关系 导致临床缺血的后果。

Coronary artery disease can cause angina, infarction and sudden death and transient ischemia underlies these symptoms and may herald the onset of ventricular damage. Holter monitoring of ischemic ST segment depression in carefully characterized patients has shown recently that transient ischemic activity is not represented by pain, it is much more frequent than symptoms would suggest and occurs mostly with no appreciable increase in heart rate, suggesting that the traditional trigger mechanisms such as exercise do not operate frequently in everyday life. This study has 3 short-term aims: 1) we plan to study transient ischemia out of hospital in characterized patients with angina and obstructive coronary disease to quantify the relative importance of extrinsic provocative factors (eg; mental arousal, exercise, cold) as against intrinsic triggers of myocardial ischemia, i.e., events unrelated to any external circumstances. 2) Having characterized the relevant trigger mechanism in each patient, we plan to use quantitative angiography and monitoring of hemodynamics to describe the effects of these trigger mechanisms on the stenosed vessels responsible for ischemia and describe the sequence of events leading to the ischemic response. 3) In similarly characterized patients, we plan to test certain specific cellular mechanisms in the atherosclerotic coronary lesions, that will, for example, assess the loss of endothelial dependent vasomotion and look for the abnormal increase in sensitivity to certain physiological vasoconstrictor agents as possible causes of myocardial ischemia. In looking for the causes of transient ischemia, the long-term aims consist firstly of determining the relative importance of internal and external trigger mechanisms to identify if external mechanisms need to be manipulated to benefit transient ischemia. In addition and more importantly, we seek to understand the relationship between the cellular activiy of atherosclerotic coronary lesions and the functional disturbances of vasomotion that lead to ischemia. This research seeks pathophysiological mechanisms in intact patients with a disease that cannot be reproduced in an animal laboratory. On the other hand, we plan to use concepts arising from the basic laboratory (eg; endothelial dependent vasomotion) in order to test in man the relationship between atherosclerotic lesion activity and functional consequences causing clinical ischemia.