NATURAL HISTORY OF MILDLY SYMPTOMATIC CORONARY ARTERY DISEASE

我们以前已经证明左心室射血分数 - （EF）在休息和运动期间分层患者轻度 症状性冠状动脉疾病（CAD），根据风险 多支冠状动脉疾病和死亡的过程中的药物治疗。到 确定EF随时间的后续变化是否意味着重要变化 在冠状动脉解剖学方面，我们研究了90例有轻度症状的两个冠状动脉病变的患者， 血管造影，时间跨度2 - 12年（平均5年）的药物治疗和连续 每1 - 2年进行一次静息和运动时的放射性核素血管造影， 停用所有抗缺血药物。我们观察到CAD的进展 冠状动脉造影在左室功能无变化的情况下是罕见的 在休息或锻炼时。然而，进步的CAD开发在大多数 表现出静息EF降低或 EF对运动的反应，即使心绞痛没有进展 症状在后一种患者中， 新发冠状动脉完全阻塞或新发左主干阻塞 狭窄 这些数据使我们能够解决另一个问题， CAD和诱导性缺血的轻度症状患者。我们发现 静息状态下左心室功能随时间推移而恶化的情况很少见， 新的100%冠状动脉阻塞，即使是在重复的患者 心肌缺血反复发作的证据。因此， 心肌缺血本身似乎并不倾向于 无CAD解剖学进展时发生LV功能障碍 在人类身上。

We have previously demonstrated that left ventricular (LV)ejection fraction -(EF) at rest and during exercise stratifies patients with mildly symptomatic coronary artery disease (CAD) according to the risk of multivessel CAD and of death during the course of medical therapy. To determine if subsequent changes in EF with time signify important changes in coronary anatomy, we studied 90 mildly symptomatic pts with two coronary angiograms spanning 2-12 yr (mean 5 yr) of medical therapy and with serial radionuclide angiograms at rest and during exercise every 1-2 yrs, after withdrawal of all anti-ischemic drugs. We observed that progression of CAD by coronary arteriography was rare in the absence of changes in LV function at rest or exercise. However, progressive CAD developed in the majority of patients manifesting either a reduction in resting EF or a deterioration in the EF response to exercise, even in the absence of progression of anginal symptoms. In these latter patients, there was also a high likelihood of the development of new total coronary artery obstructions or new left main stenoses. These data allowed us to address another issue that has been raised in mildly symptomatic patients with CAD and inducible ischemia. We found that it was rare for LV function at rest to deteriorate with time in the absence of a new 100% coronary artery obstruction, even in patients with repeated evidence of recurrent episodes of myocardial ischemia. Thus, recurrent myocardial ischemia, in and of itself, does not appear to predispose to the development of LV dysfunction in the absence of anatomic progression of CAD in humans.