Bertolet B D, Hill J A, Pepine C J
Department of Medicine, University of Florida Health Sciences Center, Gainesville.
Prog Cardiovasc Dis. 1992 Sep-Oct;35(2):97-118. doi: 10.1016/0033-0620(92)90002-h.
Recent investigations of SMI occurring during daily life have advanced our understanding of the pathophysiology of myocardial ischemia. These contributions have directed our attention away from "chest pain" alone and physical exertion as the central provoking factor toward transient myocardial ischemia and its broader triggers and consequences. Transient myocardial ischemic episodes, the majority of which are silent, are found in a subset of patients with any clinical manifestations of CAD (eg, stable angina, unstable angina, myocardial infarction, and sudden death), as well as in those patients with CAD who are and have been totally asymptomatic. These episodes are an independent predictor of increased risk for future cardiac events. Most medical therapy and revascularization therapies have the potential to prevent or relieve these silent episodes; however, we do not yet know which method is superior in reducing SMI episodes or preventing future cardiac events. Furthermore, the benefit of reducing SMI versus the cost and potential morbidity of these chosen therapies is not known. At least three trials are now underway to examine some of these concerns (Table 2). Focus on pain relief alone does not appear to be an adequate approach to alter outcome in patients with CAD and may prove insufficient to control SMI. Until these issues are resolved, we believe a conservative approach to the management of patients with CAD is warranted. Documentation of ischemia (painful or painless) is essential. Three general principles should be kept in mind. First, the presence of detectable ischemia is of central importance. This information should be used in the overall risk assessment of the patient. Second, the level of concern or aggressiveness of treatment should be based on the risk associated with the ischemic abnormalities documented (Table 3). The exercise stress test is the most useful to begin this process. The detection of ischemic-type ST-segment depression, either silent or painful, at a low workload (eg, less than or equal to 120 beats per minute or less than or equal to 6.5 metabolic equivalents [METS]) implies high risk for adverse outcome. Likewise, these ST-segment changes occurring in leads that reflect multiple coronary artery distribution, of greater than 2 mm in magnitude and persisting for greater than 6 minutes, are all markers for high risk. Thallium redistribution defects occurring at low work loads, in multiple areas, associated with increased lung uptake and enlargement of the cardiac pool all imply high risk.(ABSTRACT TRUNCATED AT 400 WORDS)
近期对日常生活中发生的无症状心肌缺血（SMI）的研究，加深了我们对心肌缺血病理生理学的理解。这些研究成果使我们的注意力从仅关注“胸痛”和体力活动这一主要诱发因素，转向短暂性心肌缺血及其更广泛的触发因素和后果。短暂性心肌缺血发作，其中大多数是无症状的，在患有任何冠心病临床表现（如稳定型心绞痛、不稳定型心绞痛、心肌梗死和猝死）的患者亚组中发现，也在那些曾经完全无症状的冠心病患者中发现。这些发作是未来心脏事件风险增加的独立预测因素。大多数药物治疗和血运重建治疗都有可能预防或缓解这些无症状发作；然而，我们尚不知道哪种方法在减少SMI发作或预防未来心脏事件方面更具优势。此外，减少SMI的益处与这些所选治疗的成本和潜在发病率之间的关系尚不清楚。目前至少有三项试验正在进行，以研究其中一些问题（表2）。仅关注疼痛缓解似乎不是改变冠心病患者预后的充分方法，可能不足以控制SMI。在这些问题得到解决之前，我们认为对冠心病患者采取保守的管理方法是必要的。记录缺血情况（有痛或无痛）至关重要。应牢记三个一般原则。首先，检测到缺血的存在至关重要。该信息应用于患者的整体风险评估。其次，治疗的关注程度或积极程度应基于所记录的缺血异常相关的风险（表3）。运动负荷试验是开始这一过程最有用的方法。在低负荷（例如，每分钟小于或等于120次心跳或小于或等于6.5代谢当量[METS]）时检测到无症状或有症状的缺血型ST段压低，意味着不良后果的高风险。同样，在反映多支冠状动脉分布的导联中出现的这些ST段改变，幅度大于2mm且持续超过6分钟，都是高风险的标志。在低负荷下多个区域出现的铊再分布缺陷，伴有肺摄取增加和心腔扩大，都意味着高风险。（摘要截断于400字）
