Bleske B E, Shea M J
College of Pharmacy, University of Michigan, Ann Arbor.
Clin Pharm. 1990 May;9(5):339-57.
The definition, pathogenesis, incidence and characteristics, detection, treatment, and prognosis of silent myocardial ischemia (SMI) are reviewed. SMI is the occurrence of myocardial ischemia for which there is objective evidence (electrophysiological, hemodynamic, and metabolic changes) but no angina. Patients with SMI are classified as type 1 (completely asymptomatic), type 2 (SMI after myocardial infarction), and type 3 (both symptomatic and silent ischemia). Episodes of SMI are true ischemic events. The absence of pain may be due to defects in pain perception, an altered physiological response to ischemia, or a lesser degree of ischemia. The incidence of SMI is 2-5% in totally asymptomatic patients, 20-30% in patients who have suffered myocardial infarction, and 44-84% in patients who have symptomatic ischemia. SMI can be detected by exercise testing, portable electrocardiographic monitoring, or imaging techniques. Patients with SMI have more frequent adverse cardiac events (except death) than patients without SMI. The frequency of adverse cardiac events is similar in patients with angina and patients with SMI. SMI has been treated with nitrates, calcium-channel blockers, and beta blockers. Beta blockers appear to be the most consistent in reducing the number and duration of episodes. Combination therapy with beta blockers and nifedipine may be more effective than therapy with either agent alone. Because of the limited number of studies and the possible contribution to the results of spontaneous variability in the occurrence of SMI, no definite conclusions can be drawn about drug efficacy. There is no evidence that the prognosis of patients with SMI is altered by drug therapy; routine treatment with anti-ischemic drugs cannot be recommended. Patients must be evaluated individually, with aggressive management being reserved for those at high risk for myocardial infarction or other serious cardiac events.
本文综述了无症状心肌缺血(SMI)的定义、发病机制、发病率及特征、检测、治疗和预后。SMI是指存在客观证据(电生理、血流动力学和代谢变化)但无心绞痛的心肌缺血情况。SMI患者分为1型(完全无症状)、2型(心肌梗死后出现SMI)和3型(既有症状性缺血又有无症状性缺血)。SMI发作是真正的缺血事件。无疼痛可能是由于疼痛感知缺陷、对缺血的生理反应改变或缺血程度较轻。完全无症状患者中SMI的发病率为2% - 5%,心肌梗死患者中为20% - 30%,有症状性缺血患者中为44% - 84%。SMI可通过运动试验、便携式心电图监测或成像技术检测。与无SMI的患者相比,SMI患者发生不良心脏事件(死亡除外)的频率更高。有症状性缺血患者和SMI患者发生不良心脏事件的频率相似。SMI的治疗药物有硝酸盐类、钙通道阻滞剂和β受体阻滞剂。β受体阻滞剂在减少发作次数和持续时间方面似乎最为一致。β受体阻滞剂与硝苯地平联合治疗可能比单一药物治疗更有效。由于研究数量有限以及SMI发生的自发变异性可能对结果产生影响,关于药物疗效尚无明确结论。没有证据表明药物治疗能改变SMI患者的预后;不建议常规使用抗缺血药物治疗。必须对患者进行个体化评估,对于心肌梗死或其他严重心脏事件高危患者应采取积极治疗措施。